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University of California • Berkeley

Regional Oral History Office
The Bancroft Library

University of California
Berkeley, California

The San Francisco AIDS Oral History Series

THE AIDS EPIDEMIC IN SAN FRANCISCO: THE MEDICAL RESPONSE, 1981-1984

Volume IV

Donald P. Francis, M.D., D.Sc,

Merle A. Sande, M.D.

John L. Ziegler, M.D., Ph.D.

EPIDEMIOLOGIST, CENTERS FOR DISEASE
CONTROL: DEFINING AIDS AND ISOLATING
THE HUMAN IMMUNODEFICIENCY VIRUS (HIV)

INFECTIOUS DISEASE SPECIALIST: AIDS
TREATMENT AND INFECTION CONTROL AT SAN
FRANCISCO GENERAL HOSPITAL

ONCOLOGIST: KAPOSI'S SARCOMA AND AIDS
RESEARCH IN SAN FRANCISCO AND GLOBALLY

Introduction by James Chin, M.D., M.P.H.

Interviews Conducted by

Sally Smith Hughes

in 1993 and 1994

Since 1954 the Regional Oral History Office has been interviewing leading
participants in or well-placed witnesses to major events in the development of
Northern California, the West, and the Nation. Oral history is a method of
collecting historical information through tape-recorded interviews between a
narrator with firsthand knowledge of historically significant events and a well-
informed interviewer, with the goal of preserving substantive additions to the
historical record. The tape recording is transcribed, lightly edited for
continuity and clarity, and reviewed by the interviewee. The corrected
manuscript is indexed, bound with photographs and illustrative materials, and
placed in The Bancroft Library at the University of California, Berkeley, and in
other research collections for scholarly use. Because it is primary material,
oral history is not intended to present the final, verified, or complete
narrative of events. It is a spoken account, offered by the interviewee in
response to questioning, and as such it is reflective, partisan, deeply involved,
and irreplaceable.

************************************

This manuscript is made available for research purposes. All
literary rights in the manuscript, including the right to publish,
are reserved to The Bancroft Library of the University of
California, Berkeley. No part of the manuscript may be quoted for
publication without the written permission of the Director of The
Bancroft Library of the University of California, Berkeley.

Requests for permission to quote for publication should be
addressed to the Regional Oral History Office, 486 Library,
University of California, Berkeley 94720, and should include
identification of the specific passages to be quoted, anticipated
use of the passages, and identification of the user.

It is recommended that this oral history be cited as follows:

To cite the volume: The AIDS Epidemic in San
Francisco: The Medical Response, 1981-1984, Volume IV,
an oral history conducted in 1993 and 1994, Regional
Oral History Office, The Bancroft Library, University
of California, Berkeley, 1997.

To cite an individual interview: [ex.] Donald P.
Francis, M.D., "Epidemiologist, Centers for Disease
Control: Defining AIDS and Isolating the Human
Immunodeficiency Virus (HIV)," an oral history
conducted in 1993 and 1994 by Sally Smith Hughes,
Ph.D., in The AIDS Epidemic in San Francisco: The
Medical Response, 1981-1984, Volume IV, Regional Oral
History Office, The Bancroft Library, University of
California, Berkeley, 1997.

Copy no.

Cataloguing information

THE AIDS EPIDEMIC IN SAN FRANCISCO: THE MEDICAL RESPONSE, 1981-1984
Volume IV, 1997, xv, 369 pp.

Donald P. Francis. M.D., D.Sc. (b. 1942), epidemiologist, Centers for
Disease Control (CDC), 1971-1989: early research with the Ebola virus;
first reports of the AIDS epidemic; defining AIDS; risk groups for AIDS;
politics and the CDC; isolating the human immunodeficiency virus (HIV);
blood screening and blood safety issues; civil rights versus public health.
Merle A. Sande, M.D. (b. 1939), infectious disease specialist; professor of
medicine, UC San Francisco (UCSF), and chief of medical services, San
Francisco General Hospital (SFGH), 1980-1996: infection control concerns;
guidelines for AIDS health workers; UCSF Task Force on AIDS; the AIDS
outpatient clinic and inpatient ward at SFGH; AIDS treatment; physician-
patient relationship; AIDS Clinical Research Forum; the San Francisco model
of AIDS care.

John L. Ziegler. M.D., Ph.D. (b. 1938) oncologist; chief of staff, Veterans
Administration Medical Center and UCSF professor of medicine: Kaposi's
sarcoma in gay men (early cases); the Kaposi's Sarcoma Study Group; the
etiology of Kaposi's sarcoma; founding the AIDS Clinical Research
Center (s); the Kaposi's Sarcoma Clinic at UCSF; AIDS research activities
and funding; treating AIDS-related lymphomas and opportunistic infections;
recognizing a global epidemic; theories of etiology of AIDS and of Kaposi's
sarcoma.

Introduction by James Chin, M.D., M.P.H., Clinical Professor of
Epidemiology, School of Public Health, University of California, Berkeley.

Interviews conducted 1993 and 1994 by Sally Smith Hughes, Ph.D. for the San
Francisco AIDS Oral History Series. The Regional Oral History Office, The
Bancroft Library, University of California, Berkeley.

ACKNOWLEDGEMENTS

The Regional Oral History Office wishes to express deep gratitude to

Evelyne and David Lennette of Virolab, Inc., for their financial support of

this project, incisive conceptual contributions, and sustaining interest
and enthusiasm.

TABLE OF CONTENTS--The History of the AIDS Epidemic in San Francisco: The
Medical Response, 1981-1984, Volume IV

PREFACE- -by David and Evelyne Lennette i
SERIES INTRODUCTION- -by James Chin iii
SERIES HISTORY- -by Sally Smith Hughes vi

INTERVIEW WITH DONALD P. FRANCIS, M.D., D.SC.
INTERVIEW HISTORY- -by Sally Smith Hughes
BIOGRAPHICAL INFORMATION

I FAMILY BACKGROUND, EDUCATION, AND EARLY CAREER 1
Early Education 1
Employment by the Centers for Disease Control 2

State Epidemiologist, U.S. Agency for International
Development, River's State, Nigeria, January- June

1971 2

Epidemic Intelligence Service Officer, Oregon State

Health Division, July 1971-December 1972 2

Smallpox in Yugoslavia, 1971 2

Smallpox Eradication in Sudan, India, and Bangladesh,

January 1973-June 1975 3

Research Fellow in Pediatrics, Harvard Medical School,
and Doctoral Student, Department of Microbiology,
Harvard School of Public Health, July 1975-November

1979 A
Research with Max Essex 5
Ebola Virus in Sudan, 1976 6
Learning Laboratory Technology 10

Assistant Director for Medical Science, Hepatitis and
Enteritis Division, CDC, Phoenix, Arizona, July 1978-

September 1983 11

Viruses and Cancer 12

Robert Gallo 13
Hepatitis B Vaccine Trials in the United States, 1979-

1980 13
Hepatitis B Vaccine Trials in China, 1982-1985 15

II THE AIDS EPIDEMIC 16
First Reports 16
The CDC Task Force on AIDS 17
Defining the Epidemic 18
Resource Crisis 20
Risk Groups 22
Problems in Communicating Data 23

The Reagan Administration's Slow Response 28

Research at the Phoenix Laboratory 29

The Move to the Centers for Disease Control in Atlanta 30

The Laboratory 32

Suspecting a Retrovirus 33

Isolation of the AIDS Virus 36

Associations with the Pasteur Institute 36

Cold Spring Harbor Meeting on HTLV, September 1983 38

Laboratory Procedures for the AIDS Virus 39

The Pasteur Group's Approach to the AIDS Virus 40
Chermann's Presentations in the U.S., February 1984 42

Distributing CDC Virus Specimens 43
Meeting at the Pasteur Institute, Early April 1984 44

V. "Kaly" Kalyanaraman 45

Mikulas Popovic's Pooling of AIDS Sera 48

Problems with Robert Gallo 48
Attempting to Coordinate NIH, CDC, and Pasteur

Institute Work on AIDS 49

Announcing the Cause of AIDS, April 23, 1984 50

Controversy and the AIDS Research Community 53

Gallo, HTLV-III, and LAV 55

The Effect on Science of Identifying the Virus 56

The Blood Banks and Blood Screening 60

Irwin Memorial Blood Bank and Hepatitis B Core Antigen

Screening 60

The January 4, 1983 Meeting at CDC on Blood Safety 61

Resistance from Blood Bankers 63

Governmental Responsibility 66

AIDS in Africa 69

Early Perceptions of AIDS 70

Risk Groups 71

The Behavioral Approach 72

AIDS in Women and Children 74

AIDS Testing 76

Isolating and Sequencing the Virus 77

The NIH-CDC Relationship 79

AIDS Units at CDC 81

Government Accounting Office Audit of CDC AIDS Activities,

1983 84

Communicating on AIDS 87

Expedited Publication 87

Censorship 88

Dealing with the Media 88

Defining AIDS 89

Broadening the Definition 89

Defining AIDS as HIV Infection 91

Including Women's Symptoms 92

Coining the Term AIDS 93

The HIV Antibody Test 94

Screening Blood Samples, 1984 94

The Issue of Safety 95

Testing Advocate 96

Contact Tracing and Partner Notification 97

Civil Rights versus Public Health 98

Community Input 99
CDC Advisor to the California Department of Health

Services, 1985-1989 101

Politicization 103

Political Interference with CDC 105

Failure at the Federal Level 107

The Epidemic's Personal Impact 109

The Epidemic's Impact on Medicine 111

AIDS and Cof actors 112

Heterosexual AIDS 113

Future Issues 114

INTERVIEW WITH MERLE A. SANDE, M.D.

INTERVIEW HISTORY- -by Sally Smith Hughes
BIOGRAPHICAL INFORMATION

I FAMILY BACKGROUND, EDUCATION, *ND EARLY CAREER 117
Early Education 117
Medical School, Internship, and Residency 117
Interest in Infectious Diseases 118
Faculty Member, Division of Infectious Diseases, University

of Virginia School of Medicine, 1971-1979 119
Professor of Medicine, San Francisco General Hospital,

University of California, San Francisco, 1980-present 120

Recruitment 120

The Setting at San Francisco General 120

II THE AIDS EPIDEMIC 124
Preparation for the Epidemic 124
First AIDS Patient 125
Infection Control 126

Initial Concerns 126

UCSF Task Force on AIDS 127

Reports of Low Infectivity 129
Julie Gerberding and the AIDS Health Care Workers

Study, 1983-present 130
The UCSF AIDS Task Force Infection Control

Guidelines, 1983 132

The Infected Health Care Worker 134

Implications of the David Acer Case 135

CDC Recommendations 135

The AIDS Outpatient Clinic, SFGH 136

The AIDS Clinical Research Forum, SFGH 137

Political Involvement 138

Medical Advisory Committee for AIDS, San Francisco

Department of Public Health 139

The Bathhouses 139

The Mayor's Task Force on AIDS 140

Mayor Dianne Feinstein 142

The AIDS Clinic and Ward, SFGH 144

Formation 144

Coordinating the Clinic and Ward 146

The AIDS Ward 147

Holistic Treatment of AIDS Patients 148

More on the AIDS Clinical Research Forum 150

Formation and Membership 150

Compound Q 151

NIH Visitors 152

Defining AIDS 153

CDC Epidemiology 156

Political Pressure 156

More on AIDS Activities at the VA 256

Early Research and Clinical Work 256

AIDS Activities from 1985 On 257

Seeing Patients 258

Laboratory Tests 259

The AIDS Specimen Bank, UCSF 260

Association with the Gay Community 261

A New Experience 261

Chairman, Sixth International Conference on AIDS,

San Francisco, June 20-24, 1990 262

NCI (National Cancer Institute) 264
Hypothesis: Separate Agents for AIDS and Kaposi's

Sarcoma 264

Early Grants for AIDS Activities 266

B-Cell Immunodeficiency in AIDS and Immuno stimulation 268

AIDS: An Autoimmune Disease 269

AIDS Education 271

Alternative Therapy 272

The San Francisco Model of AIDS Care 272

The Personal Impact of the Epidemic 273

The Epidemic's Impact on Health Care and Research 274

275

APPENDICES

A. AIDS Chronology, 1981-1985 277

B. Key Participants in San Francisco AIDS History, 1981-1984 290

C. Biographical Sketch and Curriculum Vitae, Donald P. Francis,
M.D., D.Sc. 293

D. Curriculum Vitae, Merle A. Sande, M.D. 307

E. Declaration of Merle Sande, M.D., dated October 10, 1984 329

F. Curriculum Vitae, John L. Ziegler, M.D. 338

INDEX

355

PREFACE--by David A. Lennette, Ph.D., and Evelyne T. Lennette, Ph.D.

As two young medical virologists working in Pennsylvania, we
experienced first hand some of the excitement of medical detective work.
We had our first glimpse of how personalities can shape the course and
outcome of events during the swine influenza and Legionnaires' disease
outbreaks.

On our return to California, we were soon embroiled in another much
more frightening epidemic. In 1981, our laboratory began receiving samples
for virologic testing from many of the early San Francisco AIDS patients--
whose names are now recorded in Randy Shilts1 book And the Band Played On.
Our previous experience with the legionellosis outbreak had primed us for
this new mystery disease. While the medical and scientific communities
were hotly debating and coping with various issues during the following
three years, we were already subconsciously framing the developments in an
historical point of view. In San Francisco, dedicated junior physicians
and researchers banded together to pool resources and knowledge out of
necessity, and in doing so, organized part of the local medical community
in a very unusual way. Once again, we were struck by how the personalities
of each of these individuals shaped the course of events. Even before HIV
was discovered, we knew we were witnessing a new page in the history of
science and medicine.

The swine flu and legionellosis outbreaks were both very local and
short lived. We now speak of them in the past tense. The AIDS epidemic,
sadly, is still spreading unimpeded in much of the world. We know that it
will be with us for a long time and that it is very unlikely that either of
us will live long enough to read the closing chapter on AIDS.

Future generations will some day want to know how it all got started.
The existing scientific reports and publications provide depersonalized
records of some of the events, while newspaper articles and books give
glimpses as summarized by observers. What are missing are the
participants' own accounts and perspectives.

It is now more than a dozen years after the recognition of the AIDS
epidemic in the United States. So much has happened and changed--already,
some of the participants in early events have retired, records are being
discarded and destroyed, and memories of those days are beginning to fade.
We felt their oral histories had to be recorded without delay.

We had previously sponsored oral histories on virology with Dr. Edwin
H. Lennette, David's father, and Dr. Harald N. Johnson, and were familiar
with the methods and work of the Regional Oral History Office. We met to
talk over the recording of the AIDS epidemic with Willa Baum, head of the
office, and Dr. Sally Smith Hughes, medical history interviewer. After

some discussion, we agreed that the events from 1981-1984 needed to be
documented and we would fund it. This was a time when many crucial
decisions on the clinical, public health, social, and political issues
pertaining to AIDS were made with little scientific information and no
precedents to rely on. The consequences of many of these decisions are
still being felt today. With the discovery of HIV, however, the framework
for decision making shifted to different ground, and a pioneering phase was
over. Once we decided on the scope of the project, it was a simple task to
identify prospective interviewees, for we worked with many of these
individuals during those years.

Dr. Sally Hughes has shared our enthusiasm from the beginning. We
are pleased that her efforts are now coming to fruition.

David A. Lennette, Ph.D.
Evelyne T. Lennette, Ph.D.

November 1994
Virolab, Inc.
Berkeley, California

iii

SERIES INTRODUCTION- -by James Chin, M.D., M.P.H.

As the California state epidemiologist responsible for communicable
disease control from the early 1970s to the late 1980s, I had the privilege
and opportunity to work with all of the participants who were interviewed
for the San Francisco AIDS Oral History Project. I consider it an honor to
have been asked to provide a brief introduction to the role that these
individuals played in the history of AIDS in San Francisco during the early
years. Before I begin, the following quote from Dr. James Curran, in a
December 1984 issue of the San Francisco Chronicle sums up what has
happened to all of the participants in this oral history project:

I ' d like to sound more upbeat about this , but
there are some unavoidable facts we need to face.
AIDS is not going away. Gay men don't want to hear
that. Politicians don't want to hear that. I
don't like to hear that. But for many of us, AIDS
could well end up being a lifelong commitment.

The first recognized cases of AIDS were reported in the Morbidity and
Mortality Weekly Report (MMWR) on June 5, 1981. I recall this report
vividly. A few months earlier, the Centers for Disease Control (CDC) had
begun sending an advance copy of the MMWR text to state health departments.
The advance text of the June 5 MMWR had a lead article on the sudden and
unexplained finding of five apparently unrelated cases of Pneumocystis
carinii pneumonia in five young gay men from Los Angeles. The MMWR text
was received in my office just before our weekly Tuesday afternoon staff
meeting was to start. I handed the text to Tom Ault, who was responsible
for the state's venereal disease field unit and asked him to have some of
our federal- or state-assigned staff in Los Angeles assist in the
investigation of these cases. I remember saying to him that it may not
turn out to be much of anything, but it may be the start of something. I
never imagined that that something would eventually develop into a
worldwide epidemic of disease and death.

In the ensuing weeks and months, it became apparent that the
mysterious illness reported from Los Angeles was also present among gay men
in San Francisco. From 1981 to 1984, the numbers of AIDS cases reported
from San Francisco rose almost exponentially—from a handful in mid- 1981 to
well over 800 towards the end of 1984. The impact that AIDS has had in San
Francisco is unequaled on a per capita basis anywhere in the developed
world. If the AIDS prevalence rate of about one AIDS case per 1,000
population that was present in San Francisco at the end of 1984 was applied
nationally, then there would have been about a quarter of a million AIDS
cases nationwide instead of the 7,000 that were actually reported. During
the first few years of what was initially referred to as GRID (gay-related
immune deficiency), there was general denial of the severity of this newly

recognized mystery disease even in San Francisco. The enormity of the AIDS
problem was first fully accepted by the gay community in San Francisco, and
physicians and researchers in the city rapidly became the leading experts
in the country on the medical management, prevention, and control of AIDS.
In contrast to Los Angeles and New York, which also have had large
concentrations of AIDS cases, the gay community in San Francisco has been
more unified and organized in developing political and community support
for the treatment and care of AIDS patients.

The epidemiology of AIDS, namely, that it is caused primarily by a
sexually transmitted agent, was fairly well established by 1983, well
before HIV was eventually isolated and etiologically linked to AIDS in
1984. Public health investigations in San Francisco, spearheaded by Selma
Dritz in 1981 and 1982, provided much of the key epidemiologic data needed
to understand the transmission and natural history of HIV infection. The
more formal epidemiological studies of AIDS among gay men in San Francisco
were carried out by Andrew Moss at San Francisco General Hospital (SFGH)
and Warren Winkelstein at the University of California at Berkeley. All of
these studies were helpful to Mervyn Silverman (who during this period was
director of the San Francisco Department of Public Health) to support his
decision in October 1984 to close the San Francisco bathhouses. Selma
Dritz retired from her position with the health department in 1984, and
Mervyn Silverman has moved on to become the premier HIV/AIDS frequent flier
in his current position as president of the American Foundation for AIDS
Research, which is now supporting studies internationally.

Jay Levy was an established virologist when AIDS was first detected
and reported in 1981. His laboratory isolated and characterized a virus
which he initially called ARV--AIDS Related Virus. He continues to play a
prominent role in the quest to better understand the pathogenesis of HIV.
Herbert Perkins was the scientific director of the Irwin Memorial Blood
Bank in San Francisco during the critical period around 1982-1985 when data
began accumulating to indicate that the cause of AIDS might be an
infectious agent which could be transmitted via blood. Under his
direction, the Irwin Memorial Blood Bank in May 1984 was the first blood
bank in the country to begin routine surrogate testing of blood units for
the AIDS agent using a hepatitis B core antibody test. He retired as
director of Irwin Memorial in April 1993, but remains very much involved in
defending the blood bank from legal suits arising from transmission of HIV
via blood transfusions during the early years. Don Francis did not work in
California during the early 1980s, but directed epidemiologic and
laboratory studies on AIDS as the first head of the AIDS laboratory at CDC
in Atlanta during this time period. Following his request to become more
directly involved with field work and HIV/AIDS program and policy
development, he was assigned to work in my office in Berkeley in 1985. Don
took an early retirement from CDC in 1992 and continues to actively work in
the San Francisco Bay Area as well as nationally and internationally on the
development of an AIDS vaccine.

The clinical staffs of San Francisco General Hospital and the
University of California at San Francisco established the two earliest AIDS
clinics in the country, and in 1983, Ward 5B at SFGH was set up exclusively
for AIDS patients. In the early 1980s, Don Abrams and Paul Volberding were
two young physicians who found themselves suddenly thrust into full-time
care of AIDS patients, a responsibility which both are still fully involved
with. As a result of their positions, experience, and dedication, both are
acknowledged national and international experts on the drug treatment of
HIV and AIDS patients. Merle Sande, John Ziegler, Arthur Ammann, and
Marcus Conant were already well established and respected clinicians,
researchers, and teachers when AIDS was first detected in San Francisco.
Their subsequent work with HIV/AIDS patients and research has earned them
international recognition. The Greenspans, Deborah and John, have
established themselves as the foremost experts on the oral manifestations
of HIV/AIDS, and Constance Wofsy is one of the leading experts on women
with HIV/AIDS. There is rarely a national or international meeting or
conference on AIDS where most, if not all, of these San Francisco clinical
AIDS experts are not present and speaking on the program. The number of
HIV/AIDS clinicians and research scientists from San Francisco invited to
participate in these medical and scientific meetings usually far exceeds
those from any other city in the world. All of these individuals have made
tremendous contributions to the medical and dental management of HIV/AIDS
patients in San Francisco and throughout the world.

As of late 1994, more than a decade since the advent of AIDS in San
Francisco, Jim Curran's remark in 1984 that "...for many of us, AIDS could
well end up being a lifelong commitment" has been remarkably accurate for
virtually all the participants in this San Francisco AIDS Oral History
Project.

James Chin, M.D., M.P.H.

Clinical Professor of Epidemiology

School of Public Health,

University of California at Berkeley

September 1994
Berkeley, California

SERIES HISTORY- -by Sally Smith Hughes, Ph.D.

Historical Framework

In 1991, Evelyne and David Lennette, virologists and supporters of
previous Regional Oral History Office (ROHO) projects in virology and
horticulture, conceived the idea for an oral history series on AIDS. They
then met with Willa Baum (ROHO director) and me to discuss their idea of
focusing the series on the medical and scientific response in the early
years (1981-1984) of the AIDS epidemic in San Francisco, believing that the
city at this time played a particularly formative role in terms of AIDS
medicine, organization, and policy. Indeed San Francisco was, with New
York and Los Angeles, one of the three focal points of the epidemic in the
United States, now sadly expanded worldwide.

The time frame of the oral history project is historically
significant. Nineteen eighty-one was the year the epidemic—not until the
summer of 1982 to be officially christened "AIDS"--was first recognized and
reported. A retrovirus was isolated in 1983, and by early 1985, diagnostic
tests were being marketed. These achievements signaled a turning point in
the response to the epidemic. Its science shifted from a largely
epidemiological approach to one with greater emphasis on the laboratory.
As soon as the virus was determined, scientific teams in the United States
and Europe raced to characterize it in molecular terms. Information about
the molecular biology of the human immunodeficiency virus (HIV), as it was
named, was in turn expected to transform AIDS medicine by providing a basis
for treatment and prevention of the disease through new drugs and vaccines.

San Francisco continued to make important contributions to combating
the epidemic, but by early 1985 it had lost its pioneering role. The AIDS
test showed that the epidemic reached far beyond the three original
geographic centers and involved large numbers of symptomless HIV-positive
individuals, who were not identifiable prior to the test's advent. AIDS
funding increased; the number and location of AIDS researchers expanded;
research interest in the newly identified virus took center stage. San
Francisco's salient position in the AIDS effort faced competition from new
players, new research interests, and new institutions. The first phase of
the epidemic was history.

Project Structure

Within the limits of funding and the years of the project (1981-
1984), the Lennettes suggested eight potential interviewees whom they knew
to have played important medical and scientific roles in the early years of
the San Francisco epidemic. (Both Lennettes have close connections with
the local AIDS research community, and Evelyne Lennette was a scientific
collaborator of three interviewees in this series, Jay Levy and John and

vii

Deborah Greenspan.) I then consulted Paul Volberding, an oncologist at San
Francisco General Hospital with an international reputation as an AIDS
clinician. He and others in the oral history series made several
suggestions regarding additional interviewees, expanding my initial list to
fourteen individuals.1 My reading of primary and secondary sources and
consultation with other authorities confirmed the historical merit of these
choices.

The series consists of two- to ten-hour interviews with seventeen
individuals in epidemiology, virology, public health, dentistry, and
several medical specialties. By restricting phase one to San Francisco's
early medical and scientific response to the epidemic, we aim to provide
in-depth documentation of a major aspect, namely the medicine and science
it generated in a given location, at a given time, under near-crisis
conditions. Like any human endeavor, medicine and science are embedded in
the currents of the time. As these oral histories so graphically
illustrate, it is impossible to talk about science and medicine without
relating them to the social, political, and institutional context in which
they occur. One of the strengths of oral history methodology is precisely
this.

This concentration on physicians and scientists is of course elitist
and exclusive. There is a limit—practical and f inancial--to what the
first phase of a project can hope to accomplish. It was clear that the
series needed to be extended. Interviews for phases two and three of the
oral history project, a series with AIDS nurses and a third with community
physicians with AIDS practices, have been completed and serve to broaden
the focus. The long-range plan is to interview representatives of all
sectors of the San Francisco community which contributed to the medical and
scientific response to AIDS, thereby providing balanced coverage of the
city's biomedical response.

Primary and Secondary Sources

This oral history project both supports and is supported by the
written documentary record. Primary and secondary source materials provide
necessary information for conducting the interviews and also serve as
essential resources for researchers using the oral histories. They also
orient scholars unfamiliar with the San Francisco epidemic to key
participants and local issues. Such guidance is particularly useful to a

1 A fifteenth was added in 1994, when the UCSF AIDS Clinical Research
Center provided partial funding for interviews with Warren Winkelstein,
M.D., M.P.H., the epidemiologist directing the San Francisco Men's Health
Study. A sixteenth and seventeenth, with Lloyd "Holly" Smith, M.D., and
Rudi Schmid, M.D., were recorded in 1995 when the UCSF Academic Senate
allocated funds for transcription.

viii

researcher faced with voluminous, scattered, and unorganized primary
sources, characteristics which apply to much of the AIDS material. This
two-way "dialogue" between the documents and the oral histories is
essential for valid historical interpretation.

Throughout the course of this project, I have conducted extensive
documentary research in both primary and secondary materials. I gratefully
acknowledge the generosity of Drs. Arthur Ammann, Marcus Conant, John
Greenspan, Herbert Perkins, Warren Winkelstein, and John Ziegler in opening
to me their personal documents on the epidemic. Dr. Frances Taylor,
director of the Bureau of Infectious Disease Control at the San Francisco
Department of Public Health, let me examine documents in her office related
to closure of city bathhouses in 1984. Sally Osaki, executive assistant to
the director of the health department, gave me access to documents from
former Mayor Dianne Feinstein's papers on her AIDS activities. I am
grateful to both of them.

Dr. Victoria Harden and Dennis Rodrigues of the NIH Historical Office
assisted by sending correspondence and transcripts of a short telephone
interview with John Ziegler, which Rodrigues conducted.1 I thank Dr. James
Chin for his introduction to this series, which describes his first-hand
experience of the epidemic as state epidemiologist at the California
Department of Health Services where he was responsible for communicable
disease control. I also thank Robin Chandler, head of Special Collections,
UCSF Library, and Bill Walker, former archivist of UCSF's AIDS History
Project and the San Francisco Gay and Lesbian Historical Society, for their
assistance in accessing these rich archival collections.

The foregoing sources have been crucial in grounding the interviews
in specifics and in opening new lines of questioning. A source to be
noted, but untapped by this project, is the California AIDS Public Policy
Archives, which is being coordinated by Michael Gorman, Ph.D., at San
Francisco General Hospital.

Of the wealth of secondary historical sources on AIDS, the most
pertinent to this project is Randy Shilts1 And the Band Played On.2
Although criticized for its political slant, it has been invaluable in
providing the social, political, and ideological context of early AIDS
efforts in San Francisco, particularly in regard to San Francisco's gay
community.

1 Telephone interview by Dennis Rodrigues with John L. Ziegler, M.D.,
January 5, 1990. Tapes and transcripts of the interview are available in
the NIH Historical Office, Bethesda, MD.

2 Randy Shilts. And the Band Played On: Politics, People, and the
AIDS Epidemic. New York: Penguin Books, 1988.

Oral History Process

The oral history methodology used in this project is that of the
Regional Oral History Office, founded in 1954 and producer of over 1,400
archival oral histories. The method consists of background research in
primary and secondary sources; systematic recorded interviews;
transcription, editing by the interviewer, and review and approval by the
interviewee; deposition in manuscript libraries of bound volumes of
transcripts with table of contents, introduction, interview history, and
index; cataloging in national on-line library networks (MELVYL, RLIN, and
OCLC); and publicity through ROHO news releases and announcements in
scientific, medical, and historical journals and newsletters and via the
UCSF Library web page (http://www.library.ucsf.edu/).

Oral history as an historical technique has been faulted for its
reliance on the vagaries of memory, its distance from the events discussed,
and its subjectivity. All three criticisms are valid; hence the necessity
for using oral history documents in conjunction with other sources in order
to reach a reasonable historical interpretation.1 Yet these acknowledged
weaknesses of oral history, particularly its subjectivity, are also its
strength. Often individual perspectives provide information unobtainable
through more traditional sources. For example, oral history in skillful
hands provides the context in which events occur—the social, political,
economic, and institutional forces which shape the evolution of events. It
also places a personal face on history which not only enlivens past events
but also helps to explain how individuals affect historical developments.

The foregoing criticisms could be directed at the AIDS oral history
series. Yet this series has several mitigating characteristics. First, it
is on a given topic in a limited time frame with interviewees focused on a
particular response, namely the medical and scientific. Thus although each
interviewee presents a distinctive view of the epidemic, multiple
perspectives on the same events provide an opportunity for cross-checking
and verification, as well as rich informational content. Furthermore, most
of the interviewees continue to be actively engaged in AIDS work. Hence,
the memory lapses resulting from chronological and psychological distancing
from events discussed are less likely to occur than when the interviewee is
no longer involved.

An advantage of a series of oral histories on the same topic is that
the information each contains is cumulative and interactive. Through
individual accounts, a series can present the complexities and
interconnections of the larger picture- -in this case, the medical and
scientific aspects of AIDS in San Francisco. Thus the whole (the series)
is greater than the sum of its parts (the individual oral histories), and

1 The three criticisms leveled at oral history also apply in some
cases to other types of documentary sources.

should be considered as a totality. To encourage this approach, we decided
to bind several oral histories together in each volume.

Another feature of an oral history series is that later interviews
tend to contain more detailed information because as the series unfolds the
interviewer gains knowledge and insight from her informants and from
continued research in primary and secondary sources. This was indeed the
case in the AIDS series in which the later interviews benefited from my
research in private document collections made available to me as the
project progressed and by the knowledge I gained from the interviews and
others connected with the AIDS scene.

A feature of this particular series is its immediacy, a
characteristic less evident in oral histories conducted with those
distanced from the topic of discussion. These are interviews with busy
people who interrupted their tight schedules to look back, sometimes for
the first time, at their experiences of a decade or so ago. Because many
have not had the luxury of time to contemplate the full meaning of their
pasts, the oral histories could be criticized for lacking "historical
perspective." But one could also argue that documents intended as primary
historical sources have more scholarly value if the information they
contain is not filtered by the passage of years and evolving personal
opinions.

The oral histories also have a quality of history-in-progress. With
few exceptions, the interviewees are still professionally engaged in and
preoccupied by an epidemic which unhappily shows no sign of ending. The
narrators are living the continuation of the story they tell. Neither they
nor we can say for sure how it will end.

Other Oral History Projects Related to AIDS

Oral history projects on other aspects of the San Francisco epidemic
are essential for full historical documentation and also mutually enrich
one another. Unfortunately, not enough is currently being done in this
regard. Two local projects are Legacy, directed by Jeff Friedman, which
focuses on the Bay Area dance community tragically decimated by AIDS, and
Clarissa Montanaro's AIDS Oral History Project, which interviews people
with AIDS. An installation, "Project Face to Face", directed by Jason
Dilley and using excerpts from interviews with people with AIDS, was
exhibited around the San Francisco Bay Area and in 1991 was part of the
inaugural exhibit at the Smithsonian's Experimental Gallery.

AIDS oral history projects outside San Francisco include
documentation by Victoria Harden, Ph.D., Caroline Hannaway, Ph.D., and
Dennis Rodrigues of the NIH Historical Office of the contribution made by
NIH scientists, physicians, and policymakers to the AIDS effort. Gerald
Oppenheimer and Ronald Bayer at Columbia, with support from the National

Library of Medicine and the Royal Marx Foundation, are conducting
interviews with AIDS physicians in several cities across the United States.
The New Jersey AIDS Oral History Project, sponsored by the University of
Medicine and Dentistry of New Jersey, interviews faculty and staff involved
in the epidemic and representatives of organizations providing AIDS support
services. Rosa Haritos, Ph.D., at Stanford relied substantially on oral
history in her dissertation on the controversy between the Pasteur
Institute and NIH over the discovery of the AIDS virus.1 In England,
Virginia Berridge, Ph.D., co-director of the AIDS Social History Programme
at the London School of Hygiene and Tropical Medicine, employs oral history
in her research on AIDS policy in the UK.2 And Maryinez Lyons, Ph.D., at
the University of London, uses interviews in her work on the political
economy of AIDS in Uganda.3 In France, Anne Marie Moulin, M.D., Ph.D.,
Director of Research at INSERM, Paris, has relied on oral history in some
of her work on the epidemic in France. The anthropologist, Paul Farmer,
used interviews heavily in his work on AIDS in Haiti.*

Emerging Themes

What themes can be extracted from these oral histories? What do they
convey about the medical response to AIDS in San Francisco? Was it unique,
or are there parallels with responses to other epidemics? What do these
interviews tell us about the complex interweaving of factors — social,
political, economic, and personal—which shaped reactions to this epidemic,
in this city, in these years?

The short answer is that it is too soon to attempt definitive
answers. This is the third volume in a lengthy series, and most of the
oral histories are not completely processed nor has the information they
contain been fully assessed.

Furthermore, there is an inherent danger in reaching definitive
conclusions on the basis of oral histories with only seventeen individuals.

1 Rosa Haritos. Forging a Collective Truth: A Sociological Analysis
of the Discovery of the AIDS Virus. Ph.D. dissertation, Columbia, 1993.

2 See: Virginia Berridge and Paul Strong, eds. AIDS and Contemporary
History. Cambridge: Cambridge University Press, 1993.

3 Maryinez Lyons. AIDS and the Political Economy of Health in Uganda,
paper presented at a conference, AIDS and the Public Debate: Epidemics and
their Unforeseen Consequences, sponsored by the AIDS History Group of the
American Association for the History of Medicine, Lister Hill Center, NIH,
Bethesda, MD, October 28-29, 1993.

* Paul E. Farmer. AIDS and Accusation: Haiti and the Geography of
Blame. Berkeley: University of California Press, 1992.

xii

Obviously, this is not a statistical sampling. On the other hand, because
these seventeen have been at the front line of the epidemic and in a city
hit hard by the epidemic, their voices "count" more than their numbers
might suggest. They also "count" because these individuals helped devise
organizations and policies that have served as models for AIDS programs
across the country and around the world. Thus, if used in conjunction with
the traditional documentary sources, these oral histories "count" as rich
historical sources on several levels.

Remembering these caveats, I will make some tentative suggestions
about a few of the many themes which come to the fore as I put the first
volume together. My thoughts will doubtless be modified and extended as I
examine the oral history collection as a whole and assess it in the context
of the existing literature on AIDS history.

--Professional and personal "preparation" for the epidemic:

Narrators invariably mentioned how their prior education and
professional training and experience had prepared them for participation in
the epidemic. Their training as oncologists or epidemiologists or
infectious disease specialists "fitted them" in a deterministic sense to
take notice when the epidemic was first recognized in San Francisco. Their
interest piqued, they chose to become engaged because their professional
knowledge, experience, and responsibility placed them in a position to
contribute. How then to explain why others with similar backgrounds chose
not to become involved? The interviews indicate that psychological makeup,
humanitarian concerns, career ambition, sexual orientation, and simply
being needed and on the scene also played a role.

--Organizing for the epidemic:

The oral histories describe at length, in detail, and on many levels
how the academic medical profession in San Francisco organized to respond
to the epidemic. The focus is on university physicians, but the oral
histories show that it is impossible to talk about the medical response
without at the same time mentioning its interconnections with the community
physician, nursing, psychiatric, and social service professions, the gay
community, and volunteer AIDS support organizations. Discussion of the
coordinated medical system created in the early years of the epidemic,
capsulized in the so-called San Francisco model of comprehensive AIDS care,
permeates the oral histories. The complex process by which a community
organizes to diagnose, investigate, and treat a newly recognized disease is
detailed here, as are the spinoffs of these activities—the foundation of
two AIDS clinics, an AIDS ward, and a specimen bank; funding efforts;
education and prevention programs; epidemiological and laboratory studies;
political action at the city, state, and national levels; and so on.

--The epidemic's impact on the professional and personal lives of
physicians and scientists:

xiii

Surprisingly, despite the flood of AIDS literature and the centrality
of the medical profession in the epidemic, there are few accounts by
physicians of the epidemic's professional and personal impact.1 The
physicians' voices which speak--at times poignantly, but always with
immediacy --through these oral histories are a small corrective to the
impersonality of most of the literature on AIDS.

On a professional level, the narrators describe commitment, concern,
cooperation, camaraderie, and conflict as attributes of their engagement in
the epidemic. Clinicians and epidemiologists confronted by what they
perceived as a medical emergency described the prevailing sense of urgency
and dedication of the epidemic's early years—to stop the insidious spread
of disease, to discover its cause, to devise effective treatments, to
establish community care arrangements. Narrators talked of concern for an
articulate, informed, and youthful patient population, with whom some
identified and for whom most felt great sympathy. They also spoke of the
camaraderie and cooperation of the physicians, nurses, social workers, and
community volunteers assembled at UCSF and San Francisco General to run the
AIDS clinics and ward. But they also mentioned conflict- -personal and
institutional rivalries, funding problems, and run-ins with the university
administration, city politicians, and gay activists.

On a personal level, the interviews recount the epidemic's impact on
individual lives—of fear of a devastating and lethal infection, of stigma
and homophobia involved in dealing with socially marginal patient
populations, of exhaustion and burnout, and of growth in human experience
and insight.

--The epidemic as a social and cultural phenomenon:

These oral histories describe the complex interactions between
disease and its social and cultural context. They indicate how the unique
circumstances of San Francisco in the early 1980s— its large and vocal gay
community, its generally cooperative medical and political establishments,
the existence of a city budget surplus— shaped the response to the
epidemic.

AIDS, like all disease, reflects social and cultural values.
Implicit and explicit in the oral histories are evidence of stigma and
homophobia, the politicization of the AIDS effort and those associated with
it, and the tension between individual rights and social welfare.

1 A few personal accounts by physicians do exist. See, for example:
G. H. Friedlander. Clinical care in the AIDS epidemic. Daedalus 1989,
118, 2:59-83. H. Aoun. When a house officer gets AIDS. New England
Journal of Medicine 1989, 321:693-696. The Oppenheimer/ Bayer oral history
project, mentioned above, also seeks to document physicians' responses.

xiv

The foregoing themes are but a few of those inherent in these oral
histories. I hope that scholars will be persuaded to explore these further
and to discover and research those unmentioned. To serve as a rich,
diverse, and unique source of information on multiple levels is after all a
major purpose of this oral history series.

Locations of the Oral Histories

The oral history tapes and bound volumes are on deposit at The
Bancroft Library. The volumes are also available at UCSF, UCLA, and other
manuscript libraries.

Note Regarding Terminology

In this series, both interviewer and interviewee occasionally use the
term "AIDS" to refer to the disease before it had been officially given
this name in the summer of 1982. "AIDS" is also used to refer to the
disease which in recent years has come to be known in scientific and
medical circles as "HIV disease." In these oral histories, the term "AIDS"
has been retained, even when its use is not historically accurate, because
it is the term with which readers are most familiar.

Sally Smith Hughes, Ph.D.
Project Director

October 1996

Regional Oral History Office

LIST OF PARTICIPANTS IN THE AIDS MEDICAL RESPONSE ORAL HISTORY SERIES

VOLUME I

Selma K. Dritz, M.D., M.P.H, Epidemiologist, San Francisco Department of

Public Health
Mervyn F. Silverman, M.D., M.P.H., Director, San Francisco Department of

Public Health

VOLUME II

Donald I.
Marcus A.

Abrams, M.D.
Conant, M.D.

AIDS Internist at San Francisco General Hospital
AIDS Physician and Political Spokesman

Andrew A. Moss, Ph.D., Epidemiologist at San Francisco General Hospital

VOLUME III

Arthur J. Ammann, M.D., Pediatric AIDS Physician and Administrator, UCSF
Paul A. Volberding, M.D., AIDS Oncologist at San Francisco General Hospital
Constance B. Wofsy, M.D., Authority on Pneumocystis carinii Pneumonia and
Women with AIDS, San Francisco General Hospital

VOLUME IV

Donald P. Francis, M.D., D.Sc., Epidemiology and Virology at the Centers

for Disease Control
Merle A. Sande, M.D., Infectious Disease Specialist; Professor of Medicine,

UCSF-SFGH; AIDS Activities at San Francisco General Hospital
John L. Ziegler, M.D., Ph.D., Professor of Medicine, UCSF; AIDS Oncologist

at the Veterans Administration Medical Center, San Francisco

IN PROCESS

Deborah Greenspan, D.D.S., D.Sc., Oral Manifestations of AIDS
John S. Greenspan, D.D.S., Ph.D., AIDS Specimen Bank, UCSF
Jay A. Levy, M.D., Virologist, UCSF: Isolation of the AIDS Virus (On Hold)
Herbert C. Perkins, M.D., President, Irwin Memorial Blood Centers
Warren Winkelstein, Jr., M.D., M.P.H., The San Francisco Men's Health Study,
UC Berkeley

Regional Oral History Office University of California

The Bancroft Library Berkeley, California

The San Francisco AIDS Oral History Series

THE AIDS EPIDEMIC IN SAN FRANCISCO: THE MEDICAL RESPONSE, 1981-1984

Volume IV

Donald P. Francis, M.D., D.Sc,

EPIDEMIOLOGIST, CENTERS FOR DISEASE CONTROL: DEFINING AIDS AND
ISOLATING THE HUMAN IMMUNODEFICIENCY VIRUS (HIV)

Interviews Conducted by

Sally Smith Hughes

in 1993 and 1994

Donald P. Francis, ca. 1994,

Interview History—by Sally Smith Hughes, Ph.D.

Thanks partly to Randy Shilts1 book, And the Band Played On. and the
film based on it, Donald Francis is one of the most visible figures in AIDS
science and politics. In the oral history, the reader will learn of his
efforts in the 1970s as an Epidemic Intelligence Service Officer of the
Centers for Disease Control [CDC] to stamp out disease in exotic areas of
the world, including smallpox and Ebola fever in Sudan. He then tells of
his doctoral research in Max Essex's group at the Harvard School of Public
Health on feline leukemia, an immunodeficiency disease caused by a
retrovirus. This work "prepared" him in unexpected ways to deal with the
epidemic of immunodeficiency disease in gay men reported in 1981, less than
two years after he had received a doctoral degree in virology from Harvard.
Largely because of this experience, Francis was among the first to suggest
that the puzzling outbreak was caused by a retrovirus.

By this time, Francis was assistant director of the CDC hepatitis lab
in Phoenix, Arizona, a location which grew problematic as he became
increasingly involved with the frenetic work of the AIDS Task Force located
at CDC headquarters in Atlanta. In 1983, he and his young family moved to
Atlanta, where Francis became coordinator of AIDS Laboratory Activities and
a prime player in CDC efforts to isolate an infectious agent.

Of interest is his frank account of the race to isolate a virus which
involved, among others, Robert Gallo at the National Institutes of Health,
the Montagnier group at the Pasteur Institute, Jay Levy at the University of
California at San Francisco, and himself. It was a race with high stakes in
terms of scientific prestige and money. Triumphal announcement by the
United States of the isolation of a virus in April 1984 led to a bitter
controversy over credit from which science and personal reputation did not
emerge unscathed.

In addition to these headline events, Francis provides a picture of
the often frenzied and frustrating conditions under which the CDC AIDS team
operated in the first years of the epidemic. Francis is not alone in his
view that Reagan's downsizing of the federal government resulted in
inadequate national leadership and funding of early AIDS efforts. In
addition to the strain of conducting research with meager funds and
staffing, he and his colleagues were under constant pressure from the media
to "explain" the epidemic, an essential burden in CDC efforts to educate the
American public about AIDS.

The situation sorely tried those at the frontline. Speaking in the
oral history of a CDC AIDS group nicknamed the Sextet,1 Francis said: "...we
spent hours trying to economize. .. .The frustration would take all your
energy away, and you needed immense energy to deal with this epidemic."

Upon his retirement from the CDC in 1992, Francis was completing terms
as CDC advisor on AIDS to the state of California and special consultant on

1 Members of the Sextet were Walter Dowdle, John Bennett, James
Curran, Bruce Evatt, Frederick Murphy, and Francis.

AIDS to San Francisco Mayor Art Agnos. In 1992, he joined Genentech as
director of a team developing an AIDS vaccine. After these interviews were
completed, the vaccine program which was spun off as a new company,
Genenvax, which Francis currently heads.

Fascinating history indeed, but why, the purist might ask, is Francis
included in a series on San Francisco's early medical response to the AIDS
epidemic? The answer: to suggest that from the earliest days, local efforts
to confront the epidemic simultaneously influenced and were influenced by
events elsewhere. The federal institution most critical to local biomedical
responses to AIDS was the Centers for Disease Control, and Francis was key
to its early AIDS efforts.

The oral history of one individual cannot of course fully delineate
the complex interactions between the CDC and AIDS scientists and health
professionals at early centers of the epidemic. But because Francis was a
central figure at an institution central to the science, epidemiology,
information, and politics of the early epidemic, his story provides national
context for the local efforts recounted in other oral histories in this
series.

The Oral History Process

Three interviews were recorded with Dr. Francis between September 1993
and February 1994 in his office at Genentech. In shirt sleeves and slacks
and looking younger than his fifty-some years, he provided glimpses in the
interviews of the passion and purpose for which he is known. He borders on
the charismatic, a fact which nettles colleagues who have also made
significant contributions but who draw less public acclaim. He acknowledged
off tape that the fame he acquired from his leading role (played by Matthew
Modine) in the film of And the Band Played On was "embarrassing", but
recognized its political expediency in his effort to win support for AIDS
vaccine research.

Francis edited lightly, with no substantive changes. The oral history
stands as an intriguing but incomplete record of the achievements of one
individual and the institution he represented in the early years of the
epidemic. In many senses, this volume is just a beginning but, one hopes, a
tantalizing one which will inspire deeper and wider exploration of the CDC's
contributions to the AIDS effort.

The Regional Oral History Office was established in 1954 to augment
through tape-recorded memoirs the Library's materials on the history of
California and the West. Copies of all interviews are available for
research use in The Bancroft Library and in the UCLA Department of Special
Collections. The office is under the direction of Willa K. Baum, and is an
administrative division of The Bancroft Library of the University of
California, Berkeley.

Sally Smith Hughes, Ph.D.

Research Historian

Regional Oral History Office
April 1997

Regional Oral History Office
Room 486 The Bancroft Library

University of California
Berkeley, California 94720

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I FAMILY BACKGROUND, EDUCATION, AND EARLY CAREER

[Interview 1: September 30, 1993] #f

Early Education

Hughes: Please give a brief summary of your life up until the time of the
AIDS epidemic.

Francis: I'm a native Californian, actually a third-generation California
physician, with my grandfather having come from England and
practiced in L.A. My mother is also a physician. There was a
whole California tradition of physicians.

I was born in Los Angeles on October 24, 1942 and raised in
Marin County, across the bay from San Francisco, and then went to
undergraduate school at the University of California at Berkeley
[1961-1964]. I then moved off to Chicago to do medical school at
Northwestern University School of Medicine [1964-1968]. I came
back for my pediatric training [internship and residency] at L.A.
County [University of Southern California] Medical Center [1969-
1970].

It was the Vietnam War era, and I was staunchly and overtly
committed to being against the war and against supporting the
military. I was planning on moving to Canada, because I had
applied for conscientious objector status, but very few people
were getting it. I thought the odds were that I would not get it
and that I would be 1A [the top draft category], and then I'd
have to jump ship and be in an illegal situation. So I decided
that it would be better if I went to Canada.

1 ## This symbol indicates that a tape or tape segment has begun or
ended. A guide to the tapes follows the transcript.

Employment by the Centers for Disease Control

Francis: I went to the chairman of the Department of Pediatrics in Los

Angeles, Paul Wehrle, and asked him where he would get training
in Canada. He said, "Well, why don't you apply for the CDC
[Centers for Disease Control] Epidemic Intelligence Service?" I
ultimately did, but because I'd been on a pediatric fellowship in
India right out of medical school [1968], I was six months off.
Usually it's July to July in medical training; I was going
January to January.

State Epidemiologist, U.S. Agency for International
Development, River's State, Nigeria, January- June 1971

Francis: So I had six months extra, and CDC then sent me to Nigeria after
the Biafran War when things were so terrible in Nigeria. That's
when cholera hit West Africa, so I spent my first six months for
CDC fighting cholera in West Africa.

Epidemic Intelligence Service Officer, Oregon State Health
Division, July 1971-December 1972

Francis: Then I came back and did my initial assignment in CDC, which was
going to be for two years. They said, "Where do you want to be
assigned?" Because CDC has a variety of assignments, either in
Atlanta or out in the states. I said, "I want to be as close to
the West Coast as I can," so I took Oregon, for no other reason
than it was close to home. [laughs] It was actually supposed to
be two years of training in epidemiology there.

Hughes: At the university?

Francis: No, it was at the state health department.

Smallpox in Yugoslavia, 1972

Francis: But it was interrupted; there was a smallpox epidemic in

Yugoslavia in '72, I guess it was, and I got one of these urgent
calls to hit the airplane straight away, and went off to

Hughes :
Francis:

Hughes :
Francis :

Yugoslavia. I spent, I guess, a few weeks fighting the epidemic
there and stopping smallpox. I said, "Gee, that's really an
exciting thing to do."

Why were you chosen?

Probably because I had international experience, in India and
Nigeria, and I had at least seen cases of smallpox, and I had
worked in foreign areas. It was a team of about ten of us, I
think, and we ultimately immunized the whole country, and I
worked right down in the epidemic.

I met a guy named Bill Foege. He was this tall, thin, head
of smallpox eradication for CDC. I met him actually on the
opposite side of a volleyball court, which is the wrong way to
meet a six-foot-seven individual. [laughter] But I told him,
"If you ever do anything in smallpox, I'd be interested."

Was there talk of eradication at this point?

No, the worldwide program hadn't been started yet.1 Bill Foege
and others had done some initial eradication program in West
Africa, and I was really kind of an offshoot of that when I was
in Nigeria. So I knew very well what they were doing. He really
developed the concept of search and containment. Instead of
trying to vaccinate everybody, the issue was to find cases and
then do very compulsive, 100 percent vaccination around the
cases. Then you could stop the disease instead of trying to
vaccinate the whole world, which never worked, because you miss
so many people.

Smallpox Eradication in Sudan, India, and Bangladesh,
January 1973-June 1975

Francis: As I say, I said, "If you ever really want to do a big smallpox
program, I'd be interested." So even before I finished my two
years of training, I was called by the smallpox eradication
program and was sent off for two and a half years to WHO [World
Health Organization! » initially in Sudan, then in India, and then
Bangladesh.

1 See: Frank Fenner, Donald A. Henderson, Isao Arita, et al. Smallpox
and Its Eradication. History of International Public Health, no. 6.
Geneva: World Health Organization, 1988.

Research Fellow in Pediatrics, Harvard Medical School, and
Doctoral Student, Department of Microbiology, Harvard School
of Public Health, July 1975-November 1979

Francis: At the conclusion of my smallpox work—this was 1975--I felt very
isolated from any modern medicine, and asked CDC to send me for
some training. I talked them into two years of training for my
infectious disease fellowship at Harvard. I was going to do a
master's in public health at the same time, but then I decided
that was really dull. I wanted to do some laboratory work. I
had some very good advice from a guy named Roger Feldman at CDC
to get a strong laboratory background.

Hughes: Which you hadn't had before?

Francis: Which I hadn't had. So luckily, the former head of epidemiology
at CDC, called the father of epidemiology in the United States, a
fellow named Alex Langmuir, was at Harvard at that time. When I
came back from India, he set me up to have lunch with the School
of Public Health microbiology faculty and see what projects they
were doing—in case I was interested in them. We sat around with
bag lunches, and everyone mentioned what they were doing. There
were all these esoteric, mostly immunology studies, and then
there was this one guy named Max [Myron] Essex who was working
with cats and feline leukemia. I had become increasingly
interested in the late manifestations of viral infections, these
things that take years and years to develop.

Hughes: Why?

Francis: Because I think we all have this bias in virology that it's a
two-week incubation period and you develop a disease. And I
began learning more of chronic hepatitis, or possibly liver
cancer, or herpes zoster after chicken pox, and these kinds of
diseases that happen years and years after initial infection. I
just was fascinated by the fact that an acute viral infection
could produce a disease years and years later. Were some other
diseases we see in adults really a function of pediatric
infections years before?

Now realize, the only reason I went to Harvard was because I
had met a girl in Portland, and she was an undergraduate, years
younger than I was, at Harvard. So I was going back to see her,
and I thought I would try to combine a personal advantage with my
training. But we broke up when I was in Bangladesh, so by the
time I got there, we weren't together anymore. So I found myself
there for no particular personal reason whatsoever. [laughter]

Hughes: Well, it ' s a good place to be for no reason whatsoever.

Francis: I met my future wife [Karen M. Starko, M.D.] there, so it worked
out very well.

Research with Max Essex

Francis :

Hughes :
Francis :
Hughes :
Francis :

Hughes :

Francis ;

I started working with Max on feline leukemia, and I ultimately-
another kind of chancy situation—talked CDC out of an extra
year. So I was able actually to complete a doctorate in
microbiology studying feline leukemia virus, which is a
retrovirus. There were no retroviruses known in humans at that
time.

Was Essex's lab a retroviral lab at that stage?

Yes.

Did that mean anything to you at that point?

No. It was just a classification of viruses. As a matter of
fact, the infectious disease group usually stayed out of the
whole retrovirus field, because it was dominated by scientists
studying cancer viruses of mice that pass from mother to
offspring, and it didn't really seem to make any difference to
the field of virology. So it was always kind of a separate
field.

Had the myth been destroyed at that point,
animal pathogens , not human?

that retroviruses were

There was still the debate. They were pathogens, but they were
thought to be vertically transmitted instead of horizontally
transmitted. It was really some of Max's initial studies showing
that these cats actually transmitted from cat to cat, not from
dam to kitten, which indicated that retroviruses could be
horizontally transmitted. And my work was really on working out
the whole transmission and outcome, the natural history, of
feline leukemia virus.

The CDC was fighting me regarding my third year of doctoral
training. I had to finish all my laboratory work. I'd see my
patients in the morning and then rush off in the afternoon to do
my laboratory work. But I decided not to get a master's, so I
really had nothing if I didn't get my doctorate. I was working
towards the doctoral program, and completing my exams and such.

Then CDC said, "Well, we only promised to send you to Harvard for
two years . "

Ebola Virus in Sudan, 1976

Francis: Well, in the middle of my second year, I got this call from CDC
saying, "We've got this really big problem in Sudan of this new
virus that we don't know anything about. You speak some Arabic;
you know Sudan well. Would you be willing to go?" I said, "My
god, I'm right in the middle of my classes; I'm doing my
research. How can I do this? But sure, if you need someone in
Sudan, I'll go there." Then I said, "Well, what is it?"

They said, "Well, it's like Marburg virus." I knew what
Marburg was. It was this terrible virus that came into Marburg,
Germany, and killed all these people. It was one of the viruses
that we kept in the high security area in the CDC. I said,
"What! Why are you calling me?"

They said, "Well, you work with dangerous viruses." I said,
"What, feline leukemia? Just because I work in a hood? We don't
keep that as a class IV (highly pathogenic) agent." But they
said, "Oh, you've got experience," and so I naively said, "Why
not?" My father actually was living in London and came to visit
that very night. He had never met [the person who] was to be my
future wife. I had to say, "Well, it was good of you to come,
but I've got to go to Sudan." So at least they got to spend some
time together; I left straight away. [laughs]

CDC said it was going to be for two weeks. Well, this
turned out to be Ebola virus in Sudan. It was, what, two months
before we were ready to leave, and then we got thrown in
quarantine for two weeks in Juba, Sudan. So it was a huge hole
out of my academic year. But that loss actually served as the
lever to make CDC support my third year at Harvard, ultimately
allowing me to get my doctorate, so it all worked out fine. And
I survived.

Hughes: Do you want to say something about Ebola?

Francis: That was an incredible thing to be involved in. First of all, we
were quarantined out. The north of Sudan is primarily Arab and
Muslim, and the south of Sudan is really black central Africa,
with Christians and animists, local religions. They've been at
war for years; they weren't when I was there. That was the only

Hughes :
Francis:

period of time when they were not at war; they're back at war
again and now it's horrible.

The north didn't seem to really care, so they just
quarantined off the whole south, so the WHO team couldn't even
get down there. There was a CDC team that went--a large team
with helicopters and everything—into Zaire, on the other side of
the border. But I was part of a WHO team which consisted
essentially of two of us. [laughs]

Who was the other?

David Simpson, from the London School of Tropical Medicine. He
was very experienced; he had worked with Marburg a lot. Thank
goodness, because he had all the isolation experience and knew
how to survive in this environment.

Hughes: Would CDC have sent you there without proper preparation to deal
with a lethal virus?

Francis: Yes, as long as there was a senior person there.

Hughes: So Simpson was essential; they wouldn't have sent two untrained
people in there.

Francis: No, no. I learned you get military credit for being at CDC,

because you actually end up doing some things that are far more
dangerous than a doctor would ever do in a military setting, and
this was certainly one of those instances.

We finally got a plane to take us down. Then it was about a
twelve hours' drive directly west of Juba, which is way down by
the CAR [Central African Republic] -Zaire border. We got down to
Juba, and of course there were no vehicles ready. We had to get
tires on the Land Rovers and get some trucks for all of our
equipment. So it took us most of the day to do that, and we left
about three or four o'clock in the afternoon, for a twelve-hour
drive. There are no paved roads, and the rains were just ending.
But unfortunately, it had rained just the day before, so we had
this horrible muddy track to drive on until two or three o'clock
in the morning.

The driver got exhausted about three-quarters of the way, so
I drove the rest of the way. It was an incredible experience to
go into this tiny town called Maridi out in the middle of
nowhere, little government setting with a hospital and a few
government offices. Eerie silence over the whole place.
Luckily, there was a missionary family there that put us up, with
at least a bed and some food. It was all quarantined out; no

food, no nothing was coming in.
least we got some food.

They had some fruit trees, so at

Hughes:
Francis:

Hughes :
Francis:

The first few days were spent seeing patients, with
respirators on, in the hospital, and getting lists of patients.
David was setting up the lab, doing the laboratory work, trying
to get the right specimens. I did the epidemiology. I started
visiting all the survivors and the families of the dead people,
and tried to piece the epidemic together- -to figure out how it
transmitted. Because it was really scary. If there were
airborne transmission, with that kind of virus it would have been
deadly. I guess at that point, about a quarter of the nurses and
one of the doctors had already died. By the time we finished,
half the nurses in the hospital were dead.

Fitting it all together within a few days, I could really
see how the disease transmitted. It was close contact with the
blood of the dying or dead patients at funerals, or having sex
with infected people. So at least it made us more comfortable
going into these huts with these folks and wondering if you were
going to die or not. The real danger was postmortem exams to get
specimens. I did one on the ground in back of the hospital. It
was really, really dangerous, and really stupid, when I think
back on it. Because if we had stuck ourselves with one of those
scalpels or any sharp instrument, it turned out we had a 90
percent chance of dying from a stick. Pretty high.

You didn't know that at the time?

No. Well, you knew you didn't want to be stuck. Traditionally
in new epidemics, it's the investigator or the lab investigator

who are the second generation cases often,
actually find out where the virus is.

That ' s how you

Where had it come from? Was that the end of the epidemic?

No, it came out again. We traced it down to a cotton factory in
the south. Everyone else had a very close, explainable contact,
except for a group of people working at this cotton factory in
Nzara, which was about thirty or forty miles from Maridi, which
was the hospital that everyone had come to. This group of cotton
workers just worked in the cotton factory, no other thing in
common. So we traced it down to the cotton factory, and there
was a lot of controversy about that. No one believed it. It was
stated as kind of a hypothetical source in the medical
literature. The experts didn't believe it, until about four
years later, when an outbreak started again in the same cotton
factory.

We trapped bats and rats and mice and mosquitoes, and did a
huge amount of work searching for the source of the virus, and
never did find it. It will turn out some day to be some strange
insect or plant virus or the like. We still haven't found out
where it came from.

Hughes: Any clues about why it began to infect humans?

Francis: Yes. I wouldn't be surprised if it infected humans before the
1976 epidemic—silently, without being detected. It's actually
much like AIDS: the ecology changed. They built a factory down
there with lots of people and a horrible environment, full of
dust and such. So if something was there, you could sure spread
it around. And then the next thing was, they had these night
clubs, kind of social gatherings, where the first sexual
transmissions occurred in several people. Then the ultimate
amplifier was the hospital.

The owner of this night club actually got sick, and he had
enough money to be taken up to the regional hospital in Maridi.
Once he got sick, he got the nurses infected, and the nurses got
sick and would go to the hospital. In the end the hospital staff
was all but eliminated. This was a training hospital, not the
usual African hospital where you go in and die, often with very
little intensive care. These were wonderful missionary-type
nurses who were caring very closely for these patients. They all
got infected, and their friends would take care of them, and they
would get infected. It ultimately spread to Juba, and then
ultimately the doctor went all the way to Khartoum.

Hughes: Well, what are some of the principles from this experience that
are going to be useful in the AIDS epidemic?

Francis: Well, we already see the principles emerging, of tropical viruses
that exist, that unique ecological changes often allow them to
spread where they wouldn't have spread before. If these
dangerous viruses emerge, we have to take a very aggressive
approach.

We took a very aggressive approach to stop the Ebola
epidemic. When we found it was spread by funerals, we prevented
funerals, and we took care of the bodies. And that was just
totally contrary to the traditions of the local folks, and they
hated us for it. But that was a public health endeavor-
something we had to do.

Hughes: You made that decision yourself?

Francis: No, the Sudanese authorities, together with us. They really are
the power, and they made the decision. So no, you wouldn't do
that as a foreigner. That is a fine line, whether you could get
away with that or not. You certainly couldn't get away with it
if you were a foreigner making that decision.

Hughes: And then you presumably returned to Harvard to finish up your
dissertation?

Francis: Yes, I came back to Harvard. The CDC was saying, "Now, what do
you want to do?" By that time, I was married to Karen Starko.
She was interested in the Epidemic Intelligence Service program,
the EIS, the same one that Paul Wehrle recommended that I join.
That's how we met, and we started dating, and ultimately got
married. She was interested in that program and was signed up
for CDC, and I was looking for an assignment that would fit with
my virologic background, especially dealing with viruses with
late manifestations. But there were no retroviruses known in
humans at that time.

Learning Laboratory Technology

Hughes: Do you want to say what you had learned about epidemiology and
virology, and the technology therewith, that was going to be
applicable to the AIDS epidemic?

Francis: Well, if you think about the whole chance occurrence of all this
training--. At this time, I was still a CDC-type epidemiologist,
which is kind of a quick-and-dirty epidemiologist as compared to
the people I worked with at Harvard on my doctorate, who were
really sophisticated cancer epidemiologists. So I got real
strength in writing my thesis with these folks and manuscripts
about using modern epidemiologic techniques — far greater than we
used at the time at CDC.

At the same time, I developed, if nothing else, the
vocabulary to understand modern virology, nucleic acid chemistry,
all the things you needed to know for recombinant technology; at
least I was able to speak it. I was still kind of a CDC
virologist dealing with infectious diseases but not molecular
biology, but I had to take all these courses and understand
modern techniques and deal with them. Which at least set me up
when AIDS came to be. If nothing else, I spoke the language of
modern virology. One of the things we have today in science is
this incredible specialization, each one of us with our own

vocabulary within that specialty. If you can't speak it, you're
lost. It's really like speaking another language.

Hughes: And you had all that.

Francis: So I had it, at least.

Hughes: You had been exposed to the laboratory technology, as well?

Francis: Yes, that's what I mean by vocabulary, and the ability to use the
tools of modern biology. But I never felt myself to be an
accomplished laboratorian.

Hughes: Did you like lab work?

Francis: I loved the data; I hated the gruel. It's very boring, day-to
day repetitive stuff. It's an exciting experience getting the
data; it's really fun. I didn't mind doing the procedures once
or twice, but it was the repetition, over and over and over
again, that's really dull. I luckily had a very good work- study
student technician, Dawn Gazagian, who worked with me all the
time. And I think in those two and a half years in the lab, we
published something like seven or eight manuscripts. So it was
really very productive.

Hughes: How much contact did you have with Max Essex?

Francis: Oh, every day.

Hughes: So he was really right there?

Francis: Oh, yes. He was wonderful.

Assistant Director for Medical Science, Hepatitis and Enteritis
Division. CDC, Phoenix. Arizona, July 1978-September 1983

Francis: It worked out that Karen and I would go to Phoenix, Arizona,

which was the location of the hepatitis part of CDC--hepatitis
viruses, especially hepatitis B, and also what ultimately turned
out to be hepatitis C, which fit into the category of agents that
cause acute infection, produce jaundice in some people, and
ultimately produce a lot of chronic liver disease, including
cancer. So it fit very well with my field of interest of viruses
with late manifestations.

Viruses and Cancer

Hughes: The connection with cancer was known at that point?

Francis: Yes. It was at least developing at that point.

Hughes: What was the status of the concept of the viral cause of cancer?

Francis: Still very much open. There had been these reports periodically
in the literature of retroviruses causing cancer in humans, and
they were always kind of pooh-poohed, never really panned out
very well. So it was thought that all the work in retroviruses
in animals was not very applicable to human cancer- -it all came
out of the National Cancer Institute. But it actually set up a
remarkable knowledge of nucleic acid structure of human cells and
viruses which, once AIDS was diagnosed, just [snaps fingers] sent
it straight into a very rapid discovery phase following the model
of other retroviruses.

One of my early articles out of Harvard in Journal of
Infectious Disease talked about the possibility of these cancer-
producing viruses being in humans, and reviewed the animal
models.1 I think what we had at that time was hepatitis B, and
said, "We need to look for other bugs and diseases." It was an
interesting article, in retrospect.

Hughes: Why were people so doctrinaire? If viruses cause cancer in

animals, which had been known for a long time, why couldn't they
cause cancer in human beings?

Francis: I agree. The one thing I learned working with veterinarians is
they have lots of very interesting diseases, including viruses
that cause arthritis, viruses that cause cancer, viruses that
cause immunosuppression, viruses that cause a whole variety of
other diseases that look very much like human diseases. But I
think we in human medicine were doctrinaire and biased. That
certainly came through in the AIDS epidemic where early on,
people would just not believe that it was caused by a virus.

1 D. P. Francis, M. Essex. Leukemia and lymphoma: Infrequent
manifestations of common viral infections? A review. Journal of
Infectious Disease 1978, 138:916-923.

Robert Gallo

Hughes: Was Gallo 's work well known at that point?

Francis: Yes. Actually, I knew Bob Gallo at that time. He was working

with Max. He was primarily well known, unfortunately, for having
reported a virus that caused cancer which was a laboratory
contaminant and ultimately didn't pan out.

Hughes: It plays into the story, don't you think?

Francis: Yes, in a way. I wouldn't put him down for that alone—we can
all contaminate in the laboratory. That's much more acceptable
than trying to steal credit. That's a different issue.

Hughes: This is pop psychology on my part, but I would think from what I
know about his personality, there would be a real drive to get
past that one mistake.

Francis: Yes, there was. But I don't mind that drive, as long as it's an
honest drive. It's when it's dishonest that it gets in the way.

Hepatitis B Vaccine Trials in the United States, 1979-1980

Hughes: Talk about the Phoenix laboratory and hepatitis.

Francis: All right. I had worked with hepatitis as a general

epidemiologist in Oregon, but never knew too much about it.

I didn't even know much about Phoenix, Arizona, even though
by that time my mother had moved from Marin County to Prescott,
Arizona. One of the reasons I came back from WHO was because she
was diagnosed as having cancer, so it all kind of fit. Good
thing to be near her at that time.

So I started learning hepatitis. Now, there were two
remarkable things about hepatitis B at that time. One, there was
a large epidemic in gay men, because of, again, an ecological
change, not a virus change; the virus had been around for ages.
But the ecology of homosexual activity had changed with
commercialization and urbanization of homosexual activity, so
that gay men were having a lot more contact with a lot more gay
men. The spread of sexually transmitted diseases was just
astronomical—gonorrhea, syphilis, even gastrointestinal
diseases, and hepatitis B.

And the second thing was that Merck Sharpe & Dohme was
developing a vaccine for hepatitis B, and one of the reasons that
CDC wanted me to come into this field was because of my
experience with vaccines.

Hughes: Was this the recombinant vaccine?

Francis: No, this was the forerunner of the recombinant. It was a plasma-
derived vaccine, which is actually the same—the essence of it is
exactly the same. It's a surface protein of the virus. You can
either purify the plasma to get this protein, which is actually
still used in many parts of the world, or you can produce it by
recombinant technology. This early vaccine was plasma-derived.

The question was to see if it worked. It looked like it
produced pretty good antibody, but we didn't have any way to test
it, except in a few chimpanzees; the virus didn't grow in
culture. The pattern of HIV in some ways is different, but also
in some ways very similar. There was an animal model in the
chimpanzee to test the hepatitis vaccine. The hepatitis vaccine
worked in chimps, and the decision was made to move ahead in
humans--to see if it worked in them.

So I started this large vaccine study in gay men. The group
at CDC in Phoenix was already studying the spread of hepatitis B
in five cities--San Francisco, Los Angeles, Denver, St. Louis,
and Chicago—and Wolf Szmuness and Cladd Stevens were doing
similar studies in New York City. So we all started immunizing
these gay men, half with a placebo and half with the vaccine, and
then followed them over time to see if the vaccine would protect.
And indeed, it was a highly effective and safe vaccine.

But in the meantime, in doing these studies, I got to know,
at least peripherally, the whole homosexual scene. I say
peripherally—it was really in great sexual detail, but I didn't
understand homosexuality necessarily, except it was a lot of men
having sex with a lot of men. As a straight man, I couldn't
understand it totally, but they did it, and I accepted it. In
California, we can be very tolerant. [laughs]

I guess we should bring politics in here about this time,
because with the completion of those trials, we started seeing
that the efficacy of the vaccine was really quite phenomenal.1

1 D. P. Francis, S. C. Hadler, et al. The prevention of hepatitis B
with vaccine. Report of the Center's for Disease Control multi-center
efficacy trial among homosexual men. Annals of Internal Medicine 1982,
97:362-366.

We had done major epidemiologic studies across the country
looking at how much hepatitis really was type B that would be
prevented by the vaccine, and what it cost. We came out with an
estimate of about $1 million a day for the United States, and now
we had a vaccine that was 95-plus percent effective in preventing
it. We kind of used the same smallpox model: why don't we just
go out and get rid of this disease? That was our plan.

Francis: We had the tools, but as it turned out, we weren't going to be

able to apply those tools because of political short-sightedness.

Hepatitis B Vaccine Trials in China, 1982-1985

Francis: I started working in China, where there really was a huge need.

Hepatitis B virus infected 60, 70, 80 percent of the Chinese, and
cancer of the liver was one of the primary causes of death in the
middle of life. So they were very interested in studying
hepatitis B vaccine. I started working with Dr. Xu Zhi-Yi in
Shanghai, and Liu Chung Bo in Beijing, studying the efficacy of
hepatitis B vaccine to prevent the last big chunk of transmission
that remained in the developing world, which was mother to infant
transmission. We did a major study there showing that we could
use vaccine alone, give it in the first day of life, and prevent
infection of the babies to about 90 percent.1 And that really
took care of hepatitis B; we could eliminate it.

At that point, all the data were available to begin to
eliminate hepatitis B in the world. That process is,
unfortunately, just starting now. It takes years and years and
years to get going, but I think it's something that's slowly
coming in the future.

1 Z. Y. Xu, C. B. Liu, D. P. Francis, et al. Prevention of perinatal
acquisition of hepatitis B virus carriage using vaccine: Preliminary report
of a randomized, double-blind placebo-controlled and comparative trial.
Pediatrics 1985, 76:713-718.

II THE AIDS EPIDEMIC

First Reports

Francis: Then I got this call from Jim Curran at CDC in Atlanta about
these funny cases of Pneumocystis in gay men.

Hughes: When?

Francis: May, June of '81.

Hughes: Had you seen the MMWR report?

Francis: June 5, I think was the date of the article.1 Some days before

that, or a week before that, Jim called. Jim and I had worked on
the hepatitis B vaccine study. His group from the sexually
transmitted disease division of CDC actually paid—we stole their
money to do the study of hepatitis B vaccine. They had extra
money, so we worked together closely. He was kind of the
organizer and made sure it was all proper. I was more the doer
and the protocol designer. It was a good collaboration.

Hughes: What did you think right away?

Francis: Well, I immediately called Max, [laughs] as you might imagine,
saying, "You wouldn't believe what's happening; we've got this
immunosuppressive disease associated with cancer in gay men." So
Max and I started conversing--! think my first notes are actually
in June of "81. He was saying that there was some work with
Raposi's sarcoma, looking at cytomegalovirus as a possible cause,

1 Pneumocystis pneumonia- -Los Angeles. Morbidity and Mortality Weekly
Report 1981, 30:250-252 (June 5, 1981).

and he sent me a couple of articles on that,
and the data started coming in.

We started talking,

Jim said, "With your background in feline leukemia and your
experience with gay men, it seems to me that you really need to
help us on this." I said, "Sure," not realizing what it would do
to the rest of my life.

The CDC Task Force on AIDS

Francis: A task force was set up. This was a time when CDC had no

resources at all. Nobody wanted to spare anybody from any of
their projects, because they were already overwhelmed. So nobody
could get any staff to work up this new outbreak. New outbreaks
are usually CDC's bread and butter—people will line up to get
into new outbreaks and find new exciting things. This one was
exactly the opposite. No one, no supervisor at least, wanted to
give their folks up--for good reason. Because at that point, the
Reagan administration was asking us, "Would you be happy with a
10 percent cut or a 20 percent cut?" So it was just horrible.
Some of our key junior staff were being laid off and fired,
because there were no resources.

Hughes: Tell me about the task force: Whose idea it was, who was on it,
and what you thought you were doing.

Francis: I think it was really Paul Wiesner's idea. He was the head of

the Division of Sexually Transmitted Diseases. He came from King
Holmes' group in Seattle to join CDC as the head of the sexually
transmitted disease division, and he saw this epidemic was a
problem. So he said, "Well, we've got to set up a task force,"
and he really volunteered Jim Curran and Harold Jaffe and Bill
Darrow, and I think Mary Guinan was in his group at the time.

Hughes: Is this standard CDC procedure?

Francis: It is. When there's a new epidemic, you grab people who one, are
available, and two, have background to fit the epidemic, call
some senior folks to head it, and then call a bunch of junior
folks to work on it. Absolutely typical. But it usually lasts
for a couple of weeks or a couple of months. And that's at a
time when you had the resources to be able to afford the
interruption of one's ongoing work.

Here, we had no resources at all, and the problem lasted for
years and years and years. Just to get a secretary, to get money

to buy an airplane ticket, to talk someone in the laboratory into
processing a specimen, required pulling teeth--for every single
step. And it didn't last for two weeks; it lasted for years and
years. It was a horrible bind to be in.

But this task force was set up. Initially, we all had our
other jobs, and yet we'd all meet--I would usually meet by
telephone from Phoenix--and young EIS officers were sent out to
investigate these cases. Then we set up some surveillance
systems in the big cities to start reporting the cases. It's
really the typical epidemic response.

Defining the Epidemic

Hughes: Talk in more detail about that, particularly in regard to San

Francisco. What exactly did go on between the CDC and the local
people?

Francis: Well, the first thing was to count cases. If you're going to

start defining an epidemic situation, the first thing to do is to
find out what you're going to call the epidemic, what case is a
case and what case is not a case. It was relatively easy for
this disease. There were severe opportunistic infections that
had not been seen before except in immune suppressed people, and
so the case definition was set up [1982]. The case definition
was a severe opportunistic infection in someone who did not have
any underlying disease or chemotherapy.

Hughes: The task force set up that definition?

Francis: Yes. It's absolutely key in epidemic control to make a case

definition to determine who fits in and who fits out. The other
disease fitting the case definition was Kaposi's sarcoma.
Previously that didn't occur in young people; by and large it was
[found in] older, Mediterranean or Jewish males. For the
original case definition of AIDS, as long as a person was under
the age of sixty or sixty-five, I've forgotten which, and had
Raposi's sarcoma, we called him a case.

And then, we investigated the cases to find out in the
broadest sense how they got their disease. Initially, that's
often a kind of quick-and-dirty investigation. It was simple at
first. Basically the forms asked, was the case straight or gay?
And obviously, most people were gay. But soon there were some
straight people who started coming through. Investigation of
them led to the fact that they were intravenous drug users.

Hughes: But nothing much was made of that for a long time.
Francis: No.
Hughes: Why?

Francis: The unknown aspects of it. It was investigation, trying to

figure out what it was, and you needed people to collect data,
you needed information to be able to make your hypothesis of what
kind of a disease it was. So the first year was spent actually
doing an investigation of gay cases. Harold Jaffe designed and
implemented a case-control study. I think the vast majority of
all living AIDS cases in the United States were actually
contacted by one of these young epidemiologists and interviewed,
with a huge form; I remember it well. Your pets, and your sex,
and your drugs that you took, a huge thing, trying to throw a
very broad net to investigate risk factors for individuals who
had the disease. Then in each one of the cities in which a case
lived, controls were taken in the same community, and the same
questions were asked of the controls, trying to see what the
cases did that the controls didn't. It rapidly fell out that it
was sexual activity.

Now, a similar study in New York showed that it was sexual
activity, yes, but the use of amyl and butyl nitrite was also
associated. That was "poppers"--a drug that causes
vasodilatation, used for cardiac disease, that also was supposed
to be wonderful for sexual orgasm. Poppers were very popular,
and were sold over the counter as a deodorant for gyms or locker
rooms--! don't know how. [laughing] I don't know if they were
ever used for a deodorant, but that was the marketing ploy.
People would just use them as a sexual stimulant.

Harold Jaffe rapidly said that the New York conclusion was
wrong, that the primary issue here was sex, and people who have
lots of sex look for sexual stimulants and use the drug. The
risk was sex and the drug use that carried along with it.

Hughes: Why did he say that?

Francis: Well, there are very elaborate statistical techniques that are

used to try to tease out primary versus confounding risk factors
associated with any disease. Modern computers have allowed us to
do that, where you can just run the data over and over and over
again, pulling out different parameters. If someone is positive
or negative for this question, you can actually pull him out and
analyze that group separately, as if they did or did not exist.
From this multivariant analysis, Harold concluded- -and I think

logically—that poppers were a secondary factor instead of a
primary one .

Resource Crisis

Francis: Well, unfortunately, the Reagan administration didn't want to

hear any of this. They wanted an easy out for this epidemic, and
continued to think that poppers were it, at least in terms of
action. They didn't withdraw poppers, mind you. They did
nothing. They didn't want to do anything. They didn't want to
support any part of the investigation or disease control. I'm
sure you're familiar with the memos that I've written blasting
from Phoenix and Atlanta that we've got to have resources; we
have tc do this right; we can't let an epidemic as severe as this
just burn. Because what was really coming through, and indeed
was true from the first MMWR, was that it looked like once you
got this disease, you died.

That wasn't typical of most diseases that we work with.
Most people, even with bad infectious diseases, survive. You
have to go to viruses like Ebola and rabies and others to get
this kind of horribly serious situation. It was a terrible
sandwich for a public health person to be in.

I wrote a remarkable memo in April '83, which Randy Shilts
has in his book,1 saying that we're sandwiched between a huge
problem and inadequate resources. Secretary of Health and Human
Services Margaret Heckler the same day was saying, "I've just
checked with all my public health staff, and we're doing
everything we can for this disease. No rock is being left
unturned," and that kind of garbage.

So the administration was just horrible with this disease,
leaving CDC, which was the premier investigatory institution for
the world, not to mention the United States, really shackled.

Hughes: That particular memo that you wrote went to Walter Dowdle, chief
of the CDC Center for Infectious Diseases. How did he respond?

1 Randy Shilts, And the Band Played On; Politics. People, and the AIDS
Epidemic. New York: Penguin Books, 1988, p. 273.

See also: James Kinsella, Covering the Plague: AIDS and the American
Media. New Brunswick, NJ: Rutgers University Press, 1989, pp. 179-181.

Francis: Well, Walt Dowdle then reported to Bill Foege, who was by then

director of CDC--from smallpox to director of CDC--and they sent
up budget requests to deal with this epidemic to the Assistant
Secretary of Health, who I think was Ed Brandt at the time, and
at that point the requests die.

It's interesting, you don't have to have a paper trail: If
you're sitting in a director's office at CDC, and you're being
told day after day to cut your staff, cut your budget, it doesn't
take a rocket scientist to say, "Well, gee, when we apply for
more staff, they're going to say no."

So this aura starts setting in of, "We're never going to get
these resources from the administration to do anything." You sit
there and argue with them about, "We need more vaccine for
measles for children," and they say, "Why, we don't have any
measles." Well, then a decade later we get this huge measles
epidemic in the United States, and no one looks back at these
jerks in the past who said, "Well, we had to save money," in
order to buy more armaments, so that we couldn't immunize kids.
You'll never hear, it will never come up in public, that someone
back there was the villain by deciding that CDC's budget was too
high; they were going to cut it back.

So I think the reality is the requests for funds were passed
up to department level probably already cut down to what they
would realistically expect, and then they disappeared into the
never-never land of HHS [Health and Human Services].

Hughes: You never got an answer?
Francis: Oh, you got an answer.
Hughes: What was the gist?

Francis: "We'll never get these folks [the Reagan administration] to do
anything . " Everyone knew it .

Unfortunately, I think maybe, if you look back on it, one of
our [CDC's] mistakes was being "team players." The team we were
on was the team of the United States people; we were not on any
team of government, in terms of a specific elected group. And
yet, the way it's set up in democracies is that we [CDC] were not
independent from the elected government or politics. And at this
point, CDC becomes a very political organization. The director
of CDC is now a presidential appointee, essentially a political
appointee. That's not good. You need public health to be
independent, and you need CDC to have an insulation from
politics.

Now we've got the Clinton administration, and they're going
to be very good policy setters for public health. And so there's
no problem, and so things won't change. But someday, we're going
to have another Ronald Reagan in there, and they're going to get
control of an organization like CDC. I tell you, the damage done
by Reagan to CDC will be felt as American citizens and world
citizens for the next decade. Turning it around is going to take
a huge amount of time. There are people like myself and others
who were trained in the activist mode at CDC, and me, and all the
rest are going to leave. As soon as they're retirement-eligible,
they'll bail. Like me.

[tape interruption]

Here you are at CDC, earning half the money that you could
elsewhere, fighting a bureaucracy that's often very frustrating.
Why do you stay? You stay because it's fun and exciting, new
stuff, stopping disease, stomping out viruses and bacteria and
parasites. It's accomplishment that makes it fun. When you take
that accomplishment away, then you're going to really select for
people who are status-quo seekers, and status quo is totally
contrary to the philosophy of public health.

Well, that's essentially what the Reagan administration was
saying, "Let's figure out all the things we can't do instead of
the things that we can do." Public health is always very cheap
and does things with incredibly limited resources. The example
that I used from that period of time, to put this in perspective,
is that the budget of Mass [achusetts] General Hospital was the
same as the budget of CDC, which was the same as the budget of
WHO. So you can see where we put the priorities in terms of
disease. We put it in therapy. The closer we get to large-scale
prevention, the less resources we put in.

Risk Groups

Hughes: Let's get back to the framing of the disease, which initially as
you well know was framed as a gay disease. Did you buy into that
initial definition?

Francis: CDC, for good reason, never used the term GRID, which is gay-
related immune deficiency, because very rapidly, the intravenous
drug users surfaced. As infectious disease epidemiologists,
never would we ever think of a disease—an infectious disease, at
least—being exclusively associated with one group. It just
doesn't do that. Now, you can have a unique infection of someone

who received dialysis, which would be only associated with kidney
dialysis patients. It just wouldn't transmit in other ways. But
not many other diseases would fit in that paradigm. Obviously,
because of our bias, we immediately thought of infectious agents
as the cause here, because we'd been working with gay men for
years, and they just were kind of the flagship of new infections
coming through.

Hughes: By "we," you mean you or the entire AIDS task force?

Francis: I think close to the entire task force. There were people who
always said, "Well, maybe it isn't infectious, Don." But
ultimately, I had to make decisions. We had limited resources,
and we were going to search for the cause. We couldn't pursue
every possible cause—infectious or noninfectious. Nature was
telling us something. From the epidemiologic data, we had gay
men with sex; we had intravenous drug users; we soon had sexual
partners of intravenous drug users, and then we had the
hemophiliacs. Nature was telling us it was infectious. How else
could you explain the disease in these disparate groups?

Now, the hemophiliacs were unique in that they received
plasma that was filtered to sterilize it—well, those filters
will filter out anything from bacteria up in size, which was very
useful, because now I didn't have to worry about bacteria or
parasites as the possible cause of AIDS. I only had to worry
about viruses. So this framing that occurs was very useful from
the laboratory side, but it was very clear epidemiologically that
those folks who were talking about poppers, or those folks who
were talking about immune overload and all this garbage—and
those folks were almost everybody outside of CDC, it seems—were
just not looking at the data.

Problems in Communicating Data

Francis: Looking back at our failures at CDC, some of which were resource-
or at least people-related, it's clear that we didn't market the
data well enough. Everyone now looking in retrospect says, "God,
wasn't this obvious that a virus was the cause of AIDS?" Well, I
think it was obvious to us who were very familiar day in and day
out with the data.

When we pulled groups into the CDC for updating, with the
worst example being the blood bank folks, you'd bring them in and
try to educate them in a day, and it would probably take a week's
worth of education to bring them up to speed. We didn't

recognize that, because we were so close to the data. We'd sit
and give these very cold, dispassionate slide presentations of
what the data was, without really making any editorial comments,
like, "Obviously, this is infectious. Gay men are having anal
intercourse and putting semen up their rectums all across the
country; the disease only exists right now in San Francisco and
New York and Los Angeles; don't give me this immune overload
stuff." It was nonsense. And don't give me poppers, because gay
sex and poppers were all over the country.

And then came the hemophiliacs, who do reside all over the
country, and they weren't only in New York, San Francisco, and in
Los Angeles. They were everywhere-- just like their Factor VIII
material. So the epidemiology told us all of the story. It's
just that some people refused to accept it.

Hughes: Is one of the problem related to funding, in that presumably if
the results of the CDC case-control study of AIDS [in San
Francisco, New York, and Los Angeles]1 had been released sooner,
people would have more quickly accepted a viral etiology?
Because of lack of funds, it took something like two years to
tabulate the results, did it not?

Francis: A year. We were releasing data constantly—one of the things
that just plagued us at the time were conferences. There were
constant requests. We were so short-handed that we hated it when
stories would break in the newspapers, where in public health, we
usually use the media to educate the public. That's part of our
job. But when that would happen with AIDS, there were what, a
handful of us, and your telephone would ring off the hook for
three or four days, and you got nothing done. That meant that
everything else stopped. There was no one to take up the slack.

So we made this very bad precedent of saying, "Okay, the
media office has to handle this stuff," which meant that the
response then became watered down to a relatively uninformative
base which was totally contrary to CDC tradition. CDC generally
sends the New York Times [reporter] to the EIS officer doing the
epidemic for information, and that's a great way to do it. I
mean, sure young epidemiologists make mistakes, but one, they get
educated—it ' s part of a training program—and two, the public
gets the latest information.

1 H. W. Jaffe, K. Choi, et al. National case-control study of
Kaposi's sarcoma and Pneumocystis carinii pneumonia in homosexual men.
Annals of Internal Medicine 1993, 99:145-158.

Hughes :

Francis;

Hughes:

Francis:

Hughes:

Francis:

Hughes :
Francis :

Jim Curran and I and others --everyone wanted us to speak.
"What is this AIDS?" Bring us to these big conferences.
Ultimately, we all got so tired of doing these dog-and-pony
shows. They were truly very important for marketing the message
and would have really helped the public to understand the
disease. But we could only do so much, if you wanted to do your
other jobs. So it really was a resource issue.

See, we didn't get any money. CDC finally got $400,000 for
AIDS in the summer of 1983. Exactly two years into the epidemic,
we got $400.000. Now, just for laboratory equipment alone I
could have spent all that. So all that money that we had been
spending, those ten, twenty people working on AIDS at CDC, came
out of other disease control programs at CDC. I came out of
hepatitis; Jim Curran and his group came out of sexually
transmitted diseases. It was just stealing from Peter to pay
Paul, and then doing it inadequately, setting kind of a whole
trend to do this half-assed.

What you're saying is, the media went to secondary people who
really didn't have the immediacy of the data?

Or didn't get any comments at all.

The message wasn't getting out? Or it was getting out garbled?

Getting out weakly, without the strength of the CDC behind it.

What did you want to get out?

I think in a new epidemic, you want to get every bit of new
information out. "Now we have drug users with AIDS." "The gay
men with AIDS are associated with high levels of sexual
activity." Be very frank about it. Once blood safety became an
issue, the media just [noise of fist against palm]. Now the
whole issue of "them and us" stood out. Up to that time, they
could do a "them" thing very easily: "It is all junkies and
queers. What do we care?" Now, realize we at CDC had been
working with junkies and queers for an awful long time and
realized that you can have disastrous infectious disease
situations, especially with gay men, if you ignore them.

What do you mean by that?

That they can spread disease across the country extremely fast.
Traditionally, a new disease came in to coastal cities and then
would go into the more interior areas of the country.

Hughes: Yes, but there was no reason that the agent, which a lot of

people believed was infectious, was going to be limited to the
original four risk groups [gay men, drug-users, hemophiliacs, and
Haitians]. The existence of risk groups implied that people in
them are vulnerable, and people outside them aren't.

Francis: There are two sides to that. One, the disease was limited to
clear risk groups. But two, the data indicated that the
incubation period was long and therefore we may be missing some
new cases spreading out. We knew early on that there was
heterosexual transmission from intravenous drug users as women
and babies came down with AIDS. But the issue was very different
at that point. The political (not scientific) issue then became
solidarity, and "them and us," and quarantine and isolation and
all of the stuff that was starting to be bantered around.

Once CDC starts to do a weak job of both investigating and
preventing the disease, then the state and local health
departments do a weak job. They don't have the staff, to deal
with the media, to deal with intervention programs and take
action. And then appropriately, the population starts feeling
left out: "We're not being protected." The vacuum is set;
there's no defense for it, and the extremists move in.

Then the government is going to respond, as Reagan's staff
constantly tried to do, by saying, "Yes, we are working on this
disease. Don't worry, it's "them" anyway." What should have
been the message from the highest levels of government was: "You
don't have to worry about getting this disease from buses, from
breathing air, normal daily activities. This does not look like
the plague, and don't shun these people and send every gay man or
Haitian away." Because the Haitians were getting beaten on; gay
men were getting beaten on. Politicians who were looking to
really segregate these folks anyway were happy to use this
epidemic as an excuse.

Even the Secretary of Health, [Margaret] Heckler, who was
not known for her strength, came out and said, "These are limited
transmission patterns, and you've got to have intimate contact"--
which meant sexual contact; they couldn't say it--"to get AIDS."
But that argument should have raised the issue, "Well, I'm a
heterosexual having sex; am I at risk?" And yes, you could be at
risk through sexual activity, and that's where the message kind
of broke down. It kind of flipped from extremes. "It's just
these people in risk groups [who are at risk for AIDS]; it's
nobody else."

CDC always put data out, but did not necessarily market it
terribly well where everybody could understand it. But what CDC

doesn't do is hide data. It was and continues to be a gay
epidemic here. The San Francisco Health Department estimates
that two-thirds of the newly infected people per year in San
Francisco are gay men. And that doesn't mean that one-third are
not important, but what's happened is everyone's trying to shift
now, "Oh, it's all heterosexual transmission." Yes, there will
be rivulets of infection going out into the heterosexual
community, but heterosexual sex is not like homosexual sex. Most
heterosexuals don't have these large numbers of partners. And
even when you limit the number of partners in the gay community
today, there's so damn much virus around there, when 50 percent
of the population is infected, that you make two mistakes and you
get infected.

Hughes: Had this marketing, the term you used, which was not good in the
AIDS epidemic, been part of CDC efforts in the past?

Francis: Yes. We never called it that, but it was all part of our
training; we would deal with the press all the time.

Hughes: So the epidemic didn't present a new problem in that regard?

Francis: No, but you get this almost omnipotent feeling in organizations
like the CDC, that "I am the expert in this field, and I will
study this. As soon as I figure out what it is, when I say this
should be done, it shall be done." And that was really strange
that we felt that way. It works relatively well with statutory
requirements like immunizations for school. But when it comes to
community norms, such as sexual norms, it is another matter.

Francis: You (as a public health officer) bury bodies in Sudan; you do

these things in real epidemics, and you have tremendous power to
control the epidemic.

Hughes: What about smallpox? There you eradicated a disease.

Francis: Yes, we eradicated a disease. But in terms of time, [Edward]
Jenner developed the smallpox vaccine over 150 years before we
eradicated the disease. Hepatitis B vaccine was made, and twenty
years later we still have barely started to eradicate the
disease. Bacterial infection in meat, like Jack-in-the-Box, is
an old issue that's gone on for ages, and we still haven't dealt
with it, so we have these epidemics of food poisoning. We feel
very omnipotent and powerful in the midst of a fast-moving
epidemic when we decide to do something, and it's politically
acceptable to do it. But for slower moving and long-term disease
problems, we haven't figured out how to tune the politics so that

good things are demanded by the people and public health is
utilized. So we [CDC] kind of waited for the opportunities to
wake up the people and the politicians, and you can't wait for
the opportunities with an epidemic like AIDS.

The Reagan Administration's Slow Response

Francis: Also, it's really easy to fail when someone tells you to fail.
Hughes: The government was telling you to fail?

Francis: When your boss says to fail. Now, some of us get angry at that,
and some of us say, "Well, that's the system." In the movie,1
there was this feeling that Jim Curran and I were very different.
Well, we are very different in style, but I don't think Jim had
any less anger, nor at this time has any less anger, than I do
about the government's ineptness with this epidemic in the early
days. It was terrible. We would sit there and scream and yell--
at the wall, unfortunately.

Hughes: Did it hamstring you psychologically?

Francis: Oh, it sucks your energy from you. We had this group called the
Sextet (that was Steve McDougal's term) --Walt Dowdle, John
Bennett, Jim Curran, I, Bruce Evatt, and Fred Murphy. We'd sit
for hours and hours and hours talking about what we were going to
do and how we would negotiate this ten-dollar item or this
twenty-dollar item, or what study should we do or which cancel in
its place. I'd get through those sessions, and I would just be
so drained that we had so much to do, and we were so busy
already. Yet we spent hours trying to economize. Because we had
to make these horrible decisions of what we couldn't do, it would
just double-drain you. The frustration would take all of your
energy away, and you needed immense energy to deal with this
epidemic. I started to go to work at three or four o'clock in
the morning so that I could be home with my kids at night.

1 "And the Band Played On"--A Home Box Office (HBO) film based on
Randy Shilts's book by the same title, broadcast in September 1993.
Matthew Modine played Donald Francis.

Research at the Phoenix Laboratory

Hughes: We've skipped some of the story. You were at Phoenix, and now

you're talking about Atlanta. Why don't you talk about what you
actually were doing in Phoenix?

Francis: In Phoenix, the CDC wanted me to direct the laboratory work for
AIDS.

Hughes: Is it correct to call what you were doing, basic science?

Francis: This was pretty straightforward. The first thing you do with a
new epidemic is stick material from patients in animals and get
them sick, so you can try to get an agent out. And then you put
it in culture and you try to culture the agent in an incubator.

Hughes: What was the Phoenix lab doing prior to the AIDS epidemic?
Francis: Phoenix was all hepatitis or viral gastroenteritis.
Hughes: So AIDS fit in neatly with what the lab was used to doing?

Francis: Yes, in some ways. We were searching out the cause of non-A,

non-B hepatitis. Now, what was unique about Phoenix, it was kind
of a square, one-story building of about a couple hundred feet
each direction, and in the middle were chimpanzees and monkeys.
So we had primates, the chimpanzees being incredibly valuable.
We made a decision not to use them initially in research on HIV,
which was too bad in a way. Later, we found that chimps were the
only susceptible animal, although they never do get sick, but
they do get infected. But I had marmosets. We were breeding
marmosets. We were using them in hepatitis A, but they weren't
very valuable at that time. So I first injected them.

Gary Noble, who was head of viral diseases at CDC in
Atlanta, was officially in charge. We would make suggestions of
what should be done, what animals should be inoculated, and then
I said, "Well, I'll do monkeys."

Hughes: Why monkeys?

Francis: Guinea pigs and small animals didn't come down with any [AIDS-
related] disease, so we moved up the chain to more expensive
animals. It was very interesting when I asked to do that. I
turned to our animal head, Jim Ebert, and said, "Look, I want to
stick a couple of marmosets. How can we do that?" And god,
their eyes opened, and they said, "Oh, that's really scary."

At that time in our lab, since we were the World Health
Organization lab, we had this unknown hepatitis virus from
Russian troops in Afghanistan, which turned out ultimately to be
hepatitis E virus, that we injected into our animals. We also
had non-A, non-B, which turned out to be hepatitis C, we were
injecting into animals. All of which posed immense danger to the
humans working with them. These guys were very comfortable with
that. They'd done it for years—hepatitis B, hepatitis A, non-A,
non-B, whatever. They were accustomed to doing it.

But when I came in and said, "I want to take this stuff out
of AIDS patients and shove it into these animals," they very
appropriately said, "Oh, my god. We've got to do something very
different with this agent. This could really be dangerous." I
said, "Look, guys, most people don't think it's infectious." And
they turned to me, very wisely, and said, "Don, you think it's
infectious. And if you think it's infectious, we think it's
infectious, and we're going to be extremely careful."

So then I needed a $5,000 hepa-filtered enclosure to keep
these monkey cages in. I think it cost $10,000. Well, CDC said,
"We'll never get this money. How are we going to do this?" And,
I needed to modify the animal room, because I needed an anteroom
where you could come in, change clothes, go into the dirty area,
wash off, take your clothes off, get the disposals [disposable
clothing] off, throw them away, get back into your other clothes
and go back out, so you don't take this bug everywhere.

"Well, we'll never get permission to do that," I was told.
Luckily, we had a handyman on the premises there, and Bud and I
just went and got two-by-fours and sheetrock, and he built this
thing, without asking anybody. If we had to ask CDC for
permission and for funds, it would have taken months. But we had
to ask to get this $10,000--can you imagine? Here we were, this
big laboratory, and all I wanted was $10,000. I had to write
paper after paper to justify it. After months, we ordered it,
and finally we injected the marmosets.

The Move to the Centers for Disease Control in Atlanta

Francis: Now, during all that time, Gary Noble and I are discussing what
needs to be done, but I'm trying to stay relatively peripheral.
There was a personal issue on this. Atlanta was considering
closing the Phoenix laboratory and moving us to Atlanta.

Hughes: Why?

Francis: Reagan economics. "Why do you need another facility out there?"
And it was a good question: Why the hell is hepatitis out in
Phoenix? It was an old CDC building, and they started working
with Indians and gastroenteritis. That got into hepatitis A, and
once you started working on hepatitis A you work on hepatitis B,
so that's why it was in Phoenix. They didn't have the facilities
in Atlanta; they didn't have the space in Atlanta. But we were a
hotshot lab and they appropriately wanted us there. But we had
our families in Phoenix.

I had now been with CDC since '71, and this was now '81; I'd
been ten years at CDC, and been all over the world, but had never
been assigned to Atlanta. And I rather liked that. So there was
an issue there. They kept saying, "Won't you run the AIDS lab?"
I said, "I can't do it from Phoenix." They said, "Sure you can."
But I knew what the issue was: They were going to pull me and my
family back to Atlanta, and maybe ultimately the lab.

So I resisted that. I said, "Look, I'll do it from here and
do what I can, but you guys have to run the Atlanta stuff."
Well, ultimately it became ridiculous. I would go back to
Atlanta, and Jack Obijeski--he now works at Genentech; he
involved me in Genentech in the first place—was really the
hotshot molecular biologist in the CDC. I would go to a meeting,
and Jack would be there and a few others, and he'd say what
needed to be done, and I'd go back to Phoenix and do my thing,
presuming that Gary Noble would follow through. And then I would
come back to Atlanta a month later, and check what had been done.
Nothing would be done. They just couldn't do anything. They
clearly needed someone there.

So they kept pressuring me and pressuring me, and I said,
"Okay, okay, I'll do it." Then I started commuting. Again, I'd
leave my family in Phoenix. So I'd spend one week in Atlanta and
then one week in Phoenix. That was really horrible. I was
exhausted; the family was exhausted; we had young kids at that
point. My wife was head of infectious disease for the health
department in Phoenix at that time. She had discovered the cause
of aspirin in Reye's syndrome and was doing all that stuff, and
here she was trying to be a mother of two young children. It was
just god-awful.

So I finally gave up. I guess in September of '83, we moved
to Atlanta. And soon after, the whole Phoenix lab was closed,
and we would have had to move anyway. The chimps and the
freezers and everything had to be put into airplanes.

The Laboratory

Hughes: What was your setup in Atlanta?

Francis: Horrible. In Phoenix, we never felt like we really had a state-
of-the-art laboratory, but we had a relatively modern virology
lab . When you were away from headquarters , you could spend some
money and at the end of the year you'd get your hand slapped.
"Oh, god, I'm sorry, I overspent my budget. I'll never do it
again." And then you do it next year. In Atlanta, that just
wasn't the case.

So I walked into this lab in Atlanta, and this is the
Centers for Disease Control—a world-class center. It used to be
one of the most outstanding laboratories in the world. And it
was just a pile of junk. Old copper incubators, and no modern
virology at all. Now, some labs in Atlanta were well equipped,
but certainly not the one that I inherited. I got some of the
leftovers of a couple of programs, and a few people--Ci
Cabradilla, Paul Feorino, Jane Getchall--who were really
interested and really good. So it was kind of an interesting
combination- -devoted people, too much to do, and too few tools
with which to work.

Now, I was, by that time, the assistant director of the
Division of Viral Diseases [September 1983-June 1985], which is
the biggest division in CDC, and so I had access to a lot of
people. But you just can't go out and steal somebody from
influenza. You can't go down to the hot lab and steal somebody
from the Ebola group. But what you do is you kind of interest
the director of these labs in this new disease, and then they
kind of help you with some of their technicians and equipment.
It's just a god-awful way to deal with an epidemic like this, but
that's the way I had to do it.

So we patched it together, and when we got the first
$400,000, we finally bought some incubators and centrifuges and
all the plumbing and stuff that you need. Safety issues were an
incredible problem, because we weren't in the hot lab, and yet I
knew we had something that was damn dangerous. I didn't
necessarily want to be in a space suit lab, because that really
inhibits you, but I wanted space where at least you didn't have
tourists walking down the hallway. I didn't want anybody to die
in my laboratory—including me.

Hughes: You had tourists in the hallway?

Francis: Yes. Not only had we tourists walking down the hallway, we had

virus walking up the hallway in these disposal pans. Because our
autoclave, instead of being in each lab, which would be usual for
really a highly infectious material, was down at the end of the
hall. So we had just simple problems with changing doorknobs and
things that just never would be done; it would take weeks and
weeks and weeks. Actually, not until after I left Atlanta did
they put security doors in the hallway. But we all knew you
could walk through the autoclave room and bypass the security
doors anyway.

We were careful with HIV. CDC had had only one death, from
Rocky Mountain spotted fever, several years before. It increases
your caution. But other HIV labs have not been so lucky. Look
at Gallo's labs: I think they infected two people up there.

Hughes: Were you scared?

Francis: Sure. But that was part of the job. I think probably some of
the psychopathology that those of us in this field have is that
we get a certain thrill from our jobs. You don't want to get
infected, but you want to be on the edge. I'm a downhill skier,
and that kind of extra little risk-taking must be part of our
personalities. In public health we always talk about risk
reduction. We are committed to that. But the work we do is
risky. You don't want to be the one that gets infected, and you
don't want anyone in your lab to be infected. But you know that
on the other side of your gloves is something very dangerous.

Suspecting a Retrovirus

Hughes: Talk to me about the science. What actually were you doing?

Francis: Well, I had been sending specimens to Max, so that by the time I
got to Atlanta, we really were talking about an agent growing in
lymphocytes that could well be a retrovirus.

Hughes: Why were you talking about a retrovirus?

Francis: Well, it was interesting. Max had done this interesting study

where he took our sera, and he put that serum on HTLV-I-infected
cells. This one technician named Mary Frances McLane in Max's
lab could get a positive test on these cells in a high proportion
of AIDS cases. We published that, actually, in the same journal

that the French published the LAV article--Gallo's articles on
HTLV-I, Max and the CDC's article.1

Hughes: So that was 1983?
Francis: That was May of '83.

So since it was a lymphocyte-related disease, and since the
retroviruses clearly were known to infect lymphocytes, we
accelerated our search. Unfortunately for us, all our animals
were thriving. We went all the way up the phylogenetic scale to
monkeys and then ultimately to chimpanzees, but all were doing
fine. That really hurt us in terms of finding a cause. If you
don't have an animal that gets sick--.

I used to always run into Joe McDade in CDC, who's the one
who found the Legionnaire's bug. And he would always be so
sympathetic. He said, "Don, our guinea pigs bellied-up in six
weeks, so we had something to work with. If you have two
equations and one unknown, you can figure out what the unknown
is. But when you have two equations and two unknowns--." We
didn't have any antibody; we didn't have any antigen; we couldn't
do anything. In retrospect, we made mistakes. Given our lack of
resources, we never had time to think about what we were doing,
whereas the French sat down and did it right.

Anyway, Max and Bob Gallo and I were all doing the same
thing. We were culturing lymphocytes, putting fetal cord
lymphocytes in with the patient's lymphocytes, and doing reverse
transcriptase assays on them to see if a retrovirus would come
up.

Hughes: What made you think it was a retrovirus?

Francis: It wasn't anything else, [laughs] I guess was one reason. We had
retrovirus experience, and it fit in terms of a model. And Max's
preliminary results in serology. Probably Max's preliminary
serologic results were the most exciting. Bob was isolating
HTLV-I, but we absolutely knew it was not HTLV-I.

Hughes: Why?

Francis: Because early on we'd sent blood specimens to Bob Gallo 's lab for
HTLV-I testing, and only 6 percent of them tested positive. It

1 M. Essex, M. F. McLane, T. H. Lee, et al. Antibodies to human T-
cell leukemia virus membrane antigen (HTLV-MA) in hemophiliacs. Science
1983, 221:1061-1064.

Hughes:

Francis :

Hughes:
Francis:

Hughes :
Francis ;

Hughes:

didn't fit. We all thought it a was variant retrovirus of some
kind at that time.

Well, Shilts says that very early on, in 1981, you made the
correlation with feline leukemia virus.1

Yes, it was very early. Actually, Dave Morens, who was doing the
lab coordination for Gary Noble early on, actually published in
JAMA a few months back that I said to him it was a retrovirus
ages and ages before.2

What was the date?

He actually dates it exactly,
though.

I don't remember what it is,

At the first Public Health Service meeting on the cause of
the epidemic [Workshop on KS and opportunistic infections,
September 15, 1981] --it was a small group of us, mostly from N1H
and CDC. Shockingly, most of the interest was generated by Gene
Shearer from NCI who was talking about semen up the rectum
causing immunosuppression in rats. We had a one-day meeting, and
the whole morning was spent on antigen overload and poppers as a
possible cause of the epidemic.

I went up to the library at noon and made copies of my
feline leukemia work and my hepatitis B epidemiology work. When
it finally was my turn in the afternoon, I pulled them out and
said, "If you combine these two, you have the epidemic.
Everything fits. The virus with the epidemiology and
transmission of hepatitis B, and the natural history of feline
leukemia. You have it."

What was the reaction?

Absolutely fell like a lead balloon. Talk about a marketing
mistake! I'm sure I did it in about as much time as I Just
described it to you. I should have allowed more time, given more
background, described what feline leukemia was.

Why wouldn't your suggestion be followed, when they were
considering poppers and immune overload, et cetera?

1 Shilts, And the Band Played On, p. 73.

2 Morens, D. M. Mandatory testing for HIV. Journal of the American
Medical Association. March 3, 1993, v.269, 9:1115-1116.

Francis: Don't ask me. Back in the lab, I kept being influenced by those
who kept pleading, "Well, we better think broader." More
fundamentally, I didn't spend the time when we were culturing the
virus to realize that we were not talking about a transforming
retrovirus, like HTLV-I which produces cancer. We were talking
of one more like feline leukemia that killed cells.

But it didn't make any difference, retrovirus or not. I was
an infectious disease doc, trained in cytopathic viral disease.
Max and Bob Gallo were retrovirus-transforming-type docs. We
spent months putting AIDS samples on cell cultures and looking
for rapid cell death—classic virology. Then when we switched
over in the extreme to culturing lymphocytes, looking not for
rapid cell death but for cell transformation, we followed the
Gallo transforming protocol. I still don't know why I was
influenced to make such a radical change.

Hughes: Is that what the French did differently?

Francis: Yes. The French looked early for reverse transcriptase

elevation, signifying a rapidly growing cytopathic virus. They
put specimens from patients in culture and frequently did RTs
[reverse transcriptase assays] early after initiating the
culture. We did not do testing that frequently. It was
expensive to do the assay and we didn't have the resources. So
we spread them out. Usually on the first one, a few weeks after
infection, we got this small blip of elevated reverse
transcriptase. Unfortunately we ignored it, because we were
waiting for elevations weeks later as the virus transformed the
cells. As a result, we missed the indication that we were
growing the virus. It was there in that early blip. We were, in
this case, too patient.

Isolation of the AIDS Virus
[Interview 2: December 22, 1993] II

Associations with the Pasteur Institute

Hughes: Dr. Francis, we were talking last time about the isolation of the
virus. I want to start today with your memory of your first
association with the people at the Pasteur Institute, and why
that came about.

Francis: The initial contact actually originated from Pasteur. As I

recall, it was Francoise Barre who called me from Paris about
some specimens that we had reported in our May '83 article with
Essex. We went to the freezer where we kept San Francisco City
Clinic cohort specimens and pulled out samples from individuals
who developed AIDS. We had the early specimens and the late,
because we'd been following these men as part of longterm
hepatitis B studies.1 Francoise was interested in these, because
obviously if they were trying to make an association of a virus
with AIDS and developing a test for AIDS, one of the conditions
of proving the cause would be that the infection occurred at an
appropriate interval prior to the onset of the disease. So you'd
really like specimens from people many years before they came
down with disease. We fortuitously had these specimens.

So Francoise called me--it must have been in mid-'83--and
asked for some specimens. I said sure. So I sent her four
specimens blinded. There were a couple of drops of serum of each
of these very valuable specimens from two people who developed
AIDS. There were two early specimens and two late specimens.

Hughes: Where were you getting your specimens?

Francis: From our freezer. [laughter) We had ongoing hepatitis studies.
But because of our move from Phoenix to Atlanta, the freezers
were all disorganized. Since we had no resources to hire someone
to help, I had to literally go in and spend a day in the freezer
with my winter clothes, sorting the specimens and getting them
organized so that we could find the right ones.

Hughes: You were working exclusively from the hepatitis B specimens?

Francis: Well, we had lots of AIDS specimens at that point, but the French
also had access to similar ones. More interesting were the
hepatitis specimens where we had people who had a blood
[specimen] taken early on and later developed AIDS.

Hughes: Then what happened?

Francis: I think a couple of months went by, and Francoise called me and
said, "I have the antibody test results. Do you have the code?"
I said, "Sure," and she gave me the results, and I gave her the
code. She got all of them right: the two early ones were

1 For more on these studies, see the oral history with Paul O'Malley in
The AIDS Epidemic in San Francisco: The Response of Community Physicians.
1981-1984. Regional Oral History Office, Bancroft Library, University of
California, Berkeley. Hereafter, AIDS Community Physicians series.

negative and the two late ones were positive. So my interest in
their virus increased dramatically. Initially we set up
collaboration where Francoise came over and brought us virus to
inoculate into monkeys. At that time we did nothing else with
the virus besides inoculate; that was the agreement.

Hughes: Why? Did they limit it just to inoculation?

Francis: No, there wasn't much virus available at that time. It just kind
of evolved. We just never moved any further than that early on.
I got the feeling that they wanted to do the initial work. They
wanted to feel comfortable with their findings before sending out
samples to others. It wasn't until February of '84 that we got
sizeable quantities of really hot-growing virus. By that time,
they had enough virus to give out. They were producing enough to
use in an antibody test. I was sending them specimens regularly
and they would test them, and had quite good results.

Cold Spring Harbor Meeting on HTLV, September 1983

Francis: In September of '83, we had the first Cold Spring Harbor meeting
on HTLV [human T-cell lymphotropic virus]. The French reported
the results of the first four San Francisco City Clinic cohort
specimens at that time. Then, we continued to send them other
specimens, and their results were continuing to look quite good--
relatively low positivity in the AIDS patients, but that was not
surprising, because the immune system in the AIDS patients was
already compromised. So it was not too surprising that they
would have a lower level of positivity in that group compared to
patients with lymphadenopathy.

Hughes: Was that the meeting where Montagnier first presented LAV

[lymphadenopathy associated virus] as the possible cause of AIDS?

Francis: Right, that's where Montagnier initially presented the LAV

results in public where, I think, they had 30-40 percent positive
on their blood test with AIDS patients, and 80-90 percent
positive with lymphadenopathy patients. And they had electron
micrograph pictures of the virus, showing that it looked like a
lentivirus. They were making parallels between that and the
lentivirus of horses that causes equine infectious anemia.

Hughes: This comparison was based on the electron micrographs?

Francis: They were also doing some serologic comparisons, but primarily
the lead was from EMs. It was such an unusual- looking bug that
it looked like the horse lentivirus.

Hughes: What was the reaction from Gallo and the rest?

Francis: Gallo was really obnoxious. The rest of us were saying, "Well,
it's interesting; it's worth pursuing." It looked exciting and
interesting but not overwhelming at that point, because of the
lower rates of positivity in the AIDS patients.

Hughes: Were you buying Gallo 's hypothesis at that point, that the agent
was an HTLV [human T-cell lymphotropic virus] of some kind?

Francis: Max Essex at Harvard was helping us—doing work with HTLV as the
target virus against which we were testing serum from AIDS
patients. But we knew it was not HTLV-I itself because Gallo had
already done tests collaboratively with Max and me, and only 6
percent of the specimens were positive. So the cause was not
HTLV-I. Our hypothesis was that it was a variant retrovirus,
different but with some cross-reactivity to HTLV-I. It turned
out to be even more distant than that. We were clearly very
close to target, but it was not HTLV-I itself. And I think
everyone knew that. Bob was pushing the HTLV-I concept more than
Max and I were. We knew it was something like HTLV-I; our
assumption was it was something like that, but not that very one.

Laboratory Procedures for the AIDS Virus

Hughes: Well now, last time you talked about the parallels with feline
leukemia virus, and the fact that your lab protocol was still
governed by the paradigm that [the AIDS virus] was a transforming
virus. Why did you stick with that idea?

Francis: Because we were stupid. [laughter] HTLV was the only growable
human retrovirus at the time, so it's logical that if you were
looking for one retrovirus, you would use a protocol that worked
for another human retrovirus. But we didn't take the ten minutes
that it really would take to think about it : that it was not a
slowly evolving transforming agent, that it was a really rapidly
multiplying cytopathic agent. Instead of transforming cells
making them cancerous, it was more likely to be cytopathic,
killing them. If it were [transforming], it would show itself
after a few days of culture rather than a few weeks or months.

Hughes: Where were you getting the fact that it was cytopathic?

Francis: Because the pathology of the disease was that it wiped out T
cells.

Hughes: All right, so that was clear. So you didn't have to go into the
RT business to establish that fact.

Francis: No, RT was just a measurement for a retrovirus growing in

culture, and that's what we were doing. We were doing RTs on a
regular basis, carrying on for months and months and months.
It's kind of an arduous job, so you want to spread out the
assays. So we didn't do them close together in the first few
weeks. As I mentioned, we had little blips early. We had a
little increase in RTs at that time, and we ignored it and waited
for this big RT transformation later. Now, if we had just fed
those viruses more substrate, if we had given them more cells to
grow in during that early RT blip, we would have found the virus
a year before.

Hughes: But that was the mistake that everybody was making.
Francis: Yes, we all made it.

The Pasteur Group's Approach to the AIDS Virus

Hughes :
Francis :

Hughes :

It's very easy in retrospect to say it was a mistake-
It's very easy in retrospect. But the French used logic and

said, "Well, let's look early on.
time for RT to appear."

Let ' s not wait such a long

How much do you think the flexibility of the French has to do
with not buying into Gallo's hypothesis?

Francis: No, they have told me that they kind of did their work as a "Me,
too" experiment. They said, "Gallo and CDC and Essex are all
growing it, are getting a retrovirus; we'll just do the same
thing that they're doing, and grow it too, just for interest's
sake." But then when they sat there and designed their
experiment, they put a little more thought in it than we all did.
We were following the same old Gallo protocol. They said, "Well,
let's just really zero in on the early stage of culture." They
didn't realize that we were waiting and waiting and waiting for
these transforming agents.

So they had a flexibility, but they also didn't have the
bias that we did. And we were just totally overwhelmed with all

sorts of other things at the same time—and that's typical, when
you're in a rush like that. You just don't sit and discuss
everything and really outline it, and then kind of relax the way
you need to in order to search appropriately.

Hughes: Am I right that the French group was focusing on the virology,
not trying to do a lot of other things, as you at CDC were?

Francis: Right. They were just doing retrovirology of the specimens,
whereas we were doing all sorts of other stuff, and a lot of
animal inoculations and looking at other viruses. We had a very
broad approach. They did it narrowly—but properly.

Hughes: Who do you credit with the realization that this was a different,
a new, virus?

Francis: I think that you have to give the French the credit.
Hughes: Who specifically?

Francis: I don't know, [Luc] probably all three of them. It was Barre,
[Jean-Claude] Chermann, and Montagnier--and it was Barre and
Chermann I think that really did the virology. As I understand
it, Montagnier's lab didn't want to grow this virus, which was
probably a decision of laboratory safety. This is not a friendly
little virus to grow in any casual way in a laboratory. You have
to be very careful or you'll die.

Hughes: And yet, the Pasteur has a long history of working with lethal
viruses. Think of rabies, which started it all off.1

Francis: As a matter of fact, the lab at Pasteur is right over Louis

Pasteur's tomb. Francoise Barre and Jean-Claude Chermann were in
the same building, and the tomb is right down in the basement.
So the discovery was not far away from his remains.

Hughes: What difference did the conceptual framework of these three

groups make? You and Gallo were using the HTLV framework and the
Pasteur Institute group wasn't.

Francis: Oh, it's interesting. Willy Rozenbaum told the Pasteur group

that he had a patient with lymphadenopathy and asked them to look
at the tissue for a virus. They did it because they knew what we
were doing and they were just going to repeat our work. They
luckily didn't call us and ask us exactly what we were doing;

1 The Pasteur Institute was founded in 1888 to develop Louis Pasteur's
rabies vaccine and eventually other vaccines.

they sat down and thought for themselves. Francoise Barre-
Sinoussi and Jean-Claude Chermann, I think, are the ones who put
it together, saying, "Well, we should really look early at the
cell cultures, because the virus might be cytopathic."

Chermann's Presentations in the U.S., February 1984

Hughes: In February of 1984, Chermann came to the CDC. He gave a
presentation at that time?

Francis: Yes, two presentations. He gave a presentation at Park City,
Utah [February 7, 1984], l showing their data at that time. He
reported much higher rates of positive tests in AIDS patients
than before. He then gave the same talk at CDC on February 15.
It was extremely convincing, and at that point he brought us
virus (LAV). As a matter of fact, when he came in the country, I
had arranged for our quarantine people in New York to pick up the
virus and ship it down to us. By the time he arrived in Atlanta,
we already had electron micrographs of it, and we started
duplicating a lot of the work that he had done to show that this
virus really was different. It was a lentivirus; the structure
was similar to other lentiviruses--a subgroup of retroviruses .

At that point Chermann went back to our electro-
photomicrograph pictures from our early cultures. That was one
of the best and worst days of my life. Those pictures were taken
back when these low- level RT values were detected. We had taken
some electron micrographs of the cells at that time. He goes
back and points at these structures in our EMs, "There's the
virus right there."

Hughes: The virus was very clear?
Francis: Oh, yes. [tape interruption]

We had a picture of the virus in those early cultures, right
there in front of us, and we missed it. It was in the cultures
when we had these low levels of reverse transcriptase.

Now mind you, if you don't know what you're looking for with
an electron microscope, it's very difficult. We had the best
electron microscopists in the world working on it. But once you

1 John Crewdson.
1989, p. 10.

The Great AIDS Quest. Chicago Tribune. November 19,

Hughes:

Francis:

knew what the virus looked like—it's a rather strange- looking
thing—it's easy to spot. Jean-Claude said, "Look at this." And
he was absolutely right. So, we had grown it. But we just
missed it.

After Jean-Claude came, everything went like crazy, because
we knew what we were doing. By early 1984, Bob Gallo calls and
he says he's got [an antibody] test, and we had a test, and so we
all were sending tests around, and that's when the misery
started.1 [tape interruption]

Did you go to the Park City meeting where Chermann gave a
presentation that February?

No, I did not. Jim Curran did. I don't remember if other people
from CDC went.

Hughes: What was the reaction at the CDC meeting? Did people buy the LAV
hypothesis?

Francis: Oh, yes. I think everyone at CDC knew the search was over; the
cause had been found.

Distributing CDC Virus Specimens

Hughes: Two weeks after the Park City meeting, Gallo called to say that
he'd found the virus.2 Do you remember that?

Francis: I think I was talking to Max, who said that Bob had several

isolates. And then Bob called Jim Curran--I've forgotten whether
I was out of town or not—and said that he had developed a test
and wanted some specimens from us. Jim talked to me and I
arranged to send a panel of serum up to him.

Hughes: But you didn't ask for any specimens from him?

Francis: No, not at that point. We didn't know what he had and how useful
it was. It wasn't until after the results came back that it was
interesting.

'For better chronology, the preceding three paragraphs were moved from
the transcript of Interview 1.

2 Sandra Panem, The AIDS Bureaucracy. Cambridge, MA: Harvard
University Press, 1988, p. 40.

Hughes: You mean the results from what you'd sent?

Francis: Yes.

Hughes: Interesting in what sense?

Francis: I took the same panel of serum; sent it to Bob Gallo, sent it to
the Institute Pasteur, and sent it to our lab at CDC- -all
blinded. I kept the code, and then had them all report back to
me the results of the antibody tests. The results proved that
the cause of AIDS had been identified. The specimen panel was
set up with some very valuable specimens, including the San
Francisco city clinic cohort seroconverters and specimens from
the transfusion-associated cases. For these we had samples from
all the donors to a case of AIDS, and samples from the case of
AIDS. If the blood tests were correct, you should be able to
pick out the suspect donor to the case. And indeed, in all these
cases, the suspect donor tested positive.

Hughes: So every place that you sent the panel got the same-
Francis: Came out with the same results, almost identically. We had a few

plus or minuses, and a few variations which you'd expect on a new

test. But that sewed the whole thing up.

Meeting at the Pasteur Institute, Early April 1984

Francis: That's the point where I called Bob and Pasteur and arranged for
a meeting at the Institute Pasteur in early April to discuss how
we were going to deal with all this.

Hughes: That meeting was contentious, was it not?

Francis: It was bizarre. Contentious only that Bob was not very sharing,
excluded me from the discussions of his results with Pasteur, so
I never did get to see his results until the preprint came out.

Hughes: What excuse did he use for excluding you?
Francis: Didn't want me to see his information.
Hughes: You mean he said that point blank?

Francis: Yes. He said something like, "I want to have the meeting with
Pasteur in private."

Hughes: So he obviously thought of you as a competitor rather than a
collaborator.

Francis: He saw both of us as competitors.

As a matter of fact, it got even more bizarre. Because
everything was so exciting, we went out and celebrated that
night. Jean-Claude took us out to a wild French cabaret. At
that point, I didn't know, but Bob and Jean-Claude went to the
restroom and Bob turned to him and said, "We're really doing
well. Pasteur and NCI [National Cancer Institute] can do this
together; we don't need CDC." And then the next morning alone
with me at breakfast, he told me that CDC and NCI could do this;
we didn't need Pasteur. So he was playing everything to his
benefit. But it didn't take Jean-Claude and me too long before
we shared that information.

But the sad thing is that when you have a bizarre person
like Bob, who has some talent no doubt, and tremendous influence
on the field, you give him extra leeway. We gave him far too
much. Given his strange personality, all these kinds of things
become expected—and accepted. So: "Oh, that's Bob; we'll go on
our way. He acts like a seven-year-old child, and, well, we'll
just have to tolerate him."

That was silly for me, to be honest. Here I was with Gallo
in the Public Health Service in the U.S. government trying to
find the cause of AIDS, and this guy was acting like a total
lunatic. I should have reported him to the higher authorities
straight away. But you kind of work with people as collaborators
and not in some hierarchical government structure. That's one
place where I should have shifted gears and said, "Enough's
enough." Anyway, as you know, the insanity over the discovery
went on and on for years .

V. "Kaly" Kalyanaraman

Hughes: Tell me how Kalyanaraman [Kaly] fits into this story, because it
doesn't seem to me he's given enough credit.

Francis: Oh, no, he was very key for us in CDC. He's a very talented
retrovirologist who was working in a contract laboratory in
Bethesda that contracted with NCI and Bob Gallo. We put out the
word at the National Cancer Institute that we were looking for an
experienced retrovirologist, because we really thought a
retrovirus was the cause, and we needed someone to help. We

finally got money (the Reagan administration finally, after two
years, gave us I think $400,000), so we had money to support a
Ph.D. level researcher.

Hughes: This was 1983?

Francis: This was 1983. We were recruiting a scientist from NCI named

Shushil Devare, a very good guy, who was also being recruited by
Abbott Laboratories. He was from the lab that Ci Cabradilla at
CDC worked with, and Ci knew him. So we had Shushil come down
for an interview. He would have been terrific. But he decided
to go to the private sector, to Abbott.

Shushil passed the word amongst his friends, happened to be
Indian friends, that CDC was looking for somebody, and Kaly
called. Now, as soon as Kaly started looking into this job at
CDC, I knew there was a potential problem, because he was working
under a Gallo contract. Kaly was the discoverer of HTLV-II
together with Bob Gallo. Recognizing the sensitivity, I called
Bob straight away--as soon as I heard that Kaly was interested.
I said, "We didn't recruit him, but he found out through a
friend." I wanted to inform Bob about this, as a gentlemanly
act- -I mean, when you start dealing with other people's lab
workers, you have to do it rather gingerly, because it's
obviously a very touchy thing.

But we didn't initiate the contact, and I just told Bob, "We
didn't initiate it, but Kaly's interested, and I will look at him
seriously. If he's interested, that's up to him, not either you
or me." He said, "Well, I will obviously urge him to stay," and
I said, "Of course." He said, "I think he's very good." And
that was it. Kaly ultimately decided to come to CDC.

Hughes: Why?

Francis: I don't know. I think he saw this as an opportunity for him to
get out of a big lab setting. He didn't have a full-time
position with NCI; he was a contract worker at another
laboratory. And here he could have a full-time position at a
good salary that NCI apparently couldn't offer him. So we hired
him.

When the offer was made, I called Bob Gallo and said, "We
have made an offer to Kaly," and he just hit the roof. Screamed
and yelled at me, and said, "Kaly will come with no reagents.
You will never get anything published in retrovirology; I will
see to that. I find this terribly offensive." And he just went
on one of his rampages that he often does. He screams and yells
and abuses everyone in sight, including me. I said, "Well, thank

you very much, but that's not going to interfere with us hiring
him." So Kaly came, and he was very valuable.

Hughes: What did he do specifically?

Francis: He was one of our primary virologists. He was isolating viruses
from American [AIDS] patients' material; he would grow the virus,
characterizing the viral proteins. He's a virologist/biologist
and a protein chemist. So he was critical in purifying the virus
and seeing what it looked like inside, improving serologic tests,
et cetera.

Hughes :

Francis:

Hughes:
Francis :

Hughes :
Francis :

Hughes:
Francis ;

Was he using the technology that had been developed in Gallo's
lab? By [Mikulas] Popovic and others? Or was that something
that he brought to them?

The technology of tissue culture and cell culture is very
widespread, some of which he was doing at Gallo's lab.

But there were some specific cell lines that were used.

Yes, and a lot of that was done at NCI, I think most of it
outside Bob Gallo's lab. But the specific techniques used at CDC
in growing the virus were primarily the French techniques.
That's what we used.

Which techniques was Kaly using when he was on contract to NCI?

I don't think Kaly was working on AIDS at NCI.
I think he was working on HTLV.

I'm not sure, but

I see. What I'm trying to find out is whether he came with the
technology, which he then inserted into the CDC protocol.

No, he came and he really adopted the French protocol. And he
combined their information with his vast knowledge of working
with these viruses and their proteins. No doubt some of his

skills were acquired while he was working at NCI.
enough; that's progress.

That's fair

Mikulas Popovic's Pooling of AIDS Sera

Hughes: One other point: there has been criticism of Popovic's method of
pooling serum.1 What is your opinion, and how unusual is that
technique in virology?

Francis: He was not pooling serum, he was pooling cells (and, therefore,
virus) from individuals' blood, which is a very strange approach
to finding a virus. You may pool things originally to see if
something's there, but then you go back and dissect out the
individuals, and find out from which one of them [the virus]
came. Pooling is not a typical approach. As a matter of fact,
we usually separate to begin with and then maybe pool later, not
the way he did it.

Hughes: Why would he have pooled cells?

Francis: I don't know.

Hughes: It doesn't make sense to you?

Francis: No.

Problems with Robert Gallo

Hughes: I read that you believe that your publications and the

publications of some of your colleagues were blocked after this
episode with Gallo.2

Francis: He made it very clear that he would interfere with all of our

publications. Bob may work underhanded, but he also states up-
front what—in his rages, usually he will lay out all that's
coming down the way. He said that we would never approve
publishing anything in retrovirology from our lab. It was clear
how that's done: When papers are sent out to peer review, when

1 See, for example, the oral history in this series with Jay Levy.

2 Kinsella reports that papers submitted for publication with
Francis's name on them were returned with mixed reviews. Since reviewers
are anonymous and often give conflicting reviews, Francis could not state
definitively that the negative reviews stemmed from Gallo 's laboratory.
(James Kinsella, Covering the Plague; AIDS and the American Media. New
Brunswick, N.J.: Rutgers University Press, 1989, pp. 111-112.

Hughes :
Francis:

they're submitted to a journal, Bob's friends and Bob's lab- -and
Bob—would be logical reviewers for manuscripts on retroviruses
and AIDS. And he made it clear to me that regardless of the
scientific merit, he would obstruct publication.

So when we sent in our manuscripts, we would often get two
reviews: one saying it was terrific, publish rapidly, and then
making a few minor editorial comments about what needed to be
done; and then a second review consisting of a three-page
diatribe of how terrible the manuscript was. Ultimately, when we
sent in [a manuscript], we asked the journal not to send it to
anybody from Bob Gallo's laboratory. It was easier to work with
after that.

And the journals did comply?
Yes.

Attempting to Coordinate NIH, CDC, and Pasteur Institute
Work on AIDS

Hughes: I understand that sometime in the spring of 1984, you attempted
to set up a meeting of the NCI, the CDC, and the Pasteur
Institute, with the idea of arranging a joint announcement about
the discovery of the virus.1 Can you tell me about that?

Francis: This was the early April meeting that I had described before,
when we were trying to get all three of us together. It was
obviously difficult with all of our schedules, but it happened
that Bob was going to be speaking in Switzerland in early April,
and he said, "Well, I could come back through Pasteur if you
wanted," and I said, "Sure, I'll fly over." So we all met at
Pasteur and discussed the various findings. That's when he
excluded me from his discussions, but I laid out all of our
findings, including the panel of serum that I mentioned before.
It was clear that we had the cause of AIDS at that point.

The discussions were, as much as anything else, how to
manage the chaos, how to come out with a single message to the
public and to the scientific community that we had the virus,
that the virus at Pasteur, the virus at CDC, the virus at NCI
were all the same virus—we were talking about the same agent.
And indeed, unstated but obvious at this point was that the

1 Shilts, And the Band Played On. p. 435.

French had discovered it, and now we had all proved that this was
the cause. We had virus in the United States—both in Bob
Gallo's lab, I presumed, and certainly at CDC--that was growing
from American people that looked just like the French virus; had
all the same characteristics. So we were most likely talking
about the same agent. Clearly, we wanted a single voice speaking
here, so as not to confuse science or the public at large that
was so concerned about the disease.

Part of this was selfish, wanting some sort of press
management system, because the press would just drive you crazy.
Reporters would call individually, and major stories could
consume days. Every time there was a new discovery, it would
take days just to get back to the lab and start working on stuff.
So we wanted to keep each other informed and share reprints and
know that we were going to have announcements coming from the
different labs.

We all decided that we would publish joint papers. Bob was
going to do the nucleic acid comparisons of the isolates, the
French were going to do the proteins, and we were going to do the
serologic comparisons. We would then come out with joint papers
with all this information, recognizing that the spotlight would
be on a different laboratory at different times. It was not
expected that we would all be dealing with this as a group all
the time; it was just too hard to logistically coordinate that.
But we would keep each other informed, and we would work jointly.
That obviously didn't happen.

Announcing the Cause of AIDS, April 23, 1984

Hughes: Is the next step your conversation with Edward Brandt?

Francis: The next step was the CDC press office coming to me with a press
release from the National Cancer Institute announcing a press
conference where Mrs. [Margaret] Heckler was going to announce
that the Americans had discovered the cause of AIDS. Even though
we had all agreed that we would keep each other informed about
what was going on, nothing came from Gallo's lab. That was the
next piece of information.

That was late in the week, and then over the weekend, Jim
Curran and I--I think Jim on Saturday, me on Sunday—called Bob
at home and said, "You just can't do this. This is ridiculous."

Hughes: In what sense?

Francis: That Gallo had changed the name of the virus, said that he had
discovered the virus.

Hughes: Was the agreement with the French that it was to be LAV?

Francis: The final name had not been chosen, but in virology the

discoverer of a virus carries considerable weight in naming it.

Hughes: You called Edward Brandt to urge that Heckler's announcement
include the French?1

Francis: When Bob refused to change his whole approach over the weekend,
we then called Ed Brandt--! presume it was Monday—from the
director of CDC's office. We all got together on the speaker
phone there and said how unethical this was for Gallo to exclude
the French. It would set the Americans up for future terrible
criticism, because Bob was going to claim he had discovered the
cause of AIDS--a new virus called HTLV-III. And we had
manuscripts already in preparation that were going to say the
American isolates are identical to the French virus called LAV.
And how could the U.S. government explain that.

Little did we know that this was a big deal within the U.S.
government. The NIH had already applied for a patent. We had no
idea that that was all going on at the same time. So there were in
some ways conflicts of interest here, and political desire from
Reagan to do something on AIDS. He'd been criticized heavily for
never mentioning it, and so having his Secretary of Health saying,
"We've found the cause," was no doubt an important political advan
tage for Reagan's administration. With that, there was pressure on
Bob and it hit Bob's weakest point, his total inability to give
credit to other people unless it's within his own little club.

Hughes: How did Brandt respond to that phone call?

Francis: Brandt seemed to be very accepting of our comments, and said that
he would move it up channels. It was clear that he was not in a
position to make a decision without the Secretary [of Health] ,
because the Secretary had already called the press conference. I
don't know this for sure- -but I think Brandt probably then
inserted a line into Heckler's comments that this may be the
French virus. Secretary Heckler had such a line in her written
press release but never read it. She said her voice was hoarse
and she couldn't carry on.

1 Shilts, And the Band played On. p. 448.

Hughes: On the day before the announcement, April 22, there was a front
page story by Larry Altman in the New York Times.1

Francis: Larry Altman from the New York Times, who would come down

regularly to CDC and asked us how we were doing on a variety of
things, including AIDS, was actually in my office the week
before.

It was very difficult for me. I had sent an announcement
around CDC saying, "We have to be very careful about this
information, because the primary source of this information is
Institute Pasteur, and they should be the ones making the
announcement and not us." I was saying exactly the opposite of
Bob Gallo, and I was giving individuals advice on how to deal
with the press, saying, "Well, we've got some information about
the virus; it's not proven yet." You didn't want to lie, but you
didn't want to fan the flames of public excitement until the
Pasteur had announced.

So Larry Altman came into my office, and he never asked me
the right question. He said, "How are things going?" And I
said, "Fine. We're getting some interesting information." He
didn't ask more. And I never said a thing. So I think Larry
left thinking this is all rather dull, but then went up to Jim
Mason, the director of CDC, whom I had briefed on all the data
concerning LAV. And for some reason, Jim just opened up. I
guess Larry asked Jim Mason the right question. Jim Mason just
opened up and gave him all the information.

But by this time, we had had word that NCI was going to make
an announcement. So Jim Mason asked Larry Altman not to put the
article out until after the NCI announcement, so it didn't look
like we were trying to steal any credit for the work that NCI was
doing. Larry didn't know what that meant until he got a copy of
the press release. He told me he called Jim Mason and said, "I'm
sorry, I have to violate our understanding about this, and I'm
going to go ahead and publish the article now." So I think he
put it out in the Sunday edition of the New York Times.2 Gallo
saw that as a clear move by CDC to try to undermine him, and
further fanned his paranoia.

1 Kinsella. Covering the Plague, pp. 83-8A.

2 According to Kinsella, the New York Times ran a front-page article
stating that James Mason believed LAV to be the cause of AIDS. (Kinsella,
Covering the Plague, p. 83.)

Hughes: I am assuming that your main problem with all this is where
credit should be laid. But is there also a concern about
publicizing science before it has appeared in a peer-reviewed
journal?

Francis: No, not at all. I think that's nonsense, this waiting for peer
review. That's a New England Journal, try-to-sell-magazines,
thing. If you're confident about your science and it has
important public health information, you should never wait to
announce it. That's just garbage. If the New England Journal
doesn't want it, then screw them. Don't even give the paper to
them.

Controversy and the AIDS Research Community

Francis: The issue was not just on the credit. The issue, in a public

health sense from my standpoint at CDC, was giving the message to
the public that we had the cause and we were moving ahead. We
certainly didn't want the message to be that we had two causes.
It was horrible. And what it did, which I don't think I saw
coming--! probably felt it, but I didn't think it would be so
bad—was you ended up dividing the whole relatively small
virology community now working on this bug into two camps: one
which had to collaborate with Pasteur, and the other one had to
collaborate with Gallo. It was very hard to walk those two
lines, because Gallo said, "Work with me and not them." So the
relatively small world's effort on AIDS was divided. To be
effective in this field you need collaboration, sharing reagents
and resources and information.

Hughes: And the division got worse over time?

Francis: Oh, for the next year and a half, two years. And to this day,

it's still there. To this day! It's less now, because there are
a lot of labs working on AIDS, and they don't need Bob Gallo or
the Pasteur. So they can go on their own.

Hughes: But you did need Gallo in the beginning.

Francis: Oh, we all needed each other. The divisiveness set AIDS research
back years. This guy was a paranoid, childish fellow who could
not share credit and undermined the whole AIDS field, for years
and to this day. Here we are, spending national resources
investigating his lab, going over his records, having testimony
and lawyers coming to talk to me and all this stuff. If he had
just been an honorable person this would never have happened, and

the resources would never have been wasted, not only inhibiting
science in its collaboration to advance prevention and treatment,
but all of the other spin-offs and nonsense that came from it.

Hughes: Do you think it also deterred people from entering the field?

Francis: Sure. There were people who called me who were very good

virologists--and asked, What was the field like; what about
Gallo? We needed virologists in this endeavor, not just cancer
virologists who dominated the field early on. We needed people
who were working with horizontally transmitted viruses, which
most retroviruses are not. It was only Max and Bob and myself
and a few others working on these horizontally transmitted ones.
We needed these other people in the field.

Hughes: You were working on horizontally transmitted retroviruses?
Francis: Feline leukemia virus is a horizontally transmitted retrovirus.

Hughes: But you were also seeing horizontal transmission in the field.
Right?

Francis: Right, for AIDS from person to person, not from the mother to
infant.

Hughes: Why wouldn't everybody have seen that transmission could be
horizontal?

Francis: I think by that time they ultimately did. There were still

people harping about other causes. But what I'm talking about
are people with experience only in vertically transmitted
retroviruses now having to work in [the field of horizontally
transmitted viruses]. We needed broader experience. But they
stayed out of it, because the field was ugly. Why would you want
to work in an ugly field?

Hughes: And the money for AIDS research wasn't there yet.
Francis: No, you had to sacrifice your existing grants and/or work.

Hughes: In her press announcement, Heckler made some predictions that

since have proven very wide of the mark. On what basis did she

predict that a blood test would be available in six months, and a
vaccine in two years?

Francis: I have no idea. I presume some of it came from Bob Gallo, but I
don't know.

Hughes: What did you think, once that you had the virus?

Francis: Well, those were a bit overly optimistic predictions. But I

probably would have predicted optimistically too. I don't know
if it would be those exact ones. I never thought about it
really. I think I'd probably be a little cagier; I don't think I
would have put the date right on it. "Soon we will have..."

Gallo, HTLV-III, and LAV

Francis: There's etiquette that the first person who isolates a virus has
property, and you have a responsibility as a scientist working
with a virus to compare your isolates to those which predated
yours. That's where Bob fell down; he did not want to compare
his virus to the initial French isolate.

Hughes: Why?

Francis: We took our isolates from Americans and compared them to the

French, and found out that they, by several techniques, appeared
to be identical. I discussed that with Bob over the telephone,
saying that the viruses that we were growing from Americans were
identical to the initial French isolate, so the French indeed had
discovered the virus first. If Gallo had made that comparison,
then he would be admitting that he did not discover it first. If
he didn't make the comparison, it looked as if he discovered it--
at least for a time.

Hughes: Does that explain a lot of his subsequent behavior?

Francis: Sure.

Hughes: Not willing to give out the virus-
Francis: Gallo's policy was, "Let's not give it out"--at least to the CDC.

We ultimately got the virus from him, but he forbade us to
compare it to anything. That was one of the rules. Murray
Gardner at [University of California at] Davis here compared the
virus, and was told that he was not allowed to publish that
research, because that was Bob's responsibility. Gallo's
nomenclature, HTLV, was actually human T-cell leukemia virus, but
he had adjusted the name to "lymphotropic" so that it would fit
both with his initial HTLV-I and HTLV-II, and now what he called
HTLV-III.

But it was clear at that time—the electron micrographs
were- -this [the virus causing AIDS] was a different virus. This

was not a retrovirus like HTLV-I, like HTLV-II. This was a
lentivirus, which was a different subclass of retroviruses . So
it was a different agent.

Hughes: How could he not see that?

Francis: He admits to me that he did not look at the electron micrographs.
He didn't really think that that was important to him.

Hughes: Even the ones that he himself had produced?

Francis: Yes. As came out in the future, the ones that he actually

published in his manuscript were not of his virus but were of the
French virus.

Hughes: Yes. I suppose you've seen that amazing report from a contract
lab where he had sent virus specimens.

Francis: Yes, from Matt Gonda, who did the EMs [electron micrographs].

Hughes: Right. The purged version has a gap where information about the
LAV specimens had been deleted.1

Francis: Yes. As I understand it from those investigating his lab, there
were many of those kinds of "adjustments" where, despite denying
it, they really were growing LAV. Then they changed the name [of
the virus to HIV] .

The Effect on Science of Identifying the Virus

Hughes: One more question on the isolation of the virus. Research

shifted to a reductionist, bench-science approach once the virus
was isolated, where before it was a broad, epidemiological
approach.2 What was gained and lost in the process?

1 Gonda indicated in the original report that electron microscopic
pictures of only samples 6 and 7 showed a retrovirus. These samples were
labeled HUT78/LAV and T17. A/LAV. Clearly, Popovic's cell lines were
infected with the French virus. The notations concerning the two samples
were absent from a subsequent copy of the report. (Grmek, History of AIDS.
p. 76.)

2 Gerald M. Oppenheimer. In the eye of the storm: The epidemiological
construction of AIDS. In: AIDS; The Burdens of History. Elizabeth Fee and
Daniel M. Fox, eds. Berkeley: University of California Press, 1988,

Francis: Well, I was in charge of a laboratory, and it was epidemiology
that directed my laboratory effort.

Hughes: You're unusual in that regard.

Francis: Well, that's the way it should be done. I had three Ph.D.s who
were assigned from other fields, and about the same number of
technicians. You can't do everything with that size of a
laboratory, and so you have to narrow it down. Data made it very
clear that we were talking about a horizontally transmitted
agent. After the hemophilia cases came forth, the agent was
[concluded to be] a virus, because plasma was filtered to filter
out everything bigger than viruses.

Recognize that there were still lots of viruses [being
considered as the possible cause of AIDS], which was a problem.
We had other laboratories at CDC looking at whatever they were
best at. But all results to date indicated that this bug was
new. From our work with the other viruses, nothing panned out,
so we were talking about a new agent that probably multiplied in
lymphocytes. So that brought us down to a few types of bugs.

Once we had the virus, then a huge amount of information
could be gained. We had planned all of our epidemiologic studies
with the assumption that we were going to have a virus and a
test—eventually. We had all our specimens characterized and in
systematized freezers, so when we wanted specimens from a bunch
of gay men, a bunch of gay men with AIDS, a bunch of gay men with
lymphadenopathy, we wanted transfusion cases, et cetera, we could
pull those panels out. Once we had a test for infection, we
could go back to our frozen specimens from San Francisco and
figure out exactly what proportion of people came down with AIDS
with time. We could get samples from gay men in San Francisco,
Denver, Chicago, and find out how long ago this virus had been
around, and how much damage was done.

Next we could get all the epidemiologic data of how the
infection spread. We could move into families and see if it
spreads within families. We could get all this important
information fast. Recognizing that we had a disease that what we
knew at that time had a three- to ten-year incubation period, for
an accurate epidemiologic picture, we needed to use the HIV
antibody test to tell us where the disease was going. You can't
use AIDS, because that's like driving your car with the rear-view
mirror; you see what happened ten years ago. So the test was an

pp. 267-300.

incredibly valuable tool that really outlined the epidemiology of
AIDS worldwide.

Hughes: The commercial test wasn't available until March 1985.

Francis: But we had to manufacture our own [antibody test], which was a
pain in the butt.

Hughes: How long did that process take?

Francis: Within a few weeks of getting the virus from Jean-Claude.

Hughes: Why was it a pain in the butt?

Francis: Growing large volumes of viruses is a laborious process. Instead
of going out and buying a kit, you've got to grow the virus,
purify the virus, get it onto a plate, control the plates, be
sure they work, run them all, run your tests, and then grow some
more virus. We ended up having to dedicate one or two
technicians just to do that, and I didn't have that kind of
staff.

Hughes: But the technology was all there? You didn't have to invent it
as you went along?

Francis: No, no. Once you have the virus, you can just plug it into
existing technology.

Hughes: Which was the ELISA [enzyme-linked immunosorbent assay]?

Francis: Yes, together with others.

Hughes: Is that obviously the way to go?

Francis: Sure.

Hughes: What about the Western blot?

Francis: There are several other alternatives you could use for

confirmation, either the Western blot or fluorescent antibody, or
we were using RIPS [radio immunoprecipitation] . Everyone was
using different methods for confirmation. For some reason, Bob
[Gallo] liked the Western blot, and the U.S. government in
Washington got behind the Western blot. But it was probably the
most expensive, difficult thing with a new technology out there,
to be honest. It's okay. But the California state lab still
uses fluorescent antibody, which is much cheaper. It's just a
different way to look at it.

Hughes: Why Western blot, then?

Francis: I don't know. There was a guy named Lowell Haraison making

policy from high levels of HHS [Department of Health and Human
Services]. He declared the Western blot to be the standard.

Hughes: So you had the test. What did it show you?

Francis: Because we had limited resources, it took us months to generate
all the data. As I said, I had to go into the freezer and
actually sort the specimens myself, because we didn't have
anybody else to do it. But despite the limits, the data came
rolling in; we showed that the virus had come in to San Francisco
somewhere around '78. There was relatively low prevalence until
about 1981-1982, and then it shot up, infected half to three-
quarters of our cohort.

Hughes: This is the hepatitis cohort blood?

Francis: Yes, but see, we had cohorts in St. Louis, Chicago, and Denver,
so I went back and pulled specimens from them too. We showed 20
percent HIV antibody prevalence in those cohorts. So it was all
over the United States. Already 10 percent of infected cohort
members in San Francisco had developed AIDS. Now, that was
really high. That showed us that at least 10 percent of the
people who got infected with this virus developed a fatal
disease .

Hughes: Is that unprecedented?

Francis: There aren't very many human or nonhuman viruses--Lassa, Ebola,

smallpox- -that produce such high rates of fatal disease. It gets
up to about 70 percent fatality with Ebola, and then rabies is
the top with 100 percent, and then HIV sits right up there. Now,
recognize that neither rabies nor Ebola are human viruses;
they're non-human viruses that dead-end in humans. Usually
viruses that kill that proportion of individuals don't do well
epidemiologically, because they burn themselves out. HIV, it's
just more clever in that it has a long incubation period—all the
virus has to do is infect one other human before that human [the
original host] dies, and then it will stay alive.

The Blood Banks and Blood Screening

Irwin Memorial Blood Bank and Hepatitis B Core Antigen
Screening

Hughes: How long does it take to develop a vaccine, once you isolate the
virus?

Francis: Years. Decades, usually. It takes a long time. That prediction
by Secretary Heckler was overly optimistic. You should never
come down with that kind of a prediction for a vaccine. A blood
test was a little easier.

Hughes: Well, the prediction for a test was close.

Francis: It was six months off. And it hurt. The blood banks needed a
sense of urgency to screen out at-risk donors. They never had
much, and that prediction of a test around the corner just took
any urgency that they did have totally away. So they said,
"Well, we'll have a blood test in six months, so we don't need to
think about screening donors any other way." And that killed
another 5,000 people.

Hughes: Irwin started hepatitis B core antibody testing before the test
for HIV was available.1

Francis: Irwin did, and all the Bay Area blood banks did.
Hughes: Are they the only ones?

Francis: Yes, for anti-core [hepatitis B antibody testing]. But that
wasn't because they were interested in protecting recipients;
it's because they got pressure. Stanford was screening donated
blood with T-cell counts a year before [May 1983 ].2 The doctors
and patients in the Bay Area were suddenly saying, "There are two
classes of blood here." That's really important: Irwin did not

1 In May 1984, Irwin Memorial Blood Bank [IMBB] implemented hepatitis
B core antibody testing as a surrogate test for HIV in donated blood.
(IMBB AIDS documents, binder 2a.)

\ 2 Edgar Engleman, medical director of the blood bank at Stanford
University Hospital, screened blood donated at Stanford with the
fluorescent-activated cell sorter to obtain helper-suppressor cell ratios.
If the ratio was abnormal, he discarded the blood. (Shilts, And the Band
Played On. p. 308.)

want to screen blood for hepatitis B. They did it because UCSF
doctors were complaining they were losing their patients to
Stanford. Irwin dragged their feet as long as they could, and
finally were forced to do it, as they say, for political reasons.

Hughes: You're absolutely right: UCSF was losing patients to Stanford.

But Stanford didn't institute the hepatitis B core antibody test.

Francis: No. The January 1983 meeting mentioned five blood-screening
tests blood bankers could use, or if you really wanted to be
compulsive, combinations of those five tests, T-cell tests being
one of them, and the hepatitis B tests being two others.
Engleman chose T-cell testing. As a matter of fact, Ed Engleman
admits he didn't know anything about anti-core, because he never
got the information from the blood bankers who attended national
meetings where we presented the data. They chose to keep that
information about anti-core away from the folks in the field. Ed
happened to have that very expensive machine [the cell sorter] to
do T-cell tests, so it was relatively inexpensive for him to do
it, and he just did it. He was not at the meeting, but he got
the idea from an announcement about the meeting. But he never
saw the data about T-cells versus hepatitis B or any of the other
tests.

Hughes: Of course, he had an advantage in having a cell sorter, which
most people did not have.

Francis: Oh, yes. It was $100 thousand, and it would probably take a year
to order [and receive] one. He just happened to have one on the
other side of his wall.

Hughes: Is the presence of the machine related to Stanford's organ

transplantation program and the fact that it needed large amounts
of blood?

Francis: And the fact that it was a big research institution. If you

wanted to be on the cutting edge of research on surface proteins
of blood cells, you needed a cell sorter. So Stanford had one.

The January A, 1983 Meeting at CDC on Blood Safety

Hughes: I know you had some very firm things to say at that January

meeting [Workgroup to Formulate Recommendations for Prevention of
Acquired Immune Deficiency Syndrome], which followed Art Ammann's

baby, the December 1982 death of the transfusion baby who was
then linked to a donor with AIDS.1

Francis: Correct.

Hughes: Tell me about that meeting.

Francis: Oh, it was a horrendous meeting. In many ways, we [CDC] were

hoping to move the responsibility for preventing blood infections
off to the FDA and the blood banks and the plasma collectors.
Because frankly, blood transfusion was responsible for only 2
percent of our total cases of AIDS, and we had 98 percent of the
cases, and we had no resources to deal with those. So anyone
that would help was welcome, including Bob Gallo or the blood
banks. Early on with the IV drug users coming down with AIDS, we
were very suspicious that there was a problem with blood. The
hemophiliacs with AIDS came forth in the summer of '82,2 and we
had the initial meeting with the plasma collectors in Washington
D.C. in July of '82.

Hughes: The commercial plasma collectors?

Francis: Yes.

Hughes: They were receptive to your suggestion to screen blood products?

Francis: Some were certainly more receptive than the blood bankers. This
was interesting because they were always viewed as the low-class
group of blood collecting, because they're commercial and they're
seen as sucking plasma from poor people.

Hughes: Why do you think they were more receptive to screening?

Francis: I don't know. There were some people who saw the problem, at

least at Alpha Therapeutics. A guy named McCurdy, I think, and
Drees were the two that made that decision.

Hughes: Could it be that they realized that business would obviously be
hurt if the word got out that plasma was tainted?

Francis: You would certainly think so. You would think that the free
market should have led the way on this, and the competition

1 For details, see the interviews in this series with Arthur J.
Ammann, M.D., the UCSF pediatrician who handled the case.

2 Pneumocystis carinii pneumonia among persons with hemophilia A.
Morbidity and Mortality Weekly Report 1982, 31:365-367 (July 16, 1981)

between the various companies for a better product should have
increased positive action. But competition for safety didn't
last long.

By November of 1982, we at CDC were worried enough about
blood to publish precautionary steps for hospitals to take to
prevent health care workers from coming down with AIDS . ' We
figured that if it was blood-borne, the next folks to get it
would be health care workers .

Hughes: What were those precautions?

Francis: They were basically hepatitis B precautions with blood, caution
dealing with blood and labeling of blood from patients, alerting
the lab, alerting the clinicians to be careful. Realize that
there were no cases of AIDS in health care workers at that time.
But we in public health thought that we should act in advance to
prevent it.

By the January 1983 meeting, we had Art Ammann's baby and
five other cases of blood transfusion AIDS in adults around the
country. The investigations of these cases had shown—those that
were completed- -that a gay man donated a unit of blood in each of
these cases. In the one case in San Francisco, the donor had
already developed AIDS. The rest of the suspect donors were
healthy. So then the issue was, how to eliminate blood from gay
men from the donor and plasma pools? Already IV drug users and
Haitians (other groups at risk of AIDS) were supposed to be
excluded. But they were not big blood-donating groups anyway.
Gay men were not excluded but needed to be.

Resistance from Blood Bankers

Francis: Initially (at the January 1983 meeting) the blood banks refused
to accept this possibility of blood-borne AIDS. They were
willing to accept plasma-borne transmission, but were unwilling
to accept blood-borne. That's a little bit like saying, "Well,
you can get in an automobile accident with a Ford, but you can't
get in an accident with a Chevy." It just made no sense
whatsoever.

1 CDC. Acquired immune deficiency syndrome (AIDS): Precautions for
clinical and laboratory staffs. MMWR 1982, 31 (43) :577-580 (November 5,
1981).

Hughes:

Francis:
Hughes :
Francis :

They said, "Oh, you guys at CDC who are concerned about
transmitting AIDS through blood don't have enough data." As the
year went on, there were memos by blood bankers where they were
trying to push CDC out of their hair. In reality, CDC was
perfectly happy to be out of this field, but we wanted to have
some public health action before we would release all
responsibility.

There were memos from blood industry leaders wanting to get
FDA and NIH more involved in this and CDC less involved. There
was even one memo saying that CDC was using this epidemic to
generate resources for CDC [de Banfort, Red Cross]. I mean, it
was just the most amazing stuff I've ever seen. [laughs] The
CDC needs more money, so they're manufacturing this epidemic?
These guys [blood bankers] were the most status quo, inertia-
seeking people I've ever met in my life. It was very
frustrating.

And the FDA was clearly not going to move. Dennis Donohue
was head of the FDA blood products division [director, Division
of Blood and Blood Products, Office of Biologies, Food and Drug
Administration] at that time. He was just this slow-moving,
let ' s-all-work-together type person, and he was not going to
exert the FDA autonomy and say, "Do it [anti-core hepatitis B
antibody testing]."

You make it sound as though that was just his process, but was it
more than that? Was he getting pressure from the blood bankers?

He was a blood banker.
Ah.

Very recently, he had come from the blood banking field up in
Seattle. I don't think he really understood his new
responsibility when he changed hats. You can imagine the
personality of a blood banker. These are not change agents.
These are SOP [standard operating procedure] -following people;
let's make rules and follow them day in and day out exactly the
same. Which is what you need to manage a blood bank. I didn't
understand this at the time that we at CDC were epidemic-chasers,
and we were changing things all the time. We were perfectly
comfortable as agents of change. Blood bankers, when it comes to
change, get very nervous. We said, "Well, they'll change, just
give them a few more weeks or months." And they never did. I've
seen afterwards all the information that's become available
through litigation on this issue. What they were doing behind
the scenes was just unbelievable-- just unbelievable!

Hughes: Such as what?

Francis: They went out of their way to kill people. They would make these
public announcements of "one in a million risk [of getting AIDS
from a blood transfusion]," and "I don't know if there's such a
thing as transfusion-associated AIDS," and they would minimize
the whole thing. And yet, behind the scenes, they would write
these memos saying, "Well, I think there really is such a thing
[as blood transfusion AIDS], and we're probably going to have to
start screening donors, and we'd better change this, and we'd
better think about anti-core testing, and better evaluate it."
And they didn't do anything. They just kept this, "It's all
fine; don't worry about it," facade- -you can talk for hours of
why. It makes no sense at all.

Hughes: What was the main argument blood bankers were putting forward?

Francis: Donor screening and donated blood screening were going to cost
money and lose donors. Herb Perkins summarized it best, if you
get the transcripts of the December 15 or 16 Blood Products
Advisory Committee meeting in 1983. At this meeting—now a year
after the January meeting—participants were talking about anti-
core testing. Herb Perkins said, "Well, I think it's a great
idea, except that it costs money, causes trouble, and we have to
tell patients — it causes concern in patients if we have to tell
them they're hepatitis B infected." I mean— it was trouble.

Hughes: Dr. Perkins would argue, I believe, that as a blood banker, his

primary responsibility was to ensure that the nation had a supply
of blood.1

Francis: That is absolutely true, and absolutely garbage when it comes to
an excuse for causing transfusion-associated AIDS. These guys
were on the front page of Newsweek. If you wanted to change the
entire donor pool to all women with family incomes greater than
$50,000 a year, you could have done it. You would have had women
lining up a mile long around the corner of blood banks if they
wanted to use the media who were sitting there knocking at their
door. Instead they said, "Ah, no problem, one in a million,
don't worry about it. Now let's go out and put our effort into
recruiting donors." Six percent of Americans donate blood. That
leaves 94 percent that you can tap into, and when you've got
Newsweek at your door, it's not hard to do that.

1 The statement is based on the oral history in this series with
Herbert A. Perkins, M.D., in process.

When the blood banks ultimately did anti-core testing, there
was not excess trouble getting blood donors. The American public
will rally for that kind of thing [and donate] more blood than
the blood banks can take. That was an excuse to do nothing.

Hughes: And you think that's what it was?

Francis: I think they wanted to avoid trouble. It was trouble to get new
donors. They would have to say, "We need new donors," and all
the telephone calls would come in, "How do you get AIDS?" It was
trouble. They weren't willing to put up with that trouble to
save people's lives. You've got to recognize that the blood
banks deal with the donors. We dealt with the recipients. They
don't see the recipients with the disease; that's the doc's
problem, and it's public health's problem when they get hepatitis
or AIDS. So their issue really was donor interaction, keeping
their donors happy and keeping their staff in the blood banks
happy. And to hell with the poor people who received it. [tape
interruption]

Hughes: Anything more on that hot subject?

Francis: It's endless.

Hughes: Are you still testifying in the transfusion AIDS cases?

Francis: Yes, as little as I can. I could do it seven days a week, and
it's just not what I want to do for the rest of my life. I've
really urged the blood banks to settle, but it's such a huge
problem, they're just kind of holding off, waiting for it to go
away. And it will. It will go away, and these orphans will be
left without parents. I've seen cases where the father gets
infected via transfusion. He infects the mother, and then they
both die. Only the kids are left. It's a sad chapter in health
history, and I think we've got a long way to go to improve that
so it doesn't happen again, because I think it could happen
tomorrow.

Governmental Responsibility

Francis: When it comes to governmental responsibility—you have to be

careful not to have too much government, because if you do, you
cost the society in lost resources and lost spirit. But we do
need government in some areas. With AIDS the Reagan
administration totally lost the understanding of what government
(public health) responsibility was to the people. These blood

banks would have been happy as can be to do anti-core testing and
direct questioning of donors if the FDA had said, "Do it."

It's good to work in a collaborative way with the groups
that you are regulating, but there's a limit. And that limit is
when the public's health is jeopardized, and then you've got to
move fast. You've got to pull those cans of contaminated soup
off the market. It's usually done voluntarily. Look at Tylenol.
There, there was a crazy person in Chicago putting cyanide in
pills, and [the maker of] Tylenol at a huge expense pulled all
the pills off the market in the United States. Now, that was
probably overkill, but they did it because they had a
responsibility. And the FDA didn't have to say anything.

Some of these guys in the Reagan administration were jerks.
They were just jerks. They had some right-wing, conservative
ideology, extremism at its nth degree. The word seemed to be,
"Let's ignore as much as we can now and later there will
hopefully be another administration in government and we won't
have to worry about it." Meanwhile, a million Americans die.
The blood banks alone infected somewhere in the neighborhood of
28,000 Americans, and the factor VIII folks another 10,000.'

Over half of transfusion recipients die from their
underlying disease, so that leaves about 10,000 to die of AIDS--
plus 10,000 hemophiliacs. That's 20,000 Americans. If you're
driving around in your car and you're not looking and a kid runs
out in front of you and because you were looking the other way
you kill the child, you go to jail for that. For one death. And
here you've got 20,000 people who are killed, of whom easily
half, if not three-quarters, were preventable. And now we're
wondering whether we should change our blood donation system or
not. It's very strange.

We have to change things and make damn sure it doesn't
happen again. Unfortunately, it's people. If you recruit
status-quo-seeking people, you will get the status quo. And if
you don't make jobs in government exciting and fun and
responsible and prestigious, then you'll get the status-quo-
seekers who can't find a job anywhere else.

1 T. A. Peterman, H. A. Jaffe, P. M. Feorino, et al. Transfusion-
associated acquired immunodeficiency syndrome in the United States.
Journal of the American Medical Association, May 16, 1985, vol.
312(20):1293-1296.

T. A. Peterman, D. P. Drotman, J. W. Curran. Epidemiology of the
acquired immunodeficiency syndrome (AIDS). Epidemiologic Reviews, 1985,
vol. 7:1-21.

Hughes: Do you take some heart with what's happening in the Department of
Energy now, with the release of the information about the
plutonium victims?

Francis: Yes. I think I take heart with this new [Clinton]

administration. But there's a lot more than that that needs to
be done. You just can't come in with a president and change this
whole bureaucracy. It has to be a philosophy, a fundamental
policy of the government that it is going to be sleek and
efficient. We must realize that government cannot be as
efficient as the private sector, because its funds are not its
own. It runs on someone else's money. So there's going to be
more accounting, and it's going to be slower to move. But it's
got to be as close to first class as we can [make it], instead of
fourth class.

Hughes: The Constitution says nothing about assigning public health

powers to the federal government, and the way our system works,
that means the states have the responsibility. Was the Reagan
administration playing that to the hilt?

Francis: Yes. I was paid, and a half dozen other docs, a full-time salary
to work on one virus. That's at the federal level. Most states
cannot afford that level of specialization. When states require
that level of expertise, they turn to CDC for guidance. It's
worked quite well—in the past.

Sometimes CDC puts the screws to a state government to
improve their programs-

Francis: --if it's CDC money paying the bill. And then if the state
doesn't do a satisfactory job, CDC pulls its money out. In
general this collaboration can work extremely well. But you must
have first-class federal public health employees. Recognize the
size of the budgets we're talking about here. When I was in
Atlanta, Massachusetts General Hospital, one hospital in the
United States, had the same budget as CDC and CDC had the same
budget as WHO [World Health Organization]. So you're talking
about small amounts of money. I think at that time [1983], CDC
had a $700-million-a-year budget. For a country this size, the
people get a huge return in health- -not to mention worldwide
benefit. When an organization works collaboratively with other
organizations in the world and wipes out smallpox from the world,
the money that you get back year after year on that is immense.
Same with measles and polio, and whatever. Just a huge benefit.

But we as a society are not mature enough yet in a social
evolutionary sense to realize it. It will take time.

AIDS in Africa

Hughes: When did AIDS in Africa affect your thinking?

Francis: Early. You'll have to ask Joe McConnick whether word of African
AIDS first came from Europe or whether he heard it from Zaire.
Whatever the source, Joe and his team were off to Africa to
discover AIDS. CDC had had a long history of working with west
Africa with smallpox and many others diseases. The Belgian
cases, I think, were my first knowledge of AIDS in Africa. Now,
others may have heard about it elsewhere. But the Belgian cases
of AIDS were from Africa, including Zaire. Very early on, we
sent a team over to Zaire-
Hughes: Can you think of the year?

Francis: Late '82, early '83. Joe McCormick went over. Joe was the head
of the hot lab, the Lassa-Ebola lab, at CDC. He was actually a
high school teacher in Zaire years ago before he went to medical
school. He was close to Mobutu, got in the country, brought a
team over--Peter Piot from Belgium, Joe McCormick from the United
States, a couple of others from the United States, and maybe some
others from Europe. They came in and did an investigation there,
which was published in Lancet. A two weeks survey at Mama Yemu
Hospital found forty, fifty cases of AIDS or something like that.
It was incredible. So even early on it was already a big problem
in Africa.

Hughes: Now, what about the heterosexuality of the disease there?

Francis: It was obvious from their investigation. The number of men and
women were almost equal. But the female cases were younger; the
male cases were older. Many of the females were femmes libres,
"free women" who worked in bars and were sexually very active.
And the males were their customers.

Hughes: Did knowledge of the heterosexuality of the African disease
affect your perception of the disease in this country?

Francis: Well, the earliest were the Haitians in this country, which

brought a tropical nature to it. The issue of the Haitians was
confusing, though, and wasn't sorted out for years, actually. We
knew that gay men from New York were commonly coming down to

Port-au-Prince for vacations, and hiring local youths for sex.
Haiti had a very close connection to Africa, and indeed Zaire,
because post-colonial Zaire needed school teachers and imported
Haitians for that. The question was, did it come into Haiti and
then get into the gay population through Haitian interaction with
gay men in New York, or were the Haitian cases a result of gay
men who were infected giving the virus to Haiti?

The latter turns out to be the case, but initially we
thought that an African bug went to Haiti and then got into the
gay population. Obviously, it probably was an African virus--gay
men visiting Africa picked it up and got it into the bathhouses
in Europe and the United States, and then it spread like crazy.

Early Perceptions of AIDS

Hughes: What I'm trying to get at is, the early perception of AIDS is

linked with the gay population. It is seen by most people as a
gay disease.

Francis: No. When we see a disease in the gay community, our initial
instinct is that it is infectious, that it's sexually
transmitted, not that it's a gay disease. So the assumption, I
think, of all of us at CDC was it's just a matter of time before
it spreads out [into the general population]. Gay men were the
flagship of any sexually transmitted disease. We knew that.
They were always the leaders, because of their numbers of sexual
partners.

Hughes: Did you find that to be a common perception?
Francis: Yes, at CDC.
Hughes: Beyond CDC?

Francis: I think it was a common perception of anyone in the infectious
disease field who was experienced. Some of the researchers who
never put it all together would proffer their sperm hypothesis or
their immune overload hypothesis and all that dribble, but we
just kind of chuckled at them. We'd try to bring them around,
and they wouldn't come around necessarily, but we let them do
their thing.

At the January [1983] meeting on the safety of blood and
products, Dave Sencer, who was the health commissioner of New
York City, said, "Is there anyone who doesn't believe this is

infectious?" And Don Armstrong, who is an infectious disease doc
at Sloan-Kettering Memorial Cancer Center, said, "I have no doubt
that this is caused by an agent; we've got to go out and find
it." This was not magic; anyone who took ten minutes to learn
the facts would conclude it was infectious. A lot of people
didn't spend the ten minutes, that's all.

Risk Groups

Hughes: What is the implication of identifying risk groups, both for you
as a scientist and also for the public?

Francis: You have to be scientifically accurate when you're describing a
disease. When we're describing the epidemiology, as we did for
hepatitis, we interview patients and ask what behavior these
people have that would put them at risk—having a child in a day
care center, having sex, sharing needles and syringes, eating a
picnic, or whatever it may be for the given disease. We classify
cases by their risk, and have for years and years and years, and
continue to.

For AIDS, the behaviors associated with infection were: gay
sex, sharing intravenous injecting equipment, and there was
heterosexual sex, and being born to a mother who was at risk.
Those risk categories by and large haven't changed at all, except
for adding transfusion [cases] and hemophiliacs to them. All
that was cooked [up] in late 1982, and very little has changed.

Now, the problem that we had in a public health sense and a
political sense was, instead of talking like an epidemiologist
who talks about a risk group, it was important for society to
talk about risk behaviors. Inappropriate use of the "group"
terms seemed to stigmatize people. The Haitians were the ones
who ate it early on, because indeed it was not all Haitians. It
turned out to be recent Haitian immigrants who prostituted
themselves for gay men (or their sexual contacts).

But there is stigmatization that can come with any epidemic.
In public health we're always cognizant of the potential and try
to minimize it. But we recognize that sometimes to save a lot of
people, others may be injured. To prevent AIDS we needed to talk
about men as a group who were having sex with other men. The
message was, if you have sex with other men, you are risking
AIDS. That was a very important message to get out. The gay
community didn't always like it, because if you were a monogamous
gay man who had only had sex with your partner, and your partner

had only had sex with you, or if you were gay and you never had
any sex at all, you didn't have any risk. And that's true. But
that's a much more complicated education message to dispense.
What you need to do is break the ice with these sometimes
potentially stigmatizing messages, and then refine your
educational program with time. But if you try to refine it at
first and try to prevent all stigmatization, you'll take all the
bite out of your message, and no one will ever get educated.

The Behavioral Approach to AIDS Prevention

Hughes: Well, the idea of the risk group has been criticized for taking
emphasis off behavior. It also lets people off the hook who
don't fall into those risk groups; they can divorce themselves
from the problem of acquiring AIDS.

Francis: Yes. And the issue is behavior. There's no doubt that why gay

men are infected is a mathematical issue. I think maybe anal sex
has a little bit more risk than vaginal sex, but to the woman, or
the receptive male partner, it's not that great of a difference,
to be honest. So it is receptive sexual behavior that's going to
get you into trouble. And yes, that is important to get over,
and you have to be very careful about dealing with behaviors.

But frankly, we in public health were pretty naive on all of
this. Most of us were not behaviorists; we were vaccinologists.
We were people dealing with penicillin shots. We're talking
about one or two visits to prevent disease for a lifetime.
That's about the extent of public health's reach out in the
world. Sometimes we can't even do that. Often we can't even get
people immunized in this country with one, two, or three visits.
So we're accustomed to working at a relatively simple level. But
when it comes to behavior change, far more sophistication was
needed.

It was a new field of chronic disease epidemiology and
prevention, as it was called, and we luckily had some of those
people at CDC and could tap into them, but they were a very small
group. So you basically had Jim Curran, Harold Jaffe from
sexually transmitted diseases, and myself. We were one shot of
penicillin and a follow-up visit, which meant two shots-of-
vaccine people.

Hughes: [laughs] Then your problem's solved.

Francis:

Hughes:

Francis;

Then the problem's solved,
shot.

And for smallpox, it was only one

Hughes :
Francis:

Hughes :

Francis;

Was it hard for you to realize that you had to take a different
approach to this epidemic?

Yes, it was a different approach. I think we were naive about
it. When I came out to California, I just luckily, with Marc
Conant's and Jim Chin's help, was introduced to people who knew
what they were talking about.

From a behavioral standpoint?

Yes. I got to know Larry Bye and Tom Coates and Steve Morin--
these are behavioralists. I sat down with them at a variety of
lunches and dinners and had them try to convince me that there
was such a thing as changing behavior, and they convinced me.
Steve Morin and Tom Coates and Leon McKusick did some of the
earliest studies of gay male behavior. And what proved to me
that gay male behavior could be changed was their saying: "We
went into this group assuming, from our smoking research
information, that these parameters would change people's
behavior: recognition of risk, self-motivation, and feeling that
you could do something about it, having some empowerment. And we
asked questions to quantitate these parameters.

"We had in gay men a group who altered their risk-taking
behavior and a group who didn't change, and we asked the
questions of both groups. At onset they predicted factors, say,
one, two, three, and it came out to be one, three, two." It was
incredible. I was convinced. I was sold. Now the question is
how to market that message to the general population, and that's
where people like Larry Bye and Tom Coates were superb.

So do we have the answers as to exactly how to change human
behavior? No, we don't have all the answers even today. But we
have an awful lot of groundwork that was already there from other
research, and now we have a good deal of AIDS-specif ic research
to direct our "best guess" program design.

In the gay population, you have generally well-educated, well-
motivated, politically astute people. The epidemic is moving
into populations which don't have those characteristics.

The gay community is diverse. And you've got to realize in the
gay community, there was tremendous resistance, too. This was a
new political movement that had come out of the closet, and
anyone who talked about decreasing sex was anti-political. It
was against the movement. Randy Shilts and an awful lot of other

folks were seen as wanting to close the bathhouses and change gay
behavior. And certainly I was seen as an outsider. "What right
do you as a straight man have in advising us about our sex? All
you are is a messiah from Ronald Reagan saying, I want to stop
all this anal sex stuff." Realize I was saying, "You better stop
that anal sex stuff." So it was a very easy take.

AIDS in Women and Children

Hughes: Another criticism that the CDC has suffered is its reputed delay
in recognizing AIDS in women and children, and failing to
incorporate those populations in the case definition of AIDS.1
What do you have to say about that?

Francis: I don't think so. I'm sure CDC can be criticized, but CDC

recognized and reported women very early on, and the risk was
recognized as being huge.

Hughes: Yes, but the case definition of AIDS did not embrace symptoms
specific to women.2

Francis: That was nonsense. That issue was, who was going to pay for AIDS
treatment, which was not the purpose of CDC's AIDS definition.
The definition very soon should be [simply] HIV infection. If it
weren't for political pressure against it, it would be. Money
was the issue. In contrast, the several symptoms were an issue
of what disability payment one received, what kind of medical
care you required, et cetera. And unfortunately with this
primitive system we have in this country for paying for medical
care, people were using the CDC case definition to decide whether
the government would supply medical care to them. CDC never
meant to get into that.

Hughes: And it hasn't historically?

Francis: It hasn't historically. It's a little easier historically, if I
have polio, if I have hepatitis. They're easier than AIDS [to

1 The inadequacy of the federal government's response to AIDS in women
is a theme of Gena Corea's The Invisible Epidemic: The Story of Women and
AIDS. New York: Harper Collins, 1992. For discussion of resistance to the
idea of pediatric AIDS, see the oral history in this series with Arthur J.

Ammann.

2 Corea, The Invisible Epidemic,

diagnose], which is a slow-moving disease that takes so much time
[to manifest]. If there were appropriate resources available for
this epidemic, then we would have never gotten into this
discussion. We knew women were at risk [for AIDS]. We knew
women were at risk because of intravenous drug using; we knew
women were at risk from sexual contact with an IDU [intravenous
drug user], and that the chain of transmission was male IDU, or
female IDU, to baby, and baby gets infected. That was known in
1982.

If the government had put in resources, and CDC had
delivered prevention programs, they would have targeted these
folks. The problem was, there was no commitment, no money. So
what you had was a bone with a little bit of meat on it, and the
health care hyenas were trying to take care of these people who
were dying on the street, [and] the prevention hyenas were trying
to snatch their piece. All CDC had was about enough money to pay
for surveillance. They didn't need any more cases, because if
they broadened the case definition, there weren't enough people
to even interview the cases and get the forms filled out.

So the issue was a resource issue, and it got CDC caught in
a lose-lose situation. Why did I ask to leave Atlanta? I asked
to leave Atlanta because I felt I was on a losing team. It
wasn't that the team there was bad; there were some good people
in Atlanta. But the resources and government above it were going
to ensure that team would eat it, and CDC was going to get
criticized. I don't like being on a losing team, so I came to
California. In many ways, we were all going to lose on AIDS,
because of the ten-year incubation period. Even in the best
society, we were going to eat it, because societies have not
learned to deal with a ten-year incubation period phenomenon at
all. We have not yet reached that kind of social advancement.

Hughes: Because we don't look that far ahead?

Francis: Because we can't look that far ahead. Generally, government

reacts to today's crisis. AIDS is not a disease you get into if
you want to win. You're going to get criticized and screamed at
and yelled at, because the system is destined to political
failure, and you're part of the system.

But I think many of these individual issues are peripheral
to a leaderless, resource-lacking federal effort. Because of its
weakness, the federal government was going to get criticized--
deservedly. It was going to be one issue that was clear, and
everyone was going to say, "The goddamn government, we've got to
beat the shit out of it because it did a bad job." And if you're
sitting in Atlanta, you're going to get the shit beat out of you.

AIDS Testing

Hughes: You said—I'm paraphrasing—that the definition of AIDS should be
HIV infection.

Francis: Sure.

Hughes: But there were political pressures to make it otherwise. Would
you explain?

Francis: The outspoken gay community to this day resists testing.

California has been much better than the rest of the country,
especially New York. New York essentially made it impossible to
get tested, because you couldn't test unless you went to a
government facility. I believe this test should be given to
every American at risk in high prevalence areas. When they come
to their doctor, when they come to a jail clinic, when they come
to a drug treatment clinic, everyone should be getting this test
on a routine, voluntary basis.

Because of people like Bill Dannemeyer and Jesse Helms and
Ronald Reagan scaring people with the threat of quarantine,
isolation, not to mention stigmatism and loss of health
insurance, that recommendation has not been feasible politically.
I think it's horrible. Last year I wrote an editorial that the
case definition should be HIV infection, and we should care for
everyone.1 We should as a government open our arms to say,
"Come, if you're HIV infected, we'll take care of you completely.
We'll give you a job; we'll give you transportation; we'll give
you housing; we'll give you drugs; we'll give you everything.
Anything you want . "

Because infected people are potentially dangerous in a
public health perspective. We shouldn't quarantine them; that's
too expensive and it's not needed. But we should have an
isolation around them that is a voluntary isolation that we can
instill in them through ongoing education and support. Then we
teach everyone else to be damn careful, saying, "You have to
assume everyone else is infected." But burying your head in the
sand and not wanting to take on these expenses is crazy. We
should welcome these folks, and we don't.

1 Toward a comprehensive HIV prevention program for the CDC and the
nation. Journal of the American Medical Association, September 19, 1992,
v. 268, 11:1444-1447.

Isolating and Sequencing the Virus

Hughes: You've spoken of CDC and the Pasteur and Gallo regarding

isolation of the virus. What about Giovanni Battista Rossi and
his colleagues who in September 1984 isolated the virus?1

Francis: I know nothing about Rossi's work. The other one is Jay Levy.
Jay Levy got the virus from the French and then made isolates
himself. Then he did the same thing that Gallo did, and changed
the name, and did not compare his isolates to the French isolate.
I think he presumed that they were the same. That's kind of the
NCI approach. He didn't release the results in a press
conference like Bob did, but you can make the same criticism: Why
did he call it ARV [AIDS-associated retrovirus]? When we
isolated the virus at CDC, we compared it to LAV and found it to
be the same. We then called it LAV. That was the only proper
way to do it, if you're ethical.

But yes, Jay was early in on it, no doubt. I don't know the
history of Jay's lab, how long he was working on it, but he got
the virus from Jean-Claude. He was over at Pasteur and picked it
up, and said, "Let's see if we can do the same thing you did."
Which is perfectly acceptable. And he gave references to the
French in his publication, not like Gallo. He didn't go around
saying, "You've got to change the name of the virus," and all
that crap.

Hughes: What about Abraham Karpas at Cambridge who in December 1983

published an electron micrograph of a virus found in the blood of
a gay man?2

Francis: I don't know exactly what Dr. Karpas was doing.

Hughes: What about Paul Feorino?
Francis: Yes, he was at CDC.
Hughes: What did he do?

1 Mirko Grraek, History of AIDS: Emergence and Origin of a Modern
Pandemic. Princeton, NJ: Princeton University Press, 1990, p. 74.

Grmek, History of AIDS, p. 68.

Francis: He worked for me in the lab. It was the Feorino paper which
compared the American isolates to the French.1

Hughes: Let's talk about the sequencing of the virus.

Francis: Well, that was really very interesting. I had never thought that
HTLV-IIIB would be the very same isolate as LAV. I knew the
French had sent it to Gallo, and he used their techniques to grow
it, like we did. But we had LAV growing in our lab, and
ultimately IIIB growing in our lab, and we had our own various
isolates growing in our lab. With such numbers of isolates you
always have a risk of contamination; there's no doubt about that.
That's not new in virology.

Ci Cabradilla from CDC actually came to Genentech. I sent
him out here with virus to do sequencing, and one of the first
sequences came from that effort. Actually, my first
understanding of this really came from Simon Wain-Hobson from
Pasteur, who came to CDC to visit and said, "Look at these
sequences, Don." He actually was even far cleverer than that.
Not only is there a dominant sequence, but there is a defective
subtype in LAV that varies in its percentage makeup of the total
nucleic acid in the virus preparation.

Hughes: Which makes it very characteristic. Is that what you're saying?

Francis: In the LAV cultures from Pasteur, [the sequence] changed over
time. So if you take a virus and sequence it, he can tell you
exactly when that virus sample was sent. So he knew that IIIB
was LAV and he knew exactly when that was sent from Pasteur to
NCI. That put a different aura on the problem, and made it even
more outlandish.

But frankly, unless someone tells me the Gallo lab took LAV,
purposefully put it into a pool with other material, and decided
to call that IIIB--until I hear that, I will always give the
benefit of the doubt that it was a contamination in the
laboratory. Now, those who have done the investigation and seen
the lab books will probably have a different opinion than I have,
because it looks like Gallo was growing LAV in the laboratory and
put it into the pool and claimed he discovered a new virus.
That's probably what happened. And when that comes out as truth
and I get those facts, then I may change my opinion and possibly
be very critical. But until that point, I will give the benefit

1 P. M. Feorino, V. S. Kalyanaraman, et al. Lymphadenopathy
associated retrovirus infection of a blood donor-recipient pair with
acquired immunodeficiency syndrome. Science 1984, 225:753-757.

Hughes:
Francis:

of the doubt and assume it was a laboratory contaminant. It's
happened in other laboratories. That may be sloppy lab work, but
it can happen to all of us.

And it had happened to Gallo.

And had happened to Gallo, and could have happened to me. The
fact that it was a laboratory contaminant makes it even more
sleazy, but it's not a great revelation. We had more viruses
from Americans growing at CDC than they had at NCI. All this
forty, fifty, sixty isolates may be a bunch of bunk. That's my

understanding from those who have seen the lab books,
another horrible twist on the whole episode.

That puts

If then, as John Crewdson and others say,1 you can trace LAV
through MOV [another name given to the same virus isolate] into
the pool, and everyone in the Gallo lab knew that. That adds
another level of culpability and dishonesty to his laboratory's
behavior. I think the truth will come out with time. The
trouble is, the tincture of time tends to say, well, Bob does
things like that. The same thing I was telling you about when he
asked me to leave the room, instead of shouting and yelling and
saying, "You jerk, I'm not going to leave the room. We're from
the same institution, "--or the same department in different
agencies. Instead I said nothing. People will accept Bob and it
will just go on and on and on. And no one wants to deal with the
old history. It's a waste of time.

The NIH-CDC Relationship

Hughes: Let's talk about the relationship between NIH and CDC. NIH is
perceived as the bastion of basic science; CDC is perceived as
doing applied science. Yet you yourself were doing some basic
science.

Francis: Yes, but our basic science is applicatory in nature. CDC has

discovered lots of bugs, and that's their job, looking for bugs.
Legionnaire's, et cetera, et cetera. That is part of CDC's role,
and indeed does overlap with NIH to an extent in those areas.
CDC by and large is better suited to search for new causation.
My wife's work on Reye's syndrome: People had been working on
Reye's syndrome for years, including CDC in the laboratory. And

1 John Crewdson. The great AIDS quest. Chicago Tribune, section 5,
November 19, 1989.

epidemiology often breaks those nuts well before the laboratory
does. I think there are many, many examples of where CDC has
uncovered tremendous findings in infectious and noninfectious
diseases.

By and large, the basic science of NIH and the applicatory
science of CDC are really quite separate, but there is a layer of
overlap. That layer of overlap I think is great. One, we share
a lot of resources. During my work at CDC, I had always dealt
with the National Institute of Allergy and Infectious Disease
[NIAID] . We were competitors, but only in that little bit where
we overlapped. They were doing their thing and we were doing our
thing, and that allowed us one, to have a connection; and two,
some competition in government agencies is good, because it keeps
everyone working just a little bit harder.

Dr. Xu Zhi-Yi and Liu Chung-Bo and I did a remarkable study
in China addressing the question if you could interrupt perinatal
transmission, mother-to-infant transmission, of hepatitis B virus
with vaccine. HBV [hepatitis B virus] transmission from mother
to infant was the major leak in our vaccine strategy for the
developing world. An awful lot of these kids end up getting
cancer of the liver and chronic hepatitis. China was the one
place that didn't want to use any immunoglobulin because of the
expense. Thus, we could just use vaccine alone to see if it
worked. In places like the United States, immunoglobulin was
considered the standard of care.

So we did a vaccine study of infected mothers in China.
Now, what vaccine did we use? We used NIH's vaccine. Bob
Purcel, from NIAID, and I would go to China. He supplied the
vaccine; I would do the epidemiology. Some of our work was
competitive, but it was very close and we would collaborate. So
I think that was very healthy.

The relationship with NIH changed with NCI, because they
didn't collaborate well, even within NCI. They seemed to hate
each other. They are set up on the academic, kill 'em, fight 'em
mode of operation, not on the collaborative mode. They would set
out these channels of Bob Gallo's fiefdom, and Stu Aronson's
fiefdom, and George Todare's fiefdom, and all these fiefdoms, all
of which were fighting each other. Before 1982, I didn't ever
have to deal with NCI. It wasn't until AIDS came along that our
infectious agent, unfortunately, was in NCI and Bob Gallo's area.
It was a totally different working relationship compared to
NIAID.

Now, I knew Bob Gallo from Max Essex's lab and considered
him a friend. I was part of the club, recognized. I came from

Max's lab and was on the inside, and Bob would call me and say,
"Don, you only work with us. Don't work with the French. Don't
work with other people." I said, "Bob, I recognize that I am a
member of the club, but I'm also an employee of the Centers for
Disease Control and I can't define research alliances like that.
I've got to work in a general public health sphere, and if people
want specimens, I send them, if they can handle it and they're
reasonable researchers."

But in general, our relationship with NIH I think is good.
At least with NIAID I've always enjoyed it. I've kind of enjoyed
the competition.

Hughes: Shilts quotes Gallo as saying that the research that was being
done on the retrovirus at CDC was a "duplication of government
expenditures."1

Francis: Right. You had this huge epidemic, and he's saying you don't
need two laboratories to work on it. That's relatively self-
serving, [laughter] He was saying the CDC does not need a
laboratory to work on AIDS. It's just nonsense. He also made it
very clear that he wanted to close down our lab.

Hughes: Were you privy to what was going on between NCI and NIAID?

Francis: Yes. Bob called me and said, "I don't want to announce this

virus until we have full control over it, because I know it will
go over to NIAID." He saw the writing on the wall. And it did.
He still maintains a great deal of control, but NIH recognized
that there were other people who had worked with horizontally
transmitted agents that were far more talented than Bob Gallo 's
group was .

AIDS Units at CDC

Hughes:

Francis:

There were several branches of CDC that were engaged in AIDS-
related activities. For the record, the Center for Preventive
Services, the Center for Health Promotion Education, Training and
Laboratory Program- -which was you, right?

No, that was a separate group.
Disease.

I was the Center for Infectious

Shilts, And the Band Played On, p. 366,

Hughes: That's the fourth one. How coordinated were these activities?

Francis: Initially, it was a very small group of people, and relatively

easy to coordinate. Hard to do, because no one had the full time
to do it. CID, the Center for Infectious Disease, was always the
headquarters of the knowledge base, and we would bring in other
groups. By the time I left for California [1985], I within CID
had designed the first national prevention program, not from the
Center for Prevention Services [CPS] . But Prevention Services
was traditionally the one that delivers prevention programs.
With time, I moved over to Prevention Services in my California
assignment.

By that time, as the national budget started increasing, the
coordination became terrible. And to this day, there's not the
best relationship between CID and CPS. An attempt was made to
change that by putting somebody in the director's office at CDC
in charge of AIDS. That was initially Gary Noble, and now Jim
Curran. That just adds another layer of bureaucracy. There's no
center for AIDS, and that's what has to be done. You have to
make a center, and all these folks are in that center, and the
work goes out from them. We've made that recommendation through
an expert committee advising CDC. Whether it will ever happen or
not, I don't know. [Added by Dr. Francis during the editing
process: It has. ]

Hughes: Was it a CDC committee looking at CDC?

Francis: No, it was outside CDC. I was retired from CDC by that time. It
was a CDC-arranged committee, but with outside-CDC advisors.

Hughes: When was this?
Francis: Just last year [1992].

Hughes: How big a role did the Center for Health Promotion and Education
play?

Francis: Early on, it had very few people, so it was just kind of

advising. These were the experts in health promotion; they had
to come over to us, single-shot folks, and try to give us some
advice. And they were always involved in advising us. However,
with time this negative division began to emerge: the
epidemiologists on one side and the behavioral change experts on
the other. To function effectively, the expertise for the
epidemiology has to sit with or close to the prevention folks.
You can't have them separate, which is what was done. The result
has been the prevention folks with the techniques for behavioral
change without the expertise in epidemiology. So it has been a

terrible setup, because most of the scientific expertise resided
outside of the deliverers of prevention programs. With time, the
prevention program deliverers became contract-writers without any
expertise.

What CDC does is imitated by the expertise and desires of
states, and what the states do is imitated by local governments.
So what we have ended up with is these contracting-type people
running prevention programs who don't know anything about either
the epidemiology or the behavior change modalities. Hence the
CDC model has been a sadly replicated one at state and local
levels .

Hughes: How does the AIDS Activities Office fit in?

Francis: This was the centralized group that was supposed to coordinate
all of this work on AIDS.

Hughes: And does?

Francis: Oh, it tries. That is another group at the federal level trying
their best but working without true authority. Line authority is
important to get things to work. To this date, it hasn't
existed. It's been matrix managed outside of a line authority,
which is a total disaster.

Hughes: Would you talk about division of labor between Jim Curran and

Francis:

you:

Well, our responsibilities were fairly clear. This was all
CID in the Division of Viral Diseases, of which I was the
assistant director. And then we had the AIDS Activities Office,
Jim's office, in CID. I took over directing a laboratory to
complement and work with Jim's group. As I told you, Jim asked
me to do that from Phoenix. That was something that goes back to
1981. And I said, "No, I don't want to; I'm doing all my
hepatitis stuff. I'll help from the sidelines. I'll be on the
[AIDS] task force; I'll [help] by telephone, but I can't
coordinate the lab in Atlanta from Phoenix."

But, as I told you, the pressure just mounted and mounted
and mounted, and there was just no way to manage the effort.
Every time I'd go to Atlanta to get stuff organized, I'd turn my
back and it would all stop; everyone would go back and do their
own research, and AIDS would never get the appropriate attention.
At that time, everyone was defending their turf, because budgets
were being cut, cut, cut, cut. People, supplies, and equipment.
In that setting, the worst thing you can do is volunteer some of

your staff to help out on another job,
going to lose them [permanently].

because you know you're

Luckily, I was assistant director of hepatitis, so it was
easy for me to volunteer my time. But hepatitis lost me. I
don't think they ever got my position back. Jim was lost from
the Sexually Transmitted Diseases Division. STD deserves a lot
of the credit for the heroics here, where they gave all these
people—Bill Darrow, Harold Jaffe--at a really tough time. The
director of STDs, who was Paul Weisner, said, "This [AIDS]
epidemic is important, we've got to work on it. It's our [CDC's]
responsibility." And he really ate it. I don't know if STD ever
got those positions back.

General Accounting Office Audit of CDC AIDS Activities. 1983

Hughes: In 1983, the General Accounting Office [GAO] audited CDC's AIDS
surveillance program, AIDS lab studies, and AIDS epidemiology.1
Senator Ted Weiss on a subcommittee of the Committee on
Government Operations asked for an audit. Does that ring bells?

Francis: Yes, Mr. Weiss and Bill Foege [CDC director] got into a pissing
contest over it. Being from New York, Ted wanted to find out
what CDC was doing about AIDS. We in AIDS work at CDC were
letting it be known that we were not able to get done what needed
to be done.

Hughes: Why was that inquiry appropriate from New York?

Francis: Because of all the AIDS incidence in New York. Mr. Weiss sent a
woman down--I forgot her name—very good, but she wanted to see
our files. Our files are full of patients' names. And in public
health, it's really sacrosanct that you don't let people from the
outside, especially from any other branch of government, or for
that matter anyone else, come in and pull people's names out of
files.

She wasn't going to reveal anyone's names, and she knew it.
But we couldn't know that. She and Bill Foege got in a
tremendous confrontation. It progressed to: "You cannot come
into our offices." Instead of, "Come on, let's work together,
and figure--." Bill is a very collaborative person. But

1 Sandra Panem, The AIDS Bureaucracy.
University Press, 1988, pp. 31-35.

Cambridge, MA: Harvard

Hughes :

Francis:

Hughes :
Francis;
Hughes :
Francis :

something happened, and so it got to be this huge thing and she
assumed CDC had something to hide. Well, we didn't have
anything. What was hidden was that we were doing a crappy Job,
because the administration was not giving us the resources we
needed. We needed that message to get out. The whole thing
wasn't played well.

CDC had this naivete, and I had it until I came out to
California: We're doing good things; we're expected not to have
any resources; we eradicated smallpox on a shoestring; we can do
anything. Really, the opposite of NIH and NCI saying, "We need
to get into politics and raise money," because money was at least
a necessity to get your job done well. So we didn't play the
politics very well.

I don't know why Bill hit head on with Ted Weiss. It should
have been a collaborative effort, because both CDC and Ted Weiss
wanted CDC to do a better job. Instead it got into a really
horrendous privacy conflict. They thought we were hiding
something. So I guess a GAO [General Accounting Office] audit
was asked for. I think it concluded that CDC just couldn't do
what we asked it to do with the resources it had. In the end it
all came out fine, but it was not pleasant.

I remember bits of it, at least. I saw the investigation as
an invasion of my work. I had my fifteen-hour day; I didn't need
to take an extra hour for some congressional person to talk to
me. What I didn't realize is that they were the key to saving me
from this impossible, resource-strained situation. We were in
our politically isolated little place; we wanted to stay there.
It was really stupid.

Eventually, the CDC released some of the information without
reference to patient names.

Yes. It meant that staff had to go through the files and take
off every name. If someone came and told me to do that, I'd just
tell them to get out of my office. I didn't have the time to
deal with that.

But somebody apparently did it.

Yes. It's very expensive.

Did some good come out of that episode?

Oh sure. Ultimately it was Ted Weiss' committee before which I
testified about CDC's shortcomings. And Ted Weiss was terrific.
He died soon thereafter.

Hughes: Your testimony against CDC was more or less the same as what you
said in the 1992 JAMA article?1

Francis: Except the new director of CDC (William Roper), when I testified
was out of the room. I was in the leadoff group. Bud Roper,
from Roper Polls, was the first. He said, "The American public
sees AIDS as a problem, and has personalized it already. They
see it as a risk to them and their children, and they want frank
messages out there to tell us what to do." I came up and said,
"CDC has been prevented from doing its traditional job in public
health by right-wing politics."

Then Bill Roper, director of CDC, no relation to Bud Roper,
comes back into the room, having not heard our testimony, and
says, "Well, the reason that we don't have any mention of condoms
in any of our national AIDS education programs is because the
American public really hasn't personalized the risk of AIDS. The
first thing we want them to do is to feel the risk of AIDS, and
then we'll come up with the necessary information, but we don't
feel the American public has personalized it yet." He hadn't
listened to Bud Roper.

Then Ted Weiss asked him if he had had any political
interference, and he said, "No, I don't have any political
interference at all." Just after I, who had been at CDC ten
times as long as he had, said I'd never seen such political
interference in my whole career at CDC. Ultimately that ended
Bill Roper's job. I don't even think he knew what happened.
Just because he was too busy, wanted to make some telephone
calls, and wouldn't sit and listen to testimony that preceded
his.

I learned very early after coming to California that, when
you're testifying in front of a committee, you better sit through
that whole damn testimony and hear everyone's testimony. First,
because what you say, especially your written testimony, can
become meaningless or redundant. Second, you better hear what
somebody else says against you.

1 Donald P. Francis. Toward a comprehensive HIV prevention program
for the CDC and the nation. Journal of the American Medical Association
1992, 268, 11:1444-1447.

87
Communicating on AIDS

Expedited Publication
[Interview 3: February 11, 1994] ft

Hughes: Dr. Francis, I read that Edward Brandt early on in the epidemic--
I don't know the year—requested that leading medical and
scientific journals expedite publication of AIDS papers.1 Did
the major journals actually do that?

Francis: This really centered around a rather bizarre policy that the New
England Journal set—other journals tended to follow, and
certainly scientists followed- -that you couldn't talk about your
results anywhere if you expected to get them published later in
the New England Journal. That is, if they were announced
publicly, New England Journal wouldn't publish the research.
This was really a repressive policy—stifling scientific
communication. Publication takes months and months. Public
discussion in meetings and other gatherings is the best way to
announce the latest findings and get information out. So this
policy slowed scientific information exchange by several months.
It was terrible. It was primarily New England Journal. I don't
know if any other journals officially followed the NEJM, but
researchers felt that they did, or might, and so they were very
reluctant to make these announcements [before publishing] .

For the good of the public's health, we had to let AIDS
information out ASAP, and yet people who did the research were
reluctant to allow it because it would take the wind out of the
publication sails, and make it less likely that they get their
research published. It was a silly little problem, but one that
I think the Assistant Secretary of Health and Human Services did
make an active decision to do something about. I don't remember
exactly when he did that.

Hughes: How did you get critical information out?

Francis: Well, the MMWR is the way CDC gets it out primarily, and then
scientific meetings. The annual international conferences on
AIDS started in 1985, and there were always multiple conferences
even before that and in between, enough to drive you nuts. But
we would try to present the latest data that we had whenever we'd
speak.

Sandra Panem, The AIDS Bureaucracy, p. 111.

Hughes: So you didn't feel that there was a problem in disseminating
information?

Francis: Some people did; the blood banks complained that they didn't have

all the information, but indeed they did if they just listened.

Censorship

Hughes: Were you given free rein as a member of the CDC to say anything
that you wished to the press or to whomever? Was there any
censorship?

Francis: Early on, it was typical CDC where the press was sent down to the
person doing the investigation, and there was essentially no
control. Later, once Reagan came in [1980], we were almost
totally censored. Some of that was political from Reagan's side;
some of it, though, was our setup that we actually prescribed
because when something about AIDS would occur, you'd spend the
whole next day responding to the press, and it would eat up all
your time. So we said, as I mentioned earlier, "Well, let's let
the press office deal with this stuff instead of us," because we
were so understaffed. That was a mistake, because it set up a
situation which the scientists didn't control. By the mid-1980s
there was no unapproved discussion with the press, and Washington
could come down very heavy on you if you did.

Hughes: What sorts of things were censored?

Francis: Any claim for additional resources. That's what they wanted to
control. They didn't want the scientists out there saying,
"Well, we just don't have that information because we don't have
the resources to do this job." And it was not just for AIDS; it
was for everything. The administration did not want government
employees saying they can't do a job because they don't have
enough resources. If they did, they wouldn't be able to cut
budgets.

Dealing with the Media

Hughes: Was there ever a problem of translation when the press office at
the CDC handled matters?

Francis: Yes and no. They were very able people who understood at least
the general aspects of a story. Some press people really know
what's going on, and those subtleties that the press really would
like were missed.

Hughes: Were there particular people in the media that you dealt with?

Francis: Yes. Larry Altman of the New York Times was clearly a person
that I talked to, and he would drop by CDC periodically.

Hughes: Why did you choose him--or did he choose you?

Francis: Larry Altman is a doctor who was at CDC during his training, so
he knows epidemics and epidemiology very well. Who else? There
was Chris — forgotten her last name—of the Washington Post.
There was Marlene Cimons of the L.A. Times. And of course, Randy
Shilts and others from the San Francisco Chronicle. And then
there was an obsessed guy named Chuck Ortleb from the New York
Native who was always on my telephone driving me nuts about
African swine fever virus. He lost it— like Peter Duesberg at
Berkeley. These people get this pit bull approach to science and
lose all ability to look at data.

Defining AIDS

Broadening the Definition

Hughes: We talked last time about defining AIDS. What were the forces
changing that definition as time went on? Was it just science?

Francis: For the first years, it was all science. The definition enlarged
to include more opportunistic infections and some new cancers, as
we got more information. A doctor could call and say, "Lookit,
this guy doesn't have Pneumocystis; he doesn't have Kaposi's
sarcoma, but he's got cryptococcal meningitis and he's a gay man
with no T cells. He clearly has your disease [AIDS], but he
doesn't meet the definition." And so we said, "Gee, that's
really a rare situation." So with a little review of the
literature, we said, "Okay, that individual fits into the AIDS
definition."

Hughes: What would reviewing the literature accomplish?

Francis: It allowed us to estimate what the incidence of that

opportunistic infection was in other immunologically normal

individuals. And so the list of opportunistic infections that
fit increased with time. The technology to identify and diagnose
some of these organisms, cryptosporidium especially, improved
with time, as did Pneumocystis, and so some criteria changed.

And then came another scientific issue, especially with
Kaposi's sarcoma: Doctors weren't necessarily doing biopsies of
these tumors. Initially CDC required a biopsy diagnosis.
Similarly, with Pneumocystis, the doctors got so familiar with it
that there was no reason to spend the extra money or pain to do a
biopsy or bronchoscopy. They could just say, "That's
Pneumocystis, " and "that's Kaposi's sarcoma," and treat them. So
there were these provisional AIDS diagnoses that later became
acceptable.

Only in the last few years was there the political issue.
It's fascinating: Early on nobody wanted to have an AIDS
diagnosis; they didn't want to be in a risk group. But once they
realized that resources tend to be allocated to those groups with
higher incidence, the desires changed. This was highlighted with
women who had different clinical syndromes such as chronic yeast
infections and the like. That pushed the whole issue of
diagnosis of "AIDS" into being 200 helper cells [or less]. But
by that time [after March 1985], the HIV test was available, and
frankly, the diagnosis at that point should have been HIV
infection. But AIDS activists still resisted reporting HIV
infection, as they initially had for AIDS.

Hughes: Why?

Francis: Oh, I would say it's an old, old thing that if people are

healthy, you don't want their names in some government computer.
It makes no sense whatsoever. But there's sensitivity to HIV
reporting to this day; people don't want to be reported, period.
They do once they get AIDS and there is benefit from the
diagnosis because of resources that may come forth. But short of
that, they don't want their name in somebody's computer. Yet to
my knowledge, essentially nobody's name has ever leaked out of
the government computer, and there's, what, over 300,000 people
with AIDS in these computers now. Privacy has been well
protected, as it has been traditionally in public health. But
there still is a sensitivity.

The issue of wanting an AIDS diagnosis to be broadened was
also complicated by the fact that the Social Security
Administration made the clinical diagnosis of AIDS part of their
eligibility criteria for their Social Security benefits. CDC
made epidemiologic definitions that had nothing necessarily to do
with disability. For example, people with Kaposi's sarcoma can

be quite healthy early on; they just have a purple spot
somewhere, but other than that, they can work for years and do
fine. But KS patients were considered disabled because they had
an AIDS diagnosis, whereas somebody who had a wasting syndrome
didn't meet the case definition in the early days, but was sicker
than a dog, and couldn't get out of bed in the morning. But that
person was not "disabled." [tape interruption]

Defining AIDS as HIV Infection

Francis: But the real issue now is HIV infection. I've written an

editorial suggesting that we report HIV infection, and deal with
the disability issue separately, and don't connect the two.

Hughes: Why, after it was possible to determine HIV infection, were

opportunistic infections retained in the definition? Why not
just have HIV infection?

Francis: HIV infection is reported in many states, but in the big states,
the gay community has lobbied against it because they were
worried about privacy violations and other rights violations. In
California, after all, Bill Dannemeyer and his incredible group
tried to pass a quarantine proposition on the California ballot.
You can see how they might be afraid. Perception can be very
important.

Hughes: So that's where the politics comes in, rather than the science.
Francis: Yes.

Hughes: The definition would be just HIV infection, if it were based
strictly on science?

Francis: Yes, absolutely.

Hughes: What are the ramifications of the fact that it is a more
complicated definition?

Francis: Let's look at the reasons for reporting: one is to get preventive
services, two is to count new infections and get some evaluation
of the effectiveness of your prevention program, and three is to
make long-term planning for caring for these individuals. And
you want to get all that information as soon as possible after
the test has been discovered. Any delay hurts all those parts of
your program.

Including Women's Symptoms

Hughes: There has been criticism of the fact that the official case
definition, until 1993, did not include symptoms that were
specific to women. Is there any justification for that
criticism?

Francis: Some. Women's chronic yeast infections and the like can occur
without AIDS, and so it needed to be a definition that would be
linked to HIV infection. A simple solution may be to say women
meet the criteria if they're HIV positive with T cells below 200.
But again, if you really want to track the epidemic, you would
request reporting of HIV infections. If you want to evaluate the
trends compared to the old definition, then keep a subgroup where
you continue to use the old definition and say, "Ah, now they've
reached that definition, I will report them for comparison
reasons and see what the epidemic is doing in relation to what we
did in the past." The continuing debate about definition outside
of HIV infection is all kind of nonsensical, in my opinion.

Hughes: Is it common for an official definition of a disease to change
over time?

Francis: Certainly as the technology improves, yes.

Hughes: Well then, how do you ever get an accurate longitudinal study?

Francis: Makes it hard, there's no doubt. If you want to keep an accurate
longitudinal count, you'd have to at least keep a portion which
was collected in an identical manner as previously.

But with HIV, it's not a great problem, because we know the
natural history well enough where on a computer you can say,
"Okay, we know that if we shift the definition to a new one, we
can predict the effect accurately." We know what the natural
history is.

Hughes: It's a problem to some, however, who maintain that the new
definition magnifies the number of AIDS cases.1

Francis: Nobody's magnifying anything. You change the definition, we can
calculate exactly what that means. Those are critics looking for
some simple hit.

1 See, for example: S. W. Chang, M. H. Katz, S. R. Hernandez. The
new AIDS case definition: Implications for San Francisco. Journal of the
American Medical Association 1992, 267:#2:973-975 .

Hughes: Activist groups drive this politicization of the definition? Is
it as simple as that?

Francis: Yes. But they don't want to push it all the way to HIV
reporting. [laughter] Isn't that interesting?

Hughes: Yes, it really is.

Coining the Term AIDS

Hughes: Were you at the CDC meeting in July 1982, where the term AIDS was
first coined?

Francis: Yes, I was.

Hughes: Can you tell me about that?

Francis: It was at the hemophilia meeting in Washington, D.C., and Bruce

Voeller, who was I think chairman of the National Gay Task Force,
recommended that we approve that name.

Hughes: Had he thought it up?

Francis: It actually went out in the invitation to the meeting. Dr. Foege
from CDC used the name "acquired immune deficiency syndrome." So
it looks as though it came from CDC. Then Bruce is the one that
said, "This is what it should be," and everyone voted on it and
that was it.

Hughes: Did the term strike you when you received the announcement?

Francis: No.

Hughes: Because it fit your perception of the disease?

Francis: Sure.

Hughes: Was there any reaction from anybody else?

Francis: No, that was not a big deal.

Hughes: The reason I ask is because some of the previous names had been a
big deal, for example, GRID [gay-related immune deficiency].

Francis: We never used GRID. That was, I think, a local New York term.
Since we already had IV drug users, why would you call it GRID?

Hughes: What were you calling it before that meeting?

Francis: KSOI [Kaposi's sarcoma/opportunistic infections]. Rather clumsy
but descriptive.

The HIV Antibody Test

Screening Blood Samples, 1984

Hughes: Please tell me about your use of the HIV antibody test.

Francis: When we, with the collaboration of Institut Pasteur, got our test
cooking in about February of "84, I immediately went down to our
freezers and pulled out samples, primarily from the gay community
in our different study cities, to see what infection rates
existed at different times. We started studying samples straight
away. It was just a matter of how many your lab could test if it
was running full steam, all day long.

Hughes: Were other people doing the same thing?

Francis: Yes. But the test existed only in a few laboratories at that
point .

Hughes: Levy, I know, had one.

Francis: Jay Levy got his going a little later, I guess. Bob Gallo had
his; Institut Pasteur. We all had relatively crude tests. But
they were very good, very predictive for high-risk populations,
where one false positive doesn't make any difference. But in
low-risk populations, it was a problem, because the cutoff would
pick up people who were not really infected.

Hughes: Did you learn anything that surprised you?

Francis: Oh, yes. The extent of infection surprised us. We're talking
about 50, 75 percent of our samples from San Francisco being
positive, and 20, 30 percent from St. Louis, Denver, and Chicago.
Then the natural history data started to just be horrific. The
major thing that came out was that, of the people infected,
almost all had had abnormal T cells, and a lot of them had
already died, about 6 percent, I think, on our first cut. Now, 6
percent mortality for a viral infection is incredibly high.

Hughes: How did such statistics compare to your experience with other
infectious diseases?

Francis: I come from a very biased experience: Ebola, smallpox, Lassa had
extremely high mortality per infection, where something like
polio, less than one in 1,000 people died. HIV was already at 6
percent mortality; that put it up there in the viruses that we
kept in the hot lab at CDC, the really dangerous ones. And then
when we started estimating using appropriate statistics, it was
clear that the percentage was much higher than 6 percent. So
that was really incredibly impressive and worrisome.

The Issue of Safety

Hughes: What were you thinking about your own personal safety?

Francis: We were all very concerned.

Hughes: More so after you had the results of antibody testing?

Francis: No. I had very strict rules in the laboratory, because I

recognized that historically the first people that come down with
a disease after the original cases are the laboratory workers,
and I didn't want anyone in my lab dying of this disease. So we
were very strict. But as soon as the test became available in
our lab, I immediately required, asked, everyone to be tested.
There was a hue and cry at CDC, interestingly, saying, "Well, you
really can't do that, because somebody might be gay and test
positive." I already knew who was gay in my lab. CDC said, "Oh,
we've got to bring this through the ethics committee," and all
this stuff.

I just sat down with my lab folks and I said, "Lookit, I
think this is just ridiculous. We need to know whether we're
protected here or not . We have spouses , and we want to know
whether the precautions we're taking are adequate," because we
were up to our elbows in that virus for years. So they all
agreed that we be tested. The CDC told me not to, and I went
ahead and did it. I threw in a couple of positive specimens we
had from chimpanzees so that the laboratory technicians wouldn't
know if someone tested positive. I was the only one that had the
code. We tested everybody, and luckily everyone was negative.

Hughes :

Francis :

Hughes :
Francis :

Hughes:

Testing Advocate

I understand that you took quite a firm position on the necessity
of widespread testing.1 Why?

We had relatively few tools to deal with this virus in a public
health sense. When you have a disease that's relatively
difficult to transmit, not like influenza that spreads like
crazy, but rather one that goes from person to person to person,
the chain of transmission becomes terribly important. Finding an
individual who's infected, so that he/she can be advised, along
with their sexual partners, on how to protect themselves, is
incredibly important. In the end you are dealing with the ends
of the chains of transmission where an infected person is having
contact with an uninfected one. In order to do that, you have to
know who's infected and who's not. That's where the test comes
in.

So I've been a very strong proponent of widespread testing,
including in areas like California where I think essentially
everybody in a given age group should be tested so that all HIV
infected people know they're infected, so they can learn how not
to transmit it to others.

What has been the reaction to that viewpoint?

I think in California, we haven't followed through with it. The
California Medical Association was in support of it, and some of
the gay groups were in support of it, as long as it was voluntary
testing and not mandatory. What is essential is a place where
these people can go after they are identified as being infected.
We must have some medical system that can handle and take care of
them. We called it "early intervention." I think most people
are in favor of it. The trouble is, the latter part (the
medical, counseling, support system) doesn't always exist;
there's not enough money to take care of all these people, so the
program of widespread testing is only passively accepted.

I read about a workshop on HIV antibody testing that occurred in
July 1985, sponsored by the FDA, CDC, and NIH.2 Does that ring
any bells?

Francis: Yes, I remember that, but I don't think I went to it.

1 Shilts, And the Band Played On. p. 469.

2 Sandra Panem, The AIDS Bureaucracy, p. 115.

Hughes: The various manufacturers of the test made presentations in the
afternoon, and they were not forthcoming on the scientific
details, for trade secret reasons.

Contact Tracing and Partner Notification

Hughes: Contact tracing and notification go along with antibody testing?

Francis: Yes, contact tracing is clearly part and parcel of the whole
program. That was strongly resisted by the gay community. I
remember Marc Conant and me meeting with the National Gay Task
Force—at least with Jeff Levi and his group in San Francisco
Marc and I were asked to come down and discuss partner
notification, which the gay community was strongly against for
years. There we have a little different issue. Wanting to be
voluntarily tested is one thing, but if you as a male tell a
government worker that you had sex with another man, that clearly
meant that you were having homosexual sex, and the man whose name
was just given did not have any informed consent about being
mentioned as a sexual partner.

What was silly was that we had been doing this for years
with syphilis, and indeed some gonorrhea partner notification.
Much of this was with gay men, so this was not a new phenomenon
at all. But yet there was this hue and cry about it, and it
continues to this day. The reason being not that they wouldn't
support it if it were something that was important for public
health. Unfortunately it became political. The Dannemeyers and
all pushed partner notification like crazy, and so the gay
community felt an obligation to resist it. That got it into a
terrible bind. To this day, partner notification is not terribly
popular.

Now, in what we call the early intervention model, where all
infected people are brought into a medical, social, behavioral
longterm follow-up program, partner notification becomes an
integral part of what one's responsibility as an infected person
is. There's a system into which people who test positive are
enrolled, and it all works out very well. But the fifteen-minute
partner notification format is hard on client and clinic if you
don't have a well-resourced program.

Hughes: Are you saying that if a person is going to participate in one of
these programs, the understanding is that it involves partner
notification?

Francis:

Hughes:

All partner notification is voluntary,
to get names of their contacts.

We don't torture people

[laughs] Yes.
nonetheless.

But there is a certain social pressure,

Francis: Oh, yes, an ethical pressure of, if you're getting a service, and
you have contact with someone else, that exposed person should
have the right to know that they've been exposed, and they should

get the service, too.
appropriate one.

Yes, there's a pressure. I think it's an

Civil Rights versus Public Health

Hughes: There is a broader historical event that underlies these

concerns, and that is the rising consciousness of civil rights,
which escalated in this country with the civil rights movement in
the sixties, and then of course has been adopted by other groups,
including the gay and lesbian groups.

Francis: Yes. It is a new thing, and a potentially very dangerous one.

Civil rights are often easy hits. It's always easy to call civil
rights. I remember when the gay community was saying, "It's the
civil right of a gay man to be able to donate blood," the
hemophiliacs were saying, "Well, it's our civil right to be
protected from death." It was nonsense—there' s no civil right
guaranteeing that you can donate blood, and there's a health
decision that goes along with that. I think we have to be very
careful about this civil rights issue versus public health. When
there's such a dangerous virus circulating around, we will
compromise some "civil rights" for the betterment of the
community.

Now, this is a voluntarily transmitted disease by and large,
of relatively low transmissibility, and so we don't lock people
up. If it were airborne, we would isolate infected persons as
long as they were contagious, and justifiably. Isolating people
with bad infectious diseases for which there is no treatment is
something you have to do. It isn't necessary for HIV, because we
get the information out that there is a dangerous virus out
there, and hope that people change their behavior and protect
themselves. We stress individual action and responsibility. If
the government takes everyone who is infectious out of
circulation, then you give the exact opposite message, i.e., it
is safe to practice at-risk behavior.

If you give that opposite message, you better have a good
program that indeed gets all the HIV-infected people out of
circulation, because otherwise you'll have a fox in the chicken
coop phenomenon, and you'll be a lot worse off than if you did
nothing.

Hughes: Has the CDC actually quarantined people in recent years?

Francis: Sure. People with tuberculosis are periodically locked up if

they don't take their pills. And they should be. They have an
airborne disease that puts others at risk for just breathing air.

Hughes: And there's not a great public stink?

Francis: Oh, yes, there's some. But isolation rules are very strict.

We've got to be careful in America that we balance civil rights
and public health.

Community Input

Francis: Interestingly, one of the things that is new in public health is
bringing in new constituencies as part of planning programs and
dispersing information. Sometimes that has been a disaster.
Bringing the hemophiliacs in to discuss the hemophiliac thing
hurt the hemophiliacs.

Hughes: Explain why.

Francis: Because in the July meeting of 1982, the hemophiliacs' spokesman,
Charles Carmen, said, "Don't take this stuff [blood and factor
VIII concentrate] away from us. We know it's risky; we're
willing to take the risk." Well, that kind of took the wind out
of CDC's sails, and so everyone said, "Well, yeah, factor VIII is
important; we better leave it on the market." When in reality,
it was a convenience; it was not survival. There were other ways
to get clotting factor into people—less convenient, no doubt.
In this case the "responsible" community member allowed us (CDC)
to abrogate our responsibility.

We also brought the gay community into many discussions. We
had very serious discussions about the dangers of gay sex--
especially in bathhouse-type environments. Here government was
making recommendations about homosexual relations.

100

Francis: Sometimes there was reluctance to take action because some would
say, "Oh, you can't say that to gay men." Well, you may not say
it in public, but you get leaders on the side and say, "Bullshit,
this is dangerous. You must recommend change. We have to do it
to save the gay community." The preventive issue is who is
getting most of the infections in the United States right now;
it's gay men. So they ought to be screaming for prevention and
vaccines. And yet the ones who are making the most noise are the
ones who are infected, and they're screaming for drugs. They
don't want any money diverted to prevention. So we have a
conflict of interest.

Well, public health should be making those decisions,
informing the gay community, getting their support as much as
possible. But if partner notification or HIV reporting is right,
then it should be instituted.

Hughes: Well, where is the proper place for community input?

Francis: I think it's important to have it in place all the time, but what
you have to do is be sure you know whose hat everyone has on in
the room. If the gay activist is representing gay civil rights,
fine. But if you're representing public health, you better take
your words and action from your wisdom, not from complaints from
someone about civil rights. You want to listen to those, because
you want the cooperation of the community. But you should be
very matter-of-fact, saying, "For the benefit of public health
and, for example, the gay community, I am going to do this."

Hughes: Do you feel that there were instances when the CDC was hampered
in its activities because of oversensitivity to activist
concerns?

Francis: Yes. Once the Reagan administration undercut CDC, then CDC

became a half-baked organization. That is, it couldn't stand on
its laurels and say, "We did a good job on this, and therefore,
we will take a cutting-edge stand--"

Hughes: Because of budget cuts?

Francis: Both budget and policy inadequacies. The Reagan administration
had terrible policies.

Hughes: Why?

Francis: They didn't care about AIDS; they didn't care about AIDS

prevention. Bill Dannemeyer told me: "All you want to do is
teach these guys how to bugger better." And I said, "If it saves
their lives, I'll teach them how to bugger better." And Reagan

101

said, "Not with government money you won't." And the director of
CDC, Jim Mason, went along with it. For example, for an entire
year, there was no decision on what government could say
regarding homosexual health. So a year went by when there was no
government funding going out there about safe sex for gay men.

Hughes: Which year?

Francis: '85, '86. So that was real government interference. Same thing
on population-based sex surveys--it went on and on and on and on.

AIDS is a sensitive issue with the gay community, or for
that matter any other community, Haitians and others. Public
health is going to take some tough stands that are going to
irritate people. That's the reality in public health; you can't
keep everybody happy. But if public health practitioners act
appropriately, the society will support this. But when they
don't trust in public health inherently, it's very difficult to
operate in these rough waters.

So when public health practitioners start making
compromises --more political compromises in order to keep the gay
community happy- -you can hurt them. You want to walk in step
with at- risk communities; you don't want a war. But you also
want to be very forceful where necessary. It's a very fine line,
and if that balance is shifted, by statements of extremist
politicians in the Reagan administration, then it's very hard to
walk that line.

Hughes: How were you as an individual affected in terms of your

activities? From the little I know of your past, you were used
to operating in a fashion, "Let's stamp it out through
vaccination." Well, obviously, you didn't have a vaccine in the
case of AIDS.

Francis: Stomp the virus out with something else--yes.

Hughes: So what effect did political considerations have on the way you
operated?

CDC Advisor to the California Department of Health Services,
1985-1989

Francis: Well, first of all, I had to get out of a lose-lose situation in
Atlanta, so I asked to be transferred to California, where at
least the government was trying to do something about AIDS.

102

There I put myself into my Bangladesh mode: I never lost sight of
my goal. I just had to shift the time frame when I could
accomplish that goal. It was similar to what I did when I was in
the developing world working for WHO. I had my things-to-do list
in the morning, and when I first arrived, I was very frustrated
because I didn't get everything done. Then I said, "Well, I just
won't get frustrated any more. I'll just keep the items on the
list for tomorrow, and eventually I'll get done." I found a
balance between what compromise I could accept without just going
crazy, and what I must get done.

Hughes: What could you do in California that you could not do at CDC?

Francis: I could say what I needed to say here, because I was a scientific
advisor to the state of California beholden to nobody. The CDC
was perfectly happy to have me do that. They slapped my hand a
few times, but I was out there saying what should be done
concerning AIDS.

Hughes: Now, they were willing to have you do that because you were one
step removed from CDC?

Francis: Yes.

Hughes: Was it as simple as that?

Francis: And they knew they could never stop me.

Hughes: [laughs] That I can believe.

Francis: But yes, I could speak out here, including criticizing the Reagan
administration. Now, mind you, I was a guest in the state, and
even though this is my native home, I was still legally a guest,
a federal employee on a state assignment, so I was quite cautious
about criticizing the government of California.

Hughes: Which was a conservative government.

Francis: The administration was sometimes primitive. And so I would speak
out sometimes in very subtle ways. The governor's office called
me a couple of times and complained. But never did it amount to
anything .

Hughes: You sound as though the situation in California was an
improvement over Atlanta.

Francis: Oh, yes. Well, because in California we had a group of

individuals, with Marc Conant, usually the president of the
California Medical Association, Mark Madsen, who was a staffer of

103

the CMA, the gay leadership, the chairman of the State of
California Department of Health Services Task Force on AIDS, be
it Conant or Decker or whoever- -there was a mass of people that
could be rallied in fifteen seconds to stop any negative move by
extremists. So I felt fairly confident that there was a power
base behind me, and I could push the envelope a little further
than I might otherwise.

Hughes: Did you have those liaisons before you came back to California?

Francis: No, they were assembled only after my arrival. Jim Chin, the
state [State of California Department of Health Services]
epidemiologist, as soon as I came, set me up to meet all these
people, and through doing my job, I met everybody else. It was a
pretty small group at that time [1985].

Then came California Propositions 1021 and 64 and 69.
There's a very good lesson for history from this example:
Adversity is what drove us together. The California Nurses
Association, California Medical Association, the gay community
representatives, gay physicians, public health, business --when
this crazy stuff began coming from Lyndon LaRouche2 and from
Dannemeyer, they became wonderful rallying points in favor of
logic. One could really bring people together who might not
agree on other issues.

Politicization

Hughes: How do you feel about politicization of the epidemic and of Don
Francis? Were you forced to be a political animal at CDC?

Francis: In public health, you are always dealing with the public by

nature, and therefore by nature you're always out in the public
eye. But as physicians and scientists we try to stay above
politics; we like being in Atlanta and not Washington. In

1 In 1988 the voters defeated Proposition 102 which would have
required physicians to report to the state the names of all HIV-positive
patients and those suspected to be HIV positive.

2 In 1986, followers of LaRouche introduced a California initiative
which, if passed, could have resulted in quarantining and discrimination
against people with AIDS. (John Kinsella. Covering the Plague ; AIDS and
the American Media. New Brunswick: New Jersey: Rutgers University Press,
p. 267.)

104

retrospect, that was extremely naive. It's nice to have public
health be independent from politics, but it isn't, and it wasn't
in this case. I shifted all the way from a doctor and a
laboratory scientist and public health person, to almost a full-
time politician and policy person.

Hughes: Is that how you regard yourself?

Francis: In my last years in government, I was almost full-time policy. I
was writing legislation; I was reviewing legislation; I was
recommending where money went .

Hughes: That takes a very different set of skills. How did you acquire
them?

Francis: By the school of hard knocks, and from some extremely good
politicians in California, people like California state
legislators John Vasconcellos, Burt Margolin, and Jackie Speier,
their staff members, and even [California State Assembly Speaker]
Willie Brown's office. These people are really good, and they
ask, "How do you want to do this? How do you arrange testimony?"
Later I ended up in the mayor's office in San Francisco [as the
mayor's Special Consultant on AIDS, 1988-1992], and worked with
people like [Mayor] Art Agnos who are dynamite at moving those
kinds of politics. San Francisco, with its all-inclusive
politics, is a tough place to work. If you can survive in San
Francisco, you can survive anywhere.

Hughes: Were you conscious of watching politicians to learn how to
operate?

Francis: Yes. I always watched to learn, but I always kept myself a bit
above the fray. My issue was science and the public health. If
I had to maneuver politics in order to favorably affect a program
towards the logical scientific approach, I would do that. But I
learned from my experience with the World Health Organization
that if you make yourself primarily political and secondarily
scientific, you'll lose your credibility and you'll be running in
circles pretty soon because you'll compromise here and compromise
there. So as long as you stay strictly scientific and then do
the politics to accomplish that scientific endeavor, then you're
always clean, even though you're in a potentially dirty
situation.

105

Hughes: Which is precisely what you were advising the CDC to do in the
speech you gave when you retired from the Public Health Service
[1992].'

Francis: Yes. And in an editorial I just wrote for American Journal of
Public Health.2

Hughes: Referring to the CDC again?

Francis: Boards of health—keeping the separation between public health
and politics.

Political Interference with CDC

Hughes: Is CDC doing that?

Francis: No, it's terribly politicized still.

Hughes: Is that largely because of AIDS?

Francis: Largely, I think. Well, also because of some of the other

issues. First thing Reagan did was disband all of our family
planning people—no more abortion surveillance; that went
straight away. NIOSH, the National Institutes of Occupational
Safety and Health, got cut to hell. Anything that might
interfere with business or promote abortion got chopped
instantly. In all the governments I'd worked in around the
world, I had never seen anything as repressive as the Reagan and
Bush years-- just terrible.

Hughes: So CDC hasn't bounced back from the Republican administrations?
Francis: No, it will take years to bounce back.

I'll give a local example. No more than three, four years
ago, on International AIDS Day on December 1, the California
Office of AIDS decided to have a display in the main building of
the California State Department of Health Services in Sacramento,

1 Donald P. Francis. Toward a comprehensive HIV prevention program
for the CDC and the nation. Journal of the American Medical Association
1992, 268, 11:1444-1447.

2 Insulating public health from extremist politics. American Journal
of Public Health. May 1994, vol. 84, 5:720-721.

106

And the director said, "I hope you don't have any condoms there."
This was years into the epidemic, when condoms were the
foundation of AIDS prevention programs! And notice that the CDC
came out with MMWRs on condom efficacy and needle exchange
efficacy only after the Clinton administration came to power.
The data on their benefits existed for a long time, but CDC never
dared to publish them during the Reagan and Bush years.

Hughes: Well, you said last time, that one of the reasons you left the
CDC was lack of resources. But Shilts mentions policy
differences between you and Jim Curran as a reason. Shilts'
point is that Curran took an epidemiological approach where you
took that of a vaccinologist wanting control of the disease.1 Is
there truth in that, and could you talk about those different
approaches to an epidemic?

Francis: There is some truth to it, exaggerated no doubt in the movie.2
In general, Jim and I worked well together. His interest was a
little more academic than mine. I have great academic curiosity,
but when it comes to an epidemic, my job is to respond. Maybe
it ' s because I came into CDC through the Epidemic Intelligence
Service, which was this epidemic training program, and he came in
through kind of a postdoctoral study program. His interest was
research, but that was very complementary to mine in disease
control. If he wasn't interested in intervention, he had enough
business to do in research for a lifetime. So we were quite
compatible if I were more interested in prevention than he was.

Our boss, Dr. Walter Dowdle, asked me to put together a
national AIDS prevention program, which was fine.3 Jim was not
interested, and I was, so I did that. Ultimately the plan went
up to Washington for funding and was totally shot down.

Hughes: On what basis?

Francis: Money. $37 million a year. For the United States of America.

Hughes: Do you think that was the total issue?

1 Shilts, And the Band Played On. pp. 482-483.

2 "And the Band Played On"--A Home Box Office (HBO) film based on
Randy Shilts 's book by the same title, broadcast in September 1993.

3 Donald Francis, James Chin. The prevention of acquired
immunodeficiency syndrome in the United States: An objective strategy for

medicine, public health, business, and the community.
American Medical Association 1987, 257, 10:1357-1366.

Journal of the

107

Francis: That was certainly the first step. I think the rest of it was,
who cares if these guys die.

Hughes: That response was what caused you to leave Atlanta?
Francis: That was it. That was what sent me to California.

Failure at the Federal Level

Hughes: Well, I have a quote from Don Francis about government

ineptitude: "The worst thing in all this, which I only came to
recognize as the years went on, is that the government had no
concept of what its role should be in an epidemic."1

Francis: That refers to the federal government's role, the upper levels of
government, the Reagan administration. CDC was in the epidemic
business—that ' s the Center for Disease Control. It's up to its
ears in epidemics all the time. I think when you get to be very
specialized, you tend to assume that everyone around you has the
same specialty knowledge that you do. By that time, we had
become so knowledgeable and specialized that when we started
talking about AIDS control, people really did not understand what
the hell we were talking about. I didn't recognize that. I
didn't recognize that there was a knowledge and experience gap.

Hughes: Which people didn't understand?

Francis: The blood industry, the administration, whomever. Therefore,
some of our mistakes were marketing failure and upstream
management failure. But, in addition, some didn't care to listen
to us anyway.

But the administration had no idea of what their
responsibility was as a government. Second to national defense,
public health is one of the major priorities of government, and
has been since our founding. A society better have sewers and
immunizations and do whatever else you need to in public health,
otherwise people die. They had no concept of this at all. The
policy of the Reagan administration was, no government was better
government .

1 Steve Heilig. Donald Francis, M.D.--How CDC politics has botched
the fight against AIDS. California Physician 1992, July: 38-41.

108

Hughes: Yet, in the history of public health, there has always been a
quibble about how responsibility for public health should be
divided among different branches of government, and particularly,
where does it become the states' responsibility?1

Francis: In the early seventies, when I was actually assigned to a state,
and we were starting to get some good health officers out in
county and state levels, many of whom came through the CDC
training programs, the system worked reasonably well. For any
given disease, the narrow expertise was at CDC, and some at state
health department level, and then general public health was at
the local level. And by and large, the regulatory power is with
state and local health departments.

If CDC, if the federal government felt there was a very
important epidemic, be it immunizable diseases, be it
tuberculosis, be it sexually transmitted diseases, then federal
money would come down with some rules on its use, so the program
would be designed federally but with considerable local autonomy.

That worked very well—not perfectly, no doubt—because,
frankly, local authorities sometimes have very little flexibility
due to their lack of resources. Their tax base is very limited.
States, a little bit less so, but still not like the federal
government, which can come up with billions and billions by
shifting resources. Our tax structure is very federally
oriented. This typically decentralized U.S. approach was not
perfect in any way, but it was workable.

With the AIDS epidemic, the CDC should have taken its
traditional, strong, federally funded leadership role, performed
the essential research using its technically expert people, and
sent that information and money out to the state and local health
departments. Usually CDC assigns people much like me to help
deliver these programs. There should have been someone like that
in every major state. As a matter of fact, there should have
been at least three physicians, one in San Francisco, one in
L.A., and one at the state level in California—that would have
been typical CDC response in the past. CDC sent me to Bareilly,
India, (as a WHO medical officer) to head up a district smallpox
program. That's a long way from Atlanta, but we felt that if we
got rid of the disease there, we wouldn't have a problem here.
It was a very smart move.

The system can work, but what happened with the Reagan
administration compounded the difficulties of responding to a new

See, for example: Sandra Panem, The AIDS Bureaucracy, pp. 37-38.

109

epidemic. They cut back local funds for multiple programs. What
happens at the local level, unfortunately, is when poor people
get sick, they go to the hospital, and they cost money. Those
costs must be absorbed by basically a fixed budget. With less
federal support, less health insurance from business, more poor
people coming to public hospitals, more local money is going to
have to go to the hospitals. But the health budget at the local
level includes public health. And when the health demands
increase, everything else has to decrease if you're going to keep
your tax burden the same.

So what happened in those years when the federal government
was cutting back money and the AIDS epidemic was growing, the
health care budget was just eating everything else up.
Prevention programs and the ability to support preventive
medicine at the local levels was eaten up even more. This at a
time when we had a weak federal government, an impoverished local
government, and the state somewhere in between. It was a setup
for disaster.

The Epidemic's Personal Impact

Hughes: You have been in this epidemic now for over twelve years. What
sort of impact has it had on you as an individual?

Francis: Well, it's not the field that you'd recommend a young public

health person to get into and make their name. It's a difficult
and often unpleasant field. But I had already done great things.
I had eradicated smallpox; I felt really good about what I'd done
The hepatitis stuff was marvelous, and some of my other work,
like Ebola, was great. So I was old enough to look at AIDS as an
education, and it was a marvelous if not always pleasant
education. I got to know some really good people in the world--
in the community, in politics, and the upper levels of
government.

Equally important, there are some real bastards. And you
can't ignore those bastards; you have to deal with them. And you
may lose. You have to be very clever, because evil people are
often very clever. But the whole political process of bringing
opposing forces together and getting support to outdo the evil
was an education I would never have had without AIDS. So dealing
with the ugliness was valuable.

Hughes: What are you thinking of specifically when you say that?

110

Francis: Ronald Reagan and his entourage, Bill Dannemeyer and his ilk--

these almost fascist-type people who seem to be well-meaning but
do evil, evil things. We can't sit back and let them run the
show, or you'll have a really bad society.

I guess next I've learned it's extremely hard for humans to
work together. They are, especially the male of the species,
basically designed to fight. The future of our society depends
on our ability to harness that aggression, which was, no doubt,
useful during 99 percent of our evolution, for killing mastodons
and fighting off incurring tribes and such. Yet it's not very
useful any more. It seems more common to fight than it is to
work together and compromise and move ahead.

I'm not sure if I'm optimistic or pessimistic for the
future. The thing that saddens me is to see the tremendous
potential that we have in this world that we let pass; the beauty
that we have in this area of California, and still we can't build
transportation facilities, for example. We can't deal with
getting people from here to there and plan long-term and realize
what that does to the quality of life. I think we're close to
useless at planning the long-term.

So that realization has really depressed me and bothered me.
Yet I'm basically an optimist and think humans have an amazing
strength to come through in the end. I guess I've also realized
you have to have a crisis to get people to change. I think
that's terrible, because people get tired of having crises.

AIDS has been very hard on my family. My wife has been
remarkably tolerant, but not always, and I think basically she
hates AIDS, because it's taken me away from the family an awful
lot. She is a professional who has been trying to do her career,
and I was always in the lab, in the field, or on a trip or
somewhere. She recognizes that I have an inherent characteristic
that makes social good take precedence over individual good, and
I sometimes sacrifice the family for the society. I sacrifice
myself for the society, which she as a mother cannot understand.
She will sacrifice herself for the kids, me for the kids.
There's no doubt in my mind who would stand first. That's been
tough.

But I don't think I'd trade it. I would rather surround
myself with some nicer people sometimes, but it's been a
marvelous experience. Where else but at CDC could you do all
those things I have done? In twenty years, I did a dozen things
that most people wouldn't be able to do in a whole lifetime. So
I wouldn't trade it, even though it was hard.

Ill

I guess the last thing is, I hate death. I had to deal with
my parents' deaths, and patients' death, and I just hate death.
Maybe that's one of the reasons I went into preventive medicine.
And I hate having all my friends dying. God awful. I still have
Stan Hadden's [State Senator David Roberti's staff] card in my
Rolodex, Randy Shilts' card in my Rolodex, and I don't know if
they'll ever come out. I can't adjust to their absence. I guess
I plan to call them when I need them. . .

Hughes: What do you think the CDC thought of your effort in the epidemic?

Francis: Oh, I think they respected it. The CDC is a wonderful

organization underneath. They gave me awards, and Jim Curran
gave me a box of donuts. [laughter] No, I think there's a lot
of mutual respect between both CDC and myself. Maybe some of us
have different styles, but I think all of us had the same
endpoint in mind, and all of us were very disturbed that CDC was
so badly damaged. CDC is incredibly important- -it ' s an
international jewel. You destroy that organization, and the
health of the world suffers. There ain't many places in the
world like CDC.

The Epidemic's Impact on Medicine

Hughes: Would you comment on the ways in which the epidemic has impacted
medicine?

Francis: Oh, it's had huge impact, all the way from the old issue of

individual doctors treating patients with infectious diseases to
the rapid application of the most modern laboratory techniques to
day-to-day patient care.

Hughes: What do you mean by the old issue of infectious diseases?

Francis: Infectious disease were thought of as being things of the past.
This epidemic has certainly brought infectious disease back to
the front page. Interestingly, most of us who go into infectious
disease do so because patients come in very sick and go home very
healthy very quickly, or they die. It's a specialty that does
not center around chronic conditions very often. AIDS changed
that. Also the poor dermatologist who went into that field to
take care of healthy people with pimples got a rude awakening
with AIDS, just like the infectious disease folks. That's why a
lot of AIDS care is managed by oncology services instead of
infectious disease services.

112

Hughes :
Francis:

AIDS has politicized all of medicine. What the AIDS
activists did with AIDS women now want to do the same with breast
cancer. You'll see more politicization of health now. It
certainly drove a lot of things to the front—the health care
financing issue. We can't do public health unless somebody takes
care of health care financing. So it has helped pushed that to
the fore. I could go on and on and on.

We must realize that with all of its problems, the epidemic
has been important to medicine, and it's brought a lot of new
faces into public health. I wouldn't have thought of myself
working with the CMA in years past, but they are a great
organization in many ways, and really have the right approach to
medicine. It's brought practicing physicians together with
public health like never happened before.

Why were you reluctant to work with the CMA in the past?

In the sixties and seventies, I thought the AMA [American Medical
Association], because of its social stands, was one of the worst
institutions in the world. As a result, I have never joined the

AMA.

AIDS and Cofactors ##

Hughes: Do you want to comment on the suggestion that HIV needs a
cofactor or cofactors?

Francis: Of course it needs a cofactor; all infectious diseases have
cofactors.

Hughes: Well, in the Duesberg sense.

Francis: Duesberg speaks nonsense. Peter Duesberg has lost the ability to
honestly look at scientific data and adjust his understanding.
He ignores scientific facts. Warren Winkelstein and I sat down
at lunch with Peter Duesberg at the Women's Faculty Club at
Berkeley and almost got kicked out, because Warren and I became
so frustrated. That fellow could not understand that being HIV
infected was a bad thing. He wanted to infect himself with HIV
to show it was benign. He is a biochemical virologist who's
trying to understand epidemiology and infectious disease, and he
cannot make the leap and does not understand the complexity. He
has by and large lost his scientific integrity, the respect of
others, and probably some psychological sanity. He's ridiculous.

113

Cof actors are involved. But regardless of all the cof actors
such as age, genetic makeup, and whatever foreign proteins you've
got circulating around, if you take HIV away, AIDS goes away.
You put HIV in and it comes back. That's all I need to know. I
don't even know why some people get so sick with measles and some
people don't, or why some people get sick with chicken pox and
others don't. Of course there are cof actors, but God, you take
chicken pox virus away, and there won't be any chicken pox. The
bug is the essence.

Heterosexual AIDS

Hughes: The recent report on AIDS from the National Research Council
emphasized that the epidemic is not democratic; it strikes
socially and economically marginal communities with greater
force.1 What are the implications?

Francis: It's true. One of the silliest things about the AIDS epidemic is
that somebody could write a book about the heterosexual myth of
AIDS, and have it published, and people read it. The expectation
of this virus coming into every automobile going down the freeway
is just naive. If you understand the epidemiology—it ' s sexually
transmitted; it's blood-borne; the more sexual contacts you have
in a community, together with some cof actors, including genital
ulcers that increase the risk, then you'll have more disease [in
that community] than you would elsewhere.

We know that there are groups in society that have more risk
behaviors than others. That's where the virus is going to
concentrate. Simple as can be. So if your expectations are it's
going to spread rapidly into every corner of society, then you
will be disappointed. The expectation was false; it is going to
dribble out, but not explode. There's no way that you can keep
HIV limited to any community. Why does the daughter of a General
Motors executive get infected with HIV? It's because her contact
was part of a river let which joined one community to another. He
got infected and gave it to her. So there are going to be these
riverlets of infections in every community. That's what happens
with infectious diseases.

In the past in public health, or even today, if we have one
importation of a virus that has a mortality rate of even 10 or 20

1 The Social Impact of AIDS in the United States. Washington, D.C.:
National Academy Press, 1993.

114

Hughes:
Francis;
Hughes :

percent per infection, we blow all the whistles in public health
and make sure it doesn't go anywhere. This one [AIDS] has a 90-
plus percent mortality, and we're saying, "Well, there aren't too
many heterosexual cases. Only 5,000 women a year come down with
AIDS." Wow! I call it the body-bag phenomenon. We just get
accustomed to this incredible misery and say, "Well, that's not
too bad. Only 1 percent of African Americans in Oakland are
infected with this virus. That's a lot better than 50 percent of
the gay community." That's a stupid way to look at it. If 1
percent of the African American heterosexuals in Oakland are
infected, you better do something.

I tell you, from having teenage kids and talking with
mothers of other teenagers, if there were a vaccine for HIV,
every mother would get it for their kid. They may say, "It's not
my problem." But they also say, "I don't want it to be my
problem, either." Under the surface, there's a much more logical
response to this than meets the eye. At least here. Because
everyone around this part of California knows somebody who's died
of AIDS.

Yes. But we're not living in-
Average Nebraska.

You've talked for something like six hours. Is there any record
that you want to set straight, or anything you want to add?

Future Issues

Francis: I think the most important thing is to look ahead to the future.
The first issue for me right now is vaccines,1 and frankly, our
free-market society is not designed to develop vaccines. In many
ways, we don't value prevention. Thus vaccines are bad business.
So a small group of us limps along trying to make a vaccine, even
for North America and Europe where there's a large potential for
profit. It's still not as potentially profitable as a Tagamet or
Tylenol, and thus it is seen as a relatively poor business
opportunity.

1 Dr. Francis retired from the Public Health Service in February 1992,
and began to work at Genentech to develop a vaccine for HIV. He currently
heads Genevax, a company spun off from Genentech in 1996, which is focused
on HIV vaccine research, development and testing.

115

We've got to change that model, even for this part of the
world. For the developing world, there will never be a vaccine
if we don't do something about it. Why would Genentech make a
vaccine for Africa? Just out of the goodness of their heart?
They could take this whole company, sell it, and buy vaccine for
Africa and still not have enough, and have a company that's
totally bankrupt. So something has to be done to change that
model. In many ways, it's similar to what we have been talking
about for six hours. There are some issues that don't fit well
into our current system yet are socially very important to
deliver—rapid transit, public health, et cetera—a nonprofit or
government institution has got to take responsibility for these.

I would like to get across that individuals make the
dif ference— whom you elect, who is your health officer. Those
who account for a difference in a specific area are often five or
ten people for the whole country. We have to have a garden where
those people can really grow and not be stultified. That is
going to require some chaos and environments where a few people
can gallop ahead and make progress. By and large, our systems
don't do that. They tend to support those who seek the status
quo. The status quo for many of these issues, like AIDS, must be
declared unacceptable.

I hear some very good cooks in this area that I have great
respect for saying, "I will not have recombinant tomatoes in my
restaurant." Well, our agriculture, and our dogs, and our cows,
have all been selected by genetic selection. This may not be by
genetic engineering, but by just selecting and breeding. Luther
Burbank did a lot of early research on breeding of flowers.

We've got to be able to accept, and indeed desire, change
for the good. Some of the technology can be dangerous, but a lot
of it is not. We've got to be able to look at scientific data
and translate it into good. That requires an incredible
educational level so that people can read newspapers and
understand the issue. And I don't think we've got enough of that
capability at this point, including for AIDS. We only get
interested when it blows up in our faces. When a mortar hits the
market in Sarajevo, we get concerned. But next week when there's
no mortar, we won't be interested, and those poor people are in
there in the midst of some primitive, tribal fighting, and we do
little to bring civilization back to them. Africa is being eaten
up by tribal warfare, and we're just going to watch and let it
die.

Another lesson: AIDS came from deep, dark Africa, way back
in the jungle somewhere. It got to the United States like that—
[snaps fingers] --once the ecology was set. And the next bug is

116

sitting out there now, somewhere in the world. The world is much
smaller than it ever was before. I've been in the most distant
parts of the world with some of the most dangerous viruses, and I
know that someone who was in contact with one of these bugs the
day before he left is in London right now. And that's the way it
is. There's no part of the world that we can ignore.

It has to be a world family, and we have to deal with these
sorts of things. But we don't seem to want to, especially
Americans. We're so insulated, because we live in such a lovely
place, wealthy, isolated from the rest of the world. Immigration
will eat us up if we don't. You can't stop the world's poor from
coming in here, because the economies elsewhere are so weak.
Let's make the economies there better so that we don't have that
kind of a stress.

So the smallness of the world has to be stressed. We are
all in the same village, and we'd better take care of each other.
That's all.

Hughes: Thank you.

Transcribed and Final Typed by Shannon Page

Regional Oral History Office
The Bancroft Library

University of California
Berkeley, California

The San Francisco AIDS Oral History Series

THE AIDS EPIDEMIC IN SAN FRANCISCO: THE MEDICAL RESPONSE, 1981-1984

Volume IV

Merle A. Sande, M.D.

INFECTIOUS DISEASE SPECIALIST: AIDS TREATMENT AND INFECTION
CONTROL AT SAN FRANCISCO GENERAL HOSPITAL

Interviews Conducted by

Sally Smith Hughes

in 1993 and 1994

Merle A. Sande, 1996.

Interview History—by Sally Smith Hughes, Ph.D.

Dr. Sande was invited to participate in the AIDS oral history series
primarily because of his role as the senior administrator at San Francisco
General Hospital [SFGH] most directly involved in the institution's
response to the AIDS epidemic. In September 1980, he arrived at SFGH as
the new Chief of Medical Services, a position to which he brought career-
long experience in infectious disease. His job as chief of medicine was,
as he succinctly put it, "to bring this place [SFGH] into national
prominence." [p. 198] The following spring, the first cases of what later
became known as AIDS were described in San Francisco and elsewhere. Such
cases were at first of only passing interest to Sande who as a key player
in a complex institution administered by both the city health department
and the University of California had multiple demands on his time. There
was no way he could have then suspected that the epidemic was going to be a
vehicle for bringing prestige to the institution and to many of those,
including Sande, involved with it.

One of Sande 's first recruits was Paul Volberding, who in the summer
of 1981 became head of the new oncology unit at SFGH and co-director, with
Marcus Conant, of the Kaposi's Sarcoma Clinic at UCSF. These units saw
many of the earliest AIDS patients in San Francisco. As an infectious
disease specialist, Sande was aware of some of these troubling cases and in
fact describes in the oral history a case of toxoplasmosis which he
tentatively dates to the spring of 1981.

By 1983, the situation had changed. The trickle of AIDS patients had
become an avalanche. As chief of medicine, Sande was not only involved in
formulating policy to handle an unforeseen number of patients with strange
and usually fatal conditions but also to stem the fear of a hospital staff
dealing with an infectious and fatal disease of unknown etiology. The
formation in 1983 of a clinic and inpatient ward dedicated to AIDS was one
of the hospital's major responses to the epidemic. Another, which Sande
describes at some length in the oral history, is the formation of infection
control guidelines erected for the primary purpose of protecting hospital
staff. In March 1983 Sande was appointed head of a committee, the UCSF
Task Force on AIDS, which, despite its comprehensive name, was focused on
devising guidelines for the safety of staff dealing with AIDS patients.
Its heated deliberations resulted in publication in the fall of 1983 of an
article on infection control in the prestigious New England Journal of
Medicine.

Perhaps because of this publication, and the fact that the task force
was composed largely of physicians, it somewhat eclipsed the work of the
hospital's long-standing infection control committee which had been
attempting, before Sande' s task force was formed, to address disease-
transmission problems presented by the epidemic.1

'For an account of the history of early infection control guidelines at
SFGH, see the oral history in the AIDS nurses series with Grace Lusby.

Sande was also chairman of the UC Systemwide Task Force on AIDS, a
committee formed in 1983 to distribute California state funds for AIDS
research and which continues today as the Universitywide AIDS Research
Program. In 1984, Mayor Dianne Feinstein appointed him chairman of her
Mayor's Advisory Committee On AIDS. Sande 's three committee chairmanships
served to give him visibility and influence in university, city, and state
AIDS politics. Such standing was doubtless helpful in the skirmishes
involved in establishing the Gladstone Institute of Virology and Immunology
at SFGH. This achievement not only abetted the institution's AIDS research
efforts but also complemented Sande 's intent to reenforce it as a site of
basic as well as clinical research, and as a rival of its sister
institution on Parnassus Avenue.

But Sande is not all politics and prestige. The oral history reveals
him as a man who has learned a lot, professionally and personally, from his
involvement in the epidemic. His views about medical education and a
physician's responsibility to his patients have changed as a result.

...I think we [physicians] have become much more sensitive to
quality-of-life issues, of dealing with the human part of the
patient. I think [AIDS] has brought the art of medicine back
into our medical education process. The idea of orchestrating
a good death, which would have been an oxymoron in my days of
training, has now become a real endpoint (p. 193).

The Oral History Process

Three interviews were conducted with Dr. Sande between September 1993
and January 1994 in his office at SFGH. Although pressed by the heavy
demands of his position, he was nonetheless willing to take time to reflect
on the early years of the epidemic. After a period of reminiscence off
tape, he entered the discussion with a seemingly new-found sense of
immediacy for the period we were about to address. When he asked how frank
he should be, I urged him to be so and assured him that he would be asked
to review and correct the transcripts. He replied that he wasn't worried,
and as the first interview progressed appeared to relax and warm to his
memories, positioning his feet on the edge of his desk and answering
reflectively and sometimes eloquently. One suspects that he is an
inspiring teacher and leader. Before the final interview, we took time off
tape to reconstruct the chronology of Dianne Feinstein 's Mayor's Advisory
Committee on AIDS, which first met under that title on October 22, 1984.
We decided that it was a formalization of an earlier informal set of
mayoral advisors, which included Marcus Conant and Paul Volberding.

Sande reviewed the edited transcripts, making no substantive changes.
In June 1996, Dr. Sande left SFGH, doubtless proud that once again an
annual survey of U.S. hospitals had judged it to provide the best AIDS
medicine in the country. He is currently chairman of the Department of
Medicine at the University of Utah.

Regional Oral History Office
April 1997

Sally Smith Hughes, Ph.D.
Research Historian

Regional Oral History Office University of California

Room 486 The Bancroft Library Berkeley, California 94720

BIOGRAPHICAL INFORMATION

(Please write clearly. Use black ink.)

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Occupation Birthplace

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Mother's full name

Occupation Birthplace_

Your spouse

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Where did you grow up? L/.vC'Th r pr^ TL'.

Present community

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117

I FAMILY BACKGROUND, EDUCATION, AND EARLY CAREER
[Interview 1: September 21, 1993] II
Early Education

Hughes: Dr. Sande, let's start with where you were born and educated.

Sande: I was born in a little town north of Seattle called Mount Vernon.
It's a small farming town. My parents [Sigvald and Clara Sande]
were first-generation Norwegian immigrants. My father worked on
the Stern wheeler boats up and down the rivers in the Northwest,
and then became involved in the Washington state ferry system.
For about thirty- five years, he was skipper on the ferries that
ran from the state of Washington to Victoria, where I worked for a
number of years with him.

I went to Mount Vernon High School [1953-1957]. From high
school I went to Washington State University [1957-1961], where I
was interested in physical metallurgy and engineering. I got
talked into taking some zoology courses, and got interested in
medicine. Then at sort of the last hour I decided to go to
medical school. I was concerned about that, because I could never
stand the sight of blood.

Medical School, Internship, and Residency

Sande: I went to the University of Washington School of Medicine [1961-

1965], and always had interest in going back and practicing family
practice in my own little home town. I was told by Bob
Peter sdorf, who was chairman of medicine then, that that wasn't
what I should do, that I should become an internist. So he sent

118

me then to New York Hospital at Cornell for my [internship and
residency] training [in internal medicine] [1965-1969].

Hughes: Why Cornell?

Sande: He had a way of selecting the top five people in the class and
orchestrating their careers. So he said, "Sande, you go to New
York Hospital," and I said, "Yes, sir."

So I took my wife [Mary Ann] and my two young children, and
we went off to Manhattan, which was quite an experience for us--
small-town boy in the big city. But it wasn't bad, because we
were on [duty] every other night for four years, and we never got
to see anything anyway.

Interest in Infectious Diseases

Sande: I finished my internal medicine training in 1969. I had an
interest in infectious diseases, although I never took a
fellowship. Even though I'm currently the president of the
Infectious Disease Society of America, I'm sort of a fraud.

Hughes: Why infectious diseases?

Sande: It was the most exciting thing that we did in medicine. They were
the most interesting diseases. They were the ones that you could
do something about; you could make a definitive diagnosis. I
think those of us who had sort of a surgical mentality but found
themselves in medicine wanted an end result to something, and I
think a lot of us were attracted to infectious disease.

But also it was the mentoring. Mentors have tremendous
influence on the way you make decisions about your career choices.
My mentors there, fellows by the name of Don Kaye and Ed [Edward]
Hook, were both very stimulating. And Petersdorf, chairman of
[medicine? at] the University of Washington, from my medical
school days, was also [in] infectious diseases and maintained an
interest, a tie with us. So I became interested in that area; did
a little investigative work while I was still a resident.

Then, during the height of the Vietnam War, I got assigned,
happily, to Lackland Air Force Base [San Antonio, Texas], where my
first year I ran the general medical clinic, and then the second
year I became an infectious disease attending at Wilford Hall
Hospital and did part-time work at University of Texas Health
Science Center, San Antonio. That was where I really got into the

119

more academic aspects of infectious diseases. I still had
interests in 1970 of going back to the state of Washington to
practice medicine.

Faculty Member. Division of Infectious Diseases, University of
Virginia School of Medicine. 1971-1979

Sande: By that time, my mentor at Cornell, Ed Hook, had become chairman

at University of Virginia. He enticed me to come back East, and I
went to Charlottesville [1971-1980], where I started actually in
family practice and medicine, again working in the general medical
clinic, but also having my academic research interests in
infectious diseases. So my career in academic ID [infectious
disease] really started in 1970. I went up the academic scale to
professor, and then to acting chairman of medicine in 1979.

Hughes: At Charlottesville?

Sande: In Charlottesville, at the University of Virginia.

My research interests were developing animal models of
infection so we could study various organisms (bacteria and fungi)
in models of endocarditis and meningitis. That's probably what I
was most known for before I came here.

Hughes: The use of animal models was a standard way of studying infectious
disease?

Sande: Yes. My philosophical approach to infectious diseases was to try
to find out how things that happened in the test tube with
bacteria and antibiotics correlated with what actually happened in
the animal models. There is often times a big difference between
things you see in broth and things that actually happen in vivo.
So we essentially developed animal models, usually using rabbits,
where you could create situations and study the in vivo effects,
which then are very directly related to patients. So I tried to
bridge the gap between the test tube and the patient by the
development of the animal model.

We were extremely successful over the years, in terms of
making significant observations- -why certain diseases develop,
particularly bacterial endocarditis, what the factors were that
influenced the development of those diseases. And then in the
field of meningitis, we designed the model which is used all over
the world now. I did this with a fellow by the name of Ralph
Dacey, who was a medical student with me and now he's chairman of

120

neurosurgery at Washington University at St. Louis, a very
creative young fellow.

When I was there [at the University of Virginia], 1 had a lot
of fellows who are still close to me, and who have now distributed
themselves around the country and around the world. But I think
my major interest was always in teaching and using infectious
diseases as a prototype for general internal medicine as a whole.

Professor of Medicine, San Francisco General Hospital, University
of California, San Francisco, 1980-19961

Recruitment

Sande: I actually looked at a job in San Francisco in the mid-seventies
as chief of infectious disease here at San Francisco General
Hospital [SFGH], and decided to stay in Virginia. I looked at a
couple of other jobs, but then when this job, as chief of the
medical service at San Francisco General, came up, it was perfect.
It fit my interests. It's a sort of hospital that I enjoy working
at, and the quality of the people on the housestaff was such that
it was a really nice fit.

So I came here in September of 1980, having had a year of
really good experience running a big department of medicine in
Virginia when Ed Hook went on sabbatical. So I was, I think,
pretty well prepared for this change.

It was a very traumatic year, because I was here five days
when the housestaff went on strike. It had been brewing. It was
a time of a lot of chaos and instability, at UC and at San
Francisco General. But it passed.

The Setting at San Francisco General

Hughes: Well, talk about the staff that was in place when you arrived, and
what the facilities were.

1 In 1996, Dr. Sande moved to Salt Lake City to become chairman of the
Department of Medicine at University of Utah.

121

Sande: At that time we were not very strong in infectious diseases, and
that was one of the reasons I think I was recruited here. But we
had a lot of space. It was these old buildings that had been used
as hospitals before. The new hospital had opened, I think, in
1978, so the old hospital building that was here had been torn
down. But the other hospital buildings around the area were
preserved almost as historical monuments. So that offered a
chance to build research labs and research institutes.

Hughes: Which was one of the things that had appealed to you?

Sande: Yes. The thing that has made us what we are today, which is the
number one public hospital in the country bar none, in terms of
any way you look at it—research grants, faculty, whatever—was
the availability of the initial space, and tremendous vision by
two people: Holly Smith [Lloyd H., Chairman, UCSF Department of
Medicine], and Julius Krevans [Dean, UCSF School of Medicine].
And there were a lot of others who had a part, but those two
really had the vision of turning San Francisco General into a
highly visible, recognized, credible extension of UCSF. It's not
an ancillary hospital; it is as important to UCSF as the Parnassus
campus is, in terms of research grants, in terms of teaching, and
everything else. It's one of the songs that I sing over and over
again.

Hughes: Had there been much of a research emphasis prior to your arrival?

Sande: Well, there had been a stable group of investigators who had used
the County [SFGH] as a base of operations. Some of them, like Y.
[Yuet] W. Kan, had left here and gone over to UC. He's now a
[Howard] Hughes [Medical Institute] investigator as one of the
giants in the field of molecular biology, probably one of the
fathers of molecular biology. Most of the investigation taking
place here was clinical investigation. There was some basic
science, but there wasn't a lot.

Now, I was recruited just a year after the Gladstone
Institute for Cardiovascular Disease opened [1979], and that was
the first major step of enticing private money into San Francisco
General. Bob Mahley was the head, and still is. He's just been
very successful. Then, a whole series of recruitments followed.
There was the Rice Liver Laboratory that Monty [D. Montgomery]
Bissell ran in the department of medicine, and that's been very
successful. About the same time I was recruited, Ira Goldstein
was recruited from NYU [New York University] to run the Rosalind
Russell Arthritis Institute.

Within a couple of years, the [Ernest] Gallo family gave
money to start the Gallo [Clinic and Research] Center, and Ivan

122

Diamond was recruited to run that. Then a year or so later, with
the help of Jay Nadel and others, the Lung Biology Center opened.
Joe LaDue was particularly influential in raising money, and
that's been extremely successful. So there's a whole series of
these things that happened that allowed us, a poor city hospital,
to develop an incredible basic and clinical science environment.

What I was offered when I came here was really nothing except
a vision, and Holly Smith, who recruited me, said, "Look at all
that space. Now you go out and fill it."

Hughes: He meant with research activities?

Sande: Yes. We had the clinical activities. This has always been a very
strong clinical training program.

Hughes: Is that somewhat related to the city's diverse population?

Sande: Yes, the clinical training program is good because of the patient
population, because it's one-third of the UCSF program, which has
a very good program in internal medicine, and because there is a
cadre of very committed and dedicated clinicians who work here. I
think they make a happy environment, a pleasant place to work,
although our patients are not always pleasant patients to deal
with—the intravenous drug users, the alcoholics. The overriding
spirit of clinical care is just outstanding, and it always has
been.

Hughes: I understand that the atmosphere, the spirit, here is really quite
different from that on Parnassus.

Sande: Yes, I think so. I take great pride in that, because I think

that's one thing that has made this place a really productive and
fun place to work. I think there is a sense of family—a sense of
family maybe because everybody here considers we're working in the
battlefield, and we're closer because of the environment and the
patient population that we serve. But I think there's also been a
sense of family in terms of sharing our accomplishments and
feeling a part of a vibrant, growing community. Success breeds
success, and success is attractive and it tends to draw people
into a shared sense of responsibility. I think that's happened.
It's been a remarkable fourteen years.

Hughes: Do you think that would have occurred regardless of the epidemic?

Sande: I think so. AIDS has only been a part of the story. The epidemic
created a new arm of the hospital that was initially primarily
focused on clinical investigation, and then more recently has been
focused with the new Gladstone Virology Institute on basic science

123

investigations. But overall, the contribution that we made in
AIDS was mostly clinical more than it was basic, while most of
these other institutes [at SFGH] were doing basic research in
other areas, not related to AIDS.

Increasingly, we try to tie them together, because if you
study AIDS and you understand AIDS, you really understand an awful
lot about human biology and human disease. As that's become more
recognized, the barriers between disease states have broken down,
and it gets down to fundamental biology. AIDS is an incredible
opening of basic knowledge. Using the virus as a probe has
increased our understanding of how the immune system works and how
cells are turned on and turned off. It's an explosion of
understanding .

124

II THE AIDS EPIDEMIC

Preparation for the Epidemic

Hughes: Do you have anything to say about retrovirology?
Sande: I didn't know what a retrovirus was.
Hughes: [laughs] A lot of people didn't.

Sande: Remember, my background is in infectious diseases, but it was in

bacterial and fungal infections and not in virology. I think that
we've all become pseudo-retrovirologists; at least we now know the
language.

One of the neat things about this environment is that you
can't help but learn what's going on, because there's so much
going on around us that, if you attend the seminars or listen to
people or interview people for jobs, you learn what's going on.
Retrovirology is one of the more common topics that we discuss.
And it really has been quite remarkable how studying AIDS has
helped our understanding of molecular biology, genetics, cell
biology, cancer, immunology, and other infectious diseases.

Hughes: Is there anything we should talk about before my next question,
which is how did you encounter the AIDS epidemic?

Sande: Well, I think that it's been written and said a lot that it was a
perfect marriage for me personally, having had a background in
infectious diseases, and to have gained a certain level of
prominence or credibility in the field, to be at the same time
chief of medicine at the hospital in which it really all first
happened. It was lucky for me. I think it was fortunate that I
had a way of thinking about diseases that had an infectious
orientation, that it was a good marriage to be here when the
epidemic happened.

125
First AIDS Patient

Hughes: Tell me how you first became aware of what later was going to be
known as AIDS?

Sande: I've thought about this a lot. The first patient I saw--my dates
are always sort of suspect these days — in the spring of '81, was a
patient on the fourth floor with three brain lesions—a young gay
male. We had biopsied him three times, and we couldn't figure out
what it was. Finally, somebody thought they saw toxoplasmosis.
We sent the specimen down to Jack Remington at Stanford, and he
confirmed that it was toxoplasmosis.

Hughes: He being an expert?

Sande: Jack Remington is an expert in toxoplasmosis. He was also a good
friend. That [case] was really bizarre; it didn't make any sense,
but we see a lot of bizarre things.

Hughes: So you didn't think too much of it?
Sande: I didn't think too much of it.

Then Paul Volberding, whom I had recruited in the middle of
'81— he's one of my first recruits, actually—to come over from
the Parnassus campus and run our oncology service here at San
Francisco General, told us about some of the KS patients that he
was seeing with Marcus Conant in the Kaposi's clinic at UC.1

Then, I remember a rumor came from the CDC that they had seen
a cluster of gay male patients with an unusual pneumonia in Los
Angeles. The report by Mike Gottlieb at UCLA came out in the MMWR
[Morbidity and Mortality Weekly Report] that summer of a cluster
of five patients with this weird pneumonia called Pneumocystis .
At about the same time, we started seeing patients here with
Pneumocystis pneumonia and we were off and running.

Hughes: Did you make connections between patients at SFGH and those
elsewhere?

Sande: Not until the Gottlieb report. It really didn't register. We

were seeing the Pneumocystis pneumonia cases, but they didn't make
any sense. They were all in gay men. The toxoplasmosis patient
was gay. The patients with Kaposi's sarcoma were gay. But it was

1 See the oral histories in this series with Drs. Volberding and
Conant .

126

the click from the Gottlieb observations that, "Gee, there's
something really bizarre going on here."

Hughes: What was clicking? The fact that all this was happening in gays?

Sande: Yes. See, that didn't make any sense. Then you said, "Why would
a gay male be different? Why would they be developing these
diseases?" Particularly Pneumocystis that had only really been
seen in very young undernourished children, or patients undergoing
cancer chemotherapy, or who were on high doses of corticosteroids,
who had immunosuppression.

So then the thoughts were, Well, there is certainly no
evidence that gay men were genetically different. There were some
theories that perhaps through their sexual activity they were
getting large doses of different antigens, and somehow these
antigens were turning on one part of the immune system, and maybe
suppressing another part of the immune system. There was some
suggestion that maybe the parasites that they were acquiring were
immunosuppressant . There was some data to suggest that the sperm
itself might be immunosuppressant, so perhaps gay men who were
experiencing very promiscuous behavior might be developing an
immunosuppression that set them up for opportunistic infections
and malignancies. But nothing really made any sense.

Infection Control

Initial Concerns

Sande: One of the personal observations that I had, that I will never
forget: It became obvious that this disease or condition was
infectious. It was clearly obvious to me that we, in this
hospital, were the most exposed, because by that time we had had
more [AIDS] patients than anybody in the country, as far as we
knew. My training in infectious diseases was actually probably a
hindrance, because I really got worried. I said, "My god, I'm
responsible for this group. I'm the responsible person for this
housestaff and these nurses, for the faculty, and I am an
'infectious disease expert.1 So what should my responsibility
be?"

I remember very clearly 1952, when three of my best friends
got polio in the summer. Do you remember this? It was a
tremendously scary situation--

127

Hughes: Yes, the swimming pools were closed.

Sande: We couldn't go swimming. My mother would ask me every morning if
I had a stiff neck. And it was that fear of the unknown. I had
exactly the same feeling with AIDS. Suddenly one night, it just
hit me. It really was scary, and very uncomfortable.

Hughes: What convinced you that the other theories were probably wrong,
and that it was an infectious agent of some kind?

Sande: I don't remember what the precipitating event was. In '82, IV
drug use was recognized as a vehicle. Then Diane Wara with Jay
Levy and Art Ammann described transfusion AIDS, and then AIDS in
children.1 Transfusion AIDS didn't really fit some of the earlier
noninfectious theories for immune deficiency. [tape interruption]

So then we started thinking about what could it be that would
cause this immunodeficiency in that group of patients. The only
thing that made any sense was that it was infectious. If it was
infectious, then how was it transmitted? If it was not culturable
and it was small, it's a virus, and how are viruses transmitted?
When you think of viruses, you think of influenza and you think of
chicken pox and you think of measles, and you think of things that
are rapidly transmitted through aerosol and through coughing and
through touching and through secretions.

This is where I was in an incredibly unique, singularly
unique, position. I was the one responsible. I had more [AIDS]
patients than anybody in the world. I had a faculty, nurses,
students, housestaff, that were incredibly exposed. And that
scared the hell out of me. It really scared me.

UCSF Task Force on AIDS

Hughes: Another factor, I should think, was that your staff was afraid, as
I learned from interviewing them.2

' A. J. Ammann, M. J. Cowan, D. W. Wara, et al. Acquired
immunodeficiency in an infant: Possible transmission by means of blood
products. Lancet 1983, 1:956-958.

2 For example, see the oral histories in this series with Donald
Abrams, Andrew Moss, and Paul Volberding.

128

Sande: Yes. And so that's what precipitated the first dean's committee
[UCSF Task Force] on AIDS, which was started in '83.

Hughes: Yes, March, '83.1

Sande: I chaired that committee [ 1983-present] , and that was a very
interesting group of people.2

Hughes: It was called the UCSF Task Force on AIDS, but wasn't it

initially conceived pretty narrowly as an infection control

committee?

Sande: Yes. Initially, [Julius] Krevans actually called me and said,

"What do you think about this epidemic?" I said, "Well, I'm sort
of worried about it." So he appointed me to put together a group
to think about it, and to try to get a real heterogenous group of
people. It was a wonderful group--Merv Silverman, the health
director, came to all the meetings. Initially I guess Geoff Lang
and then Phil Sowa, our hospital administrator, came. The head of
nursing [Mary Anne McGuire] came. We had Fran Streiker who was
from the West Bay Hospital Association, because they were starting
to see AIDS cases, and the West Bay Hospital Association was
worried about what we were going to do. We were obviously in the
driver's seat and needed to do something.

Hughes: These people were actually made committee members?

Sande: We made them committee members. Marcus Conant was part of the
group. And Paul [Volberding] was vice chairman. Then the
infection control people, John Conte.

1 H. Baine Fairley, Associate Dean, to Merle Sande, February 7, 1983.
(AIDS History Project Archives, Special Collections, UCSF Library, Ward 86
papers, carton 1, f: to PV [Paul Volberding], 1983.)

2 Acting School of Medicine Dean Robert Crede appointed the UCSF Task
Force on AIDS in March 1983, a campuswide committee charged with developing
AIDS-related infection control guidelines. In July 1988, the task force
was disbanded when Chancellor Julius Krevans established the UCSF AIDS
Coordinating Council, an advisory group of faculty and staff at UCSF and
its affiliated programs at SFGH, Mount Zion Medical Center, and the
Veterans Administration Medical Center. Many individuals who had served on
the UCSF Task Force on AIDS became members of the Coordinating Council.
(Dianne Leiker, UCSF AIDS Coordinating Council: Historical Report [n.d.,
probably 1988], binder: AIDS Coordinating Council: Historical Report, AIDS
Coordinating Council Office, UCSF Faculty Club.)

129

Sande: Keith Hadley, from infection control here. There's a really long
list of people.1 And Connie [Wofsy] and Don Abrams became part of
it.2

Now, one of the complicating features was [SFGH surgeon]
Lorraine Day. I brought her on the committee, because she was
starting to agitate about the fears and the problems with HIV.
She took my comments and made slides out of them, "So-called AIDS
expert says, "Health care workers not at risk,"1 which is not what
I said, but that's what she put in her slides.

Hughes: Can you remember when you appointed her to the committee?
Sande: No.

What was very interesting is that we really knew we had to
make some guidelines, and in a way, I guess, we were lucky,
because we didn't know that the incubation period of this virus
was ten years--incubation period meaning disease from period after
infection. Had we known that, we would have been more concerned.
In '83, two years into the epidemic, there really hadn't been any
health care workers that had developed AIDS from taking are of
patients—even people who had been working extensively with people
with AIDS.

Reports of Low Infectivity

Sande: One thing that really helped us in the decision was a couple of
the family studies came out. They suggested that if there was a
child in the family environment with AIDS, that the other siblings
or the parents didn't get it. So we said, "It really must not be
very infectious or contagious from casual contact."

See the oral histories in this series with Drs. Wofsy and Abrams.

2 For members of the task force as of fall 1983, see J. E. Conte, Jr.,
W. K. Hadley, M. Sande, et al., "Infection control guidelines for patients
with the acquired immunodeficiency syndrome (AIDS)." New England Journal
of Medicine. 1983, 309:740-744.

130

Hughes: Yet there were some scares. Remember the [James] Oleske household
contact scare and an accompanying editorial in JAMA [Journal of
the American Medical Association] that fanned the fear?1

Sande: Yes, it did, it was open. And I wrote the editorial2 for the New
England Journal of Medicine article that Rogers and Friedland
published. They had published on a group of people from
Montefiore [Hospital in New York] who had household contact with
people with AIDS, yet they didn't have any evidence of
transmission in family units. So I wrote the editorial, saying,
"It looks to me like AIDS transmission is not going to be a big
problem in hospitals."

There was a fear, because we didn't know for sure. And you
know, you're not sure, in retrospect, if you made the decision
based upon just the facts you had or if there wasn't some impact
of wishful thinking in the final decisions. Pragmatically—and
this is what Lorraine has been most critical of me for--we had
this large group of patients to take care of. Who's going to take
care of them? So given the pressure of caring for the patient
population, and then looking at the lack of cases in people that
did care for them, and the lack of transmission in that family
setting, we just said, "Look. People have to be rational, and we
have a major responsibility as health care workers and
particularly as physicians to give this care. We might be missing
something, and there might be a risk here, but right now, we can't
see it."

Then there was that nurse in England that got infected with a
needlestick. Then we started focusing much more on needles.

Julie Gerberding and the AIDS Health Care Workers Study,
1983-present

Sande: By the way, that was Julie Gerberding who just looked in here, and
Julie was the person who was working with me as a resident at the

1 J. Oleske, A. Minnefore, et al. Immune deficiency in children.
Journal of the American Medical Association 1983, 249:2345-2349; A. S.
Fauci. The acquired immune deficiency syndrome (editorial). Journal of
the American Medical Association 1983, 259:2375-2376.

2 M. A. Sande. Transmission of AIDS: The case against casual
contagion. New England Journal of Medicine 1986, 314:380-382.

131

time who took on AIDS infection control, and now is the world's
authority in that area.

Hughes: Her study began in 1983, didn't it?

Sande: Yes. We started collecting blood specimens.

Hughes: How was that study set up and conducted?

Sande: Well, what academicians should do when faced with an unanswered
question, a clinical dilemma, a clinical problem, is they should
start accumulating information. We should start saving specimens
and documenting exposures. Julie was going to be chief resident
the next year, taking a year off after she finished her residency,
and she was actually working at Kaiser. So she submitted a grant
application to the statewide AIDS task force [Universitywide Task
Force on AIDS] that I at that time [1983-1988] was chairman of,
and they funded her to set up a health care workers' study.

So she started accumulating clinical data and blood specimens
from health care workers and their patients from whom they got a
needlestick. She then collected serial samples. Over the years
she has documented over 1,000 such accidents and has documented
transmission in one episode and perhaps one other.

Hughes: The specimens were blood?

Sande: Yes. With that information and with the clinical history and the
characteristics of the needlestick, she was able with a great deal
of credibility to say, "Well, HIV infection from a needlestick
does happen, and this is the risk. The hospital is not a zero-
risk environment." Well, it's an enormous risk if it's you, or if
you work for the EPA [Environmental Protection Agency]. It's a
very small risk if it's somebody else, and you're looking at
transmissibility, or you're using hepatitis B as an example of
high infectivity. Hepatitis B is about a thousand times more
infectious than HIV.

Because Julie had started early and saved specimens, she was
able to make the statement about relative infectivity before
anybody else could.1

Hughes: Was anyone else doing this sort of research?

1 J. L. Gerberding, C. E. Bryant-LeBlanc, et al. Risk of transmitting
the human immunodeficiency virus, cytomegalovirus, and hepatitis B virus tot
health care workers exposed to patients with AIDS and AIDS-related
conditions (ARC). Journal of Infectious Disease 1987, 156:1-8.

132

Sande: The CDC was trying. They were trying to pick up cases from around
the country.

The UCSF AIDS Task Force Infection Control Guidelines, 1983

Sande: The infection control guidelines that we finally came up with in
this committee were incredibly good.1 But in some areas, we
agreed to disagree. The issues weren't just infection control.
The issues were care of patients with AIDS. We talked about the
right to refuse to care for patients with AIDS--under what
circumstances there should be a right — and we figured there were
essentially none.

Hughes: Is that based on the Hippocratic Oath?

Sande: Yes. We said that if you're a physician and you're in this

setting, and somebody comes in who's sick with HIV, then it's your
obligation to care for him. Actually, Molly Cooke, who was on
that committee, was very helpful in terms of the ethical dilemmas
that we faced.

Hughes: Had she some background in medical ethics?

Sande: Let's see, by that time, Molly was doing a Robert Wood Johnson

fellowship and had been interested in medical ethics. She had

been my chief resident in 1980 and was still involved with patient
care at SFGH.

Anyway, after we had come up with all these recommendations
and we synthesized scenarios and responses to scenarios, I called
my friends at the CDC. At the other end of the line were Jim
Curran and Harold Jaffe and Jim Hughes.

On the conference call, I read them our recommendations,
which were very bold and brave for that time. We agreed that we
didn't have all the information necessary to be sure that our

1 J. E. Conte, W. K. Hadley, M. Sande, and the UCSF Task Force on the
Acquired Immunodeficiency Syndrome. Infection-control guidelines for
patients with the acquired immunodeficiency syndrome (AIDS). New England
Journal of Medicine 1983, 309, no. 12:740-744. See also, Report from the
UCSF Task Force on AIDS, June 2, 1983. (Binder: AIDS Coordinating Council:
Historical Report, AIDS Coordinating Council Office, UCSF Faculty Club.)
For other perspectives on infection control at SFGH, see the oral histories
with Grace Lusby and Cliff Morrison, AIDS Nurses series.

133

statement was true, but this was the best we could come up with at
this time. It looked like casual contact was not going to
transmit whatever this thing was, that needlesticks may be a
problem—you had to be careful with them; you should use good
infection control guidelines, but that we didn't think that it
went beyond that, and you should take care of these patients, and
you didn't have the right to refuse.

Hughes: There was controversy about whether employees who were

immunocompromised should be allowed to take direct care of
patients.

Sande: Yes, that came later.1

What was interesting about that conference call [with the
CDC] was there was a dead silence when I was finished. They said,
"Well, Merle, why don't you publish it, and we'll react to it."
[laughter] Beautiful bureaucratic response. So we went ahead and
published our infection control guidelines, and they were very
important and accepted.

Then we revisited it--Julie really did--a couple of years
later, and we made some minor changes.2 Once the virus was
isolated they knew what was causing it. We had guessed right.

Hughes: Did the CDC endorse the 1983 guidelines?3

1 At a meeting of the UCSF AIDS Coordinating Council in November or
December, 1988, Julie Gerbering discussed the need for a UCSF campuswide
policy for, and a system for dealing with, health-care workers exposed to
HIV-contaminated secretions or other materials. [Minutes, AIDS
Coordinating Council, n.d. but between 11/18/88 and 12/20/88.] The
question of what to do about employees exposed to HIV through needlesticks
was an issue at least as early as 1983. (See, the undated, unattributed
document, Recent Questions Regarding the Care of AIDS Patients and Handling
of Specimens and Instruments, Marcus Conant ' s KS Notebook for 1983.) The
interviewer was referring to a discussion in 1983 by members of the UCSF
Task Force on AIDS on whether hospital workers with AIDS should be allowed
to provide direct patient care. [David Perlman. UC Hospitals' guidelines
on AIDS cases. San Francisco Chronicle, June 3, 1983.]

2 J. L. Gerberding, UCSF Task Foce on AIDS. Recommended infection-
control policies for patients with human immunodeficiency virus infection:
an update. New England Journal of Medicine 1986, 315:1562-1564.

3 The CDC had issued infection-control guidelines in November 1982.
(MMWR 1982, 31:577-579.) For a discussion of the CDC guidelines and those
of the SFGH infection control committee, see the oral history with Grace

ISA

Sande: Not officially, but more or less.

Hughes: Did other institutions adopt the guidelines?

Sande: Yes, I think everybody finally came along to the same conclusion.
But I think we clearly broke new territory with that.

Hughes: Did you have to get approval from the Department of Public Health,
or could you just go ahead and publish and establish these
guidelines?

Sande: We don't work for anybody. We have total academic freedom. The
dean told us, "Do the best job you can." He didn't know anything
about it. So no, we didn't have any approval from anybody, except
everybody signed off on it who was on our committee, which
included Merv Silverman, who at that time [1983] was head of the
Department of Public Health.

Hughes: Well, is there a point when other guidelines come in, from OSHA
[Occupational Safety and Health Administration] , for example?

Sande: Over time, I think that our recommendations were the ones that
carried the OSHA standards and everything else.

The Infected Health Care Worker

Sande: Now, you brought up another issue, which is a much more current
issue, really three or four years ago, and that was the infected
health care worker. That's been a very tricky one. The new
committee, which is the Chancellor's Task Force on AIDS, which I
continue to chair, made a very strong statement that we felt that
there was no justification for screening health care workers for
HIV, or if it became known that they were HIV positive, for
benching them from their clinical activities, that the data didn't
support that . '

Hughes: There wasn't enough evidence that indeed they were a significant
risk?

Lusby in the AIDS Nurses series.

1 UCSF Policy for Health Care Personnel Infected with Bloodborne
Pathogens, February 1991. (See binder: AIDS Coordinating Council
Correspondence, 12/3/90-11/18/92. Chancellor's AIDS Coordinating Council
Office, UCSF Faculty Club.)

135
Sande: Right.

Implications of the David Acer Case

Sande: This all became a problem after the Florida dentist case, Dr.

Acer's cases. We became very close to the CDC and to Dr. Jaffe
and the group, and they examined that epidemic and felt like there
was reasonably good evidence that the virus came from the dentist.
And of course, that conjured up visions of a dentist pricking
himself with a needle and bleeding through his gloves into the
mouth of the patient. And that never made much sense;
theoretically possible, but not for five different individuals.

Now the data has been questioned, but I think more than the
data being questioned, the mechanism by which that happened has
been questioned. We've heard that Dr. Acer had Kaposi's sarcoma
in his mouth, and he worked with his instruments on his mouth in
the morning before he saw the patients, and didn't clean the
instruments very well. That makes a lot more sense. Or the other
really viable option is that this man was disturbed and did it
deliberately. But we're probably never going to know for sure.

As a result of that one epidemic, there have been 20,000 or
so lookbacks, and there's not a single case of transmission from
an infected health care worker to a patient. And yet, it had such
incredible appeal to the politicians, particularly to the right
wing.

Our task force got together with the California Medical
Association and the West Bay Hospital Association, and we had a
press conference condemning attempts to test and restrict health
care workers from performing their duties.

CDC Recommendations

Hughes: Any attempt to do mandatory testing?

136

Sande: We lost the fight, because the CDC did come out with

recommendations,1 but we won the war, because it's not going to be
implemented, I don't think.

Hughes: What were the CDC recommendations?

Sande: Well, first of all, they had a list of procedures that infected
health care workers couldn't do, and that was a disaster. They
dropped that. Then they said, "Have the states come up with a
plan, but they'd better be consistent with keeping the public safe
from infected health care workers." Nobody's really responded to
any of those things. It just sort of died down, went away.

The AIDS Outpatient Clinic. SFGH

Hughes: We skimmed over the inpatient and outpatient clinics. Let's go
back. Can you start with the outpatient clinic, since that was
first to open [January 1, 1983]?

Sande: Well, it was in "81, '82, when we first realized that we were
going to have a lot of patients, and, as I said earlier, I had
recruited Paul Volberding to come over and run oncology. He had
an interest in Kaposi's. Then when we started seeing these new
patients who had this immunodeficiency disease, mostly
Pneumocystis but also other opportunistic infections, we thought
that it might be worthwhile, since Paul was particularly
interested in this, to expand the division of oncology to a
division of AIDS and oncology. It was the first such division in
the country, and I think it was important because it allowed us to
give particular attention with a new division to a new disease.
We put resources into it: we got resources from the city; we got
resources from my department, and we hired some people—Connie
Wofsy, Mark Jacobson, Connie Kaplan, Jim Kahn, and Donald Abrams—
and we had a focused division.

We established a new clinic on Ward 86 initially, and so we
asked Paul, "Why don't you start seeing the patients with this new
syndrome there?" And again, it allowed us to attract resources
from the city, saying, "Okay, here's a new disease. It seems to
be occurring particularly in gay males. Let's concentrate our
resources in this one area—in social services, the infusion
center, all these other things"— sort of bringing the community

1 CDC. Acquired immunodeficiency syndrome (AIDS): Precautions for
clinical and laboratory staffs. MMWR 1982, 31 (43) :577-580 (November 5,
1981).

137

into it. And that became the San Francisco model. It came out of
this clinic concept of using the community resources, using the
university resources, doing a lot of outpatient work, minimizing
inpatient care.

Hughes: Was there a precedent for that model?

Sande: Not really. Not that I knew of. The thing that made the model
work was the tremendous contribution and commitment of the gay
community. Because you had people out there who were willing to
donate their time and willing to work, bring people back and forth
to the hospital, care for people in the home, all of these things.
So it was real intense community involvement in the process, which
probably could have only happened here, where the gay community is
so tight and so involved. Paul was very good with the gay
community, and with keeping people informed.

The AIDS Clinical Research Forum, SFGH

Sande: I established [1988] a group [AIDS Clinical Research Forum] for
the activists that's never really gotten much publicity, but it
was really effective. I would meet once every couple of months
with the activists in San Francisco, and with Paul, John Ziegler,
Mark Jacobson, Don Abrams, and all the AIDS investigators. We
would present our research projects and the activists would react
to them, and we would have a big interaction. That was really a
successful group.

Hughes: This was entirely distinct from the mayor's AIDS advisory
committee?1

Sande: Yes. We had the active people, Jesse Dobson and Martin Delaney
from Project Inform, John James from the newspaper.

Hughes: AIDS Treatment News?

Sande: Yes. We had the lesbian groups; we had the Latino gay group and
the black gay group.2

1 Sande was chairman from 1984 to 1987 of Mayor Dianne Feinstein's
AIDS Task Force.

2 Representatives of community-based AIDS organizations and physicians
and other health care workers from SFGH and UCSF attended these meetings.
By 1991, between thirty and forty individuals were receiving meeting

138

These meetings went on for a couple of years [1988-1991]. In
fact, they were so successful that one day, Tony Fauci from the
NIH [National Institutes of Health] brought his entire core of
AIDS people—Dan Both, Jack Killen. They all came out here en
masse and we met over on Ward 30 in the solarium. We had about a
four-hour exchange between the activist groups and the NIH on the
issue of clinical trials. It was really a good forum, because it
was effective, and people had a voice.

Hughes: What sort of issues came up?

Sande: Mostly AIDS research and AIDS care, and how you're using your

resources, and how you're doing your human experimentation, and
how you're getting patient permission, and how you're getting
access to drugs. We'd ask them, now what are you guys selling
under the counter, and what are you bringing in from China?
Because all the buyers' clubs were represented in the forum. So
it was really an interesting exchange. This group proved to be a
pivotal political force for a long time.

Political Involvement

Hughes: Were these meetings the beginning of the education of Merle Sande
in terms of the gay community?

Sande: No. That happened a lot earlier. I got into the political arena
actually in '82. Well, there are three areas where I've been very
active politically at local and state levels. One was through the
initial group that was advising the health director on the
bathhouses [Medical Advisory Committee for AIDS]. Then the second
one was the Mayor's Task Force on AIDS, which I really formed with
Feinstein. The third one was the statewide AIDS body—what did we
call it?

Hughes: Universitywide Task Force on AIDS.1

Sande: Yes. So those are the three areas where I had probably my biggest
political impact.

announcements. For the names of attendees, their affiliations, and other
details, see the folder, AIDS Clinical Research Forum, in Dr. Sande 's
personal collection.

1 The committee is now called the Universitywide AIDS Research
Program; it distributes California state funds for AIDS research.

139

Medical Advisory Committee for AIDS, San Francisco Department
of Public Health

Sande: The first one was a small advisory group that Merv Silverman

established, and there were always at least five of us there—two
from the gay community, two from the straight community- -which was
Paul Volberding and myself --and Merv Silverman. We agonized for a
long time about the bathhouses and whether the health department
should make an attempt to close them. It was very interesting.
That's where I really got my education on the gay community.

Hughes: What do you mean when you say that?

Sande: We knew by that time—probably '82, '83 — that the population which
was becoming infected were the ones who had tended to have the
most sexual experiences, the largest number of partners.

Hughes: Some of that evidence was coming from the health department. It
was Selma Dritz's epidemiology?

Sande: That was part of it. But you know, it was also part of a report
every morning here [SFGH], where you'd see these gay males, and
they'd admit to large numbers of sexual partners in a weekend, and
extremes of [sexual] activity. It seemed clear. Now, this is
all, let's say, dataless impressions. But it seemed clear that
those who were constant participants in the bathhouse activity
were the ones that were being admitted to the wards with
Pneumocystis pneumonia. And Selma' s and Andrew Moss's initial
observations fit with this. The number of partners seemed to be a
risk factor, and particularly rectal receptive intercourse seemed
to be a risk factor for acquiring HIV.

The Bathhouses

Sande: I remember saying at one of these meetings [of the Medical

Advisory Committee for AIDS], "I cannot understand this resistance
to closing the bathhouses. It looks like the data are becoming
overwhelming, and it looks like this behavior is bad for your
health." I was quickly informed that the freedom to express
yourself sexually any way you want is something that the gay
population had fought for for many years, and they were not going
to give it up. And you know, I could understand that emotionally
from their standpoint. I could not understand it medically. And
physicians who were part of this group were making these points.

140

And Merv [Silverman] wanted to do the correct thing. He also
wanted to do the politically correct thing. So he agonized a long
time, and finally [Mayor] Dianne [Feinstein] got mad and fired him.

Hughes: But not until after he had closed the bathhouses [October 9, 1983].

Sande: Yes. It was an interesting process; it was an effective process,
but it was too slow. It should have happened quicker. We knew
that the actual closing wasn't going to really make a big
difference, but the statement that we made was that we had thought
long and hard about closing the baths, and this activity looked to
us to be very bad for your health.1 And you know, the judge
reopened the bathhouses. But they died. They died because the
evidence then became increasingly convincing that unprotected
rectal intercourse with multiple sexual partners was very high-risk
activity for transmitting the infectious agent responsible for AIDS
(later found to be HIV). It was a very interesting time.

The Mayor's Task Force on AIDS

Sande: When Silverman was fired, I was made chairman of the mayor's task
force [1984].2

Hughes: Why you?

Sande: I don't know.

Hughes: That must have been Feinstein "s decision, right?

Sande: Yes. I don't know why. I was probably the highest-ranking

university person involved. As head of all the AIDS activities
down at SFGH, and independent of the health department but at least
part of the scene, I was probably the logical person to do that.

1 For Sande 's views on bathhouse closure see: Declaration of Merle
Sande, M.D., October 6, 1984. In support of a temporary restraining order
to close the bathhouses. Superior Court of California in and for the City
and County of San Francisco. Dean Echenberg papers, San Francisco
Department of Public Health, Bureau of Epidemiology and Communicable
Disease Control, drawer: Bathhouses, folder: 10-10-84, Declarations in
Support, Volume 1. See Appendix.

2 The Mayor's Task Force on AIDS, also referred to as the Mayor's
Advisory Committee on AIDS, was formed in 1984 after the bathhouse crisis.

141

Hughes: Do you think she wanted somebody independent of the health
department?

Sande: Yes. I think she wanted somebody who wasn't directly responsible
to her.

Hughes: Abrams, Volberding, and Conant were members of the committee at
one time or another, and had UC connections.

Sande: Well, once they put it together, Connie Wofsy, Moses Grossman,

Julie Gerberding, and Phil Lee joined the committee. Phil hardly
ever missed a meeting. Then David Werdegar, who became head of
the health department after I was made chairman of this committee.
I'm trying to think. Flo Stroud.

Hughes: Who is she?

Sande: She's now acting head of the health department. Then Jim Foster,
who was a health commissioner who died of AIDS, was there.1 Also
Andrew Moss, who probably made the most significant contributions
to that group, because he was good at predicting the course of the
epidemic. Do you know who he is?

Hughes: Oh, yes; I've interviewed him.2

Sande: Andrew was wonderful. Andrew had the vision before any of the
rest of us did. He's always right. [laughs] Just amazing.

Sande: He anticipated correctly the IV drug-abuser epidemic in the area.
He predicted the tuberculosis epidemic, and now has spent the last
year studying it in New York. He really was the one who taught us
most about the risk factors that caused the transmission in gay
males. So I think he, among all of the epidemiologists in the
area, was the real hero. If I were to write a Band Played On
thing, I would put Andrew Moss in there as the person who really
understood the epidemic more than anybody else.

1 Representatives of Bay Area Physicians for Human Rights, the San
Francisco Medical Society, Irwin Memorial Blood Bank, and community
physicians in private practice also attended. (Minutes, April 23, 1983,
San Francisco Department of Public Health, Irwin Memorial Blood Bank
documents, binder 2, 1-5/83.)

2 See the oral history in this series with Andrew R. Moss, Ph.D.

142

Hughes: Are clinicians likely to give as much credence to an
epidemiologist as to one of their own kind?

Sande: Oh, yes. I don't think that's a factor.
Hughes: So there was no specialty rivalry?
Sande: No.

Mayor Dianne Feinstein

Sande: But you know, I wrote in, "The AIDS Epidemic: Blueprint of a

Hospital's Response,"1 that the relationship we had with Feinstein
was absolutely magical. It was absolutely unique. Towards the
end of her administration, we were meeting once a month with her.
She really was hungry for information. She was the best-informed
mayor in the country on AIDS, by far. Nathan Clumeck is a close
friend of mine from Brussels. He was the first one to write a
scientific article on AIDS in Africa, and it came out in the New
England Journal in the mid-eighties. Within a week, I had him
here, and he met with Feinstein to talk about what was happening
in Africa.

Hughes: Meaning heterosexual transmission of AIDS?

Sande: Yes. Nobody knew AIDS was in Africa. He found that a lot of

people from the Belgian Congo that came to Belgium were infected
with AIDS, so he reported this. Warren Johnson, a good friend of
mine from Cornell, was head of a clinical investigative program in
Haiti. He identified Haiti as having a big problem with AIDS, and
Warren came out and met with us. So we kept her abreast of what
was new.

Hughes: When you say the relationship was magical, you mean in terms of
access to the mayor?

Sande: Well, let me tell you. It was really interesting. Feinstein used
us for a totally nonpolitical purpose. She used us for advice.
She would come out with some of the most outrageous things, and
we'd sit there and say, "You've got to be kidding me."

1 M. A. Sande. The AIDS epidemic: Blueprint of a hospital's response.
Transactions of the American Clinical and Climatological Association 1987,
99:185-195.

143

We had no axe to grind; we were not working for her; she had
absolutely no influence over us. We were ideal advisors. We had
nothing to gain, we had nothing to lose, by saying what we thought
was right . That ' s what was magical about this . We never went
public with anything that went on in there. There was one leak
once, and boy, she called me instantaneously, and we plugged it.
But it was a place where she could freely express herself, and we
could tell her to go to hell, that what she said was just
ridiculous.

We had an incredible respect for her sense, her judgment. So
she used us, and she would come up with these things, and we'd
say, "That won't sell; that will sell," and she never, ever went
public with anything we didn't agree with as a group. Now,
individuals might disagree. But I just think that in facing
something as explosive and new and confusing as AIDS must have
been for the politicians, she used us as well as any group of
experts could be used. It was really remarkable.

Hughes: How much was she driven by the knowledge that the gay population
was not only a significant percentage of the city—I've heard the
figure of 10 percent—but also a heavily voting percentage?

Sande: I'm sure she was driven by that. But the thing that was good

about it is she did not put members of the gay community on that
task force just because they wanted representation. She didn't
use it that way. She wanted to do the very best job she could do.
I'm sure it follows that that would be politically advantageous to
her. But she did it in a way that she separated politics from
advice. So there was no politics in the advice. It was strictly
scientific data, as best we could put it together, and she used
our judgment on a lot of those things.

I remember one time we made a statement about how something
would appear if she went public with it, and she said, "You guys
are more political than I am. I don't want to hear that; I want
to hear what you think." Which was quite remarkable. It was a
refreshing baptism to how good government could be if it was used
in a nonpolitical sense, and she did that.

144

When she became chairman of the AIDS committee for the mayors
in the country, she used us all the time.1 So that was very
positive. I was very impressed with her.

Hughes: I've heard Feinstein criticized by people connected with the
epidemic because of her straight-lacedness on sexual issues.
Putting it baldly, she didn't want these activities going on in
her city. That was particularly apparent before the Democratic
National Convention in San Francisco in '86 when she didn't want
the message going out to the rest of the country that this kind of
sexual activity went on in "her" city.

Sande: She was not a proponent of bathhouse activity, I'll tell you that.
But I don't recall ever hearing her say that. I remember her
being disgusted by the thought of the glory holes and those sorts
of things. That certainly didn't appeal to her. But I heard it
not from a moral standpoint as much as I heard it as a result of
its facilitating HIV transmission.

Hughes: So can I conclude from what you're saying that her personal
morality probably didn't have much effect on policy?

Sande: I think it did not. I remember vividly her expressing her

morality in a very outspoken way. But the policies that were
implemented never reflected that feeling. When she went public
with something, it had been well tested on a number of people in
our group. So who knows the motivations for things, but I can
tell you that in my experience of her, that it was pretty well
thought out and pretty well censored by thoughtful people before
it was expressed.

The AIDS Clinic and Ward, SFGH

Formation

Hughes: Well, I haven't heard enough about the AIDS Clinic and ward.

1 Dr. Sande refers to the Mayors' Task Force on AIDS of the U.S.
Conference of Mayors; Feinstein chaired the task force from 1983 until her
resignation as mayor, January 17, 1988. (Information courtesy of Sally
Osaki, Office of the Executive Assistant to the Director of Health, San
Francisco Department of Public Health.)

145

Sande: Well, the clinic was developed because it was expedient to develop
it. We had no high-falutin ideas about turning this clinic into
anything more than a clinic, but it clicked. It really clicked,
because it became a place where the gay community could commit
themselves to their constituency and also to fight the disease.

Now, the ward was a little bit different. In reality, I
started the ward, which was initially 5B and then became 5A,
because I was worried. My initial vision for the ward was to make
it an infection-control ward, to make it an isolation ward, to
treat AIDS like tuberculosis. This was when we were going through
this agony of writing our [infection control] guidelines. But we
didn't really know how contagious it was. That's why we always
had private rooms for patients with HIV. The initial development
of the AIDS ward was to protect ourselves and protect other
patients from what we thought was a contagious agent.

Now, that's not the way it was sold once it was--I mean,
after the AIDS ward opened, and we had written our infection
control guidelines, and we had decided that AIDS probably wasn't
that contagious, and it became a center where every politician in
the country and many from Europe would want to have their pictures
taken, and we generated tremendous resources because of it, we
looked like geniuses. It had nothing to do with that initially.
We did it because we were scared. I did it because I was scared.
And then everything else just flowed. We used words like, "Well,
it was a great place to focus our resources, and we got the Shanti
Project involved, and it was a great place to train housestaff,
and it was a great place to take care of patients--" all those
things flowed in. It turned out to be a very, very successful
endeavor.

Hughes: You mentioned going to the city for funding. Who arranged the
funding?

Sande: It was Feinstein, to the health department, to us for the AIDS
program, and it still flows. She was putting up to $17, $20
million into AIDS from city dollars, unlike any other city in the
country. We got out ahead of everything. She supported
clinicians here; she supported the beds here; she supported nurses
here. So a lot of that was her doing. It also helped being her
advisors, because we could point out where the needs were, and she
responded I think very appropriately. And it worked.

Hughes: Well, talk about what happened once a patient was admitted.

Sande: The San Francisco model that was developed in the clinic is

because we wanted to minimize inpatient utilization. But say, for
example, a gay male with a new interstitial pneumonia comes into

146

the clinic or is seen in general medical clinic or in the
emergency room. The patient probably has Pneumocystis.

Now, a number of things along this line were just wonderful.
Keith Hadley and his group in the clinical micro [biology] lab
developed a new way to diagnose Pneumocystis through sputum
induction. So that was done up here by Phil Hopewell and his
chest service, and then microbiologists would look at the smear,
make a diagnosis and initiate therapy. We developed a whole
approach to management of Pneumocystis pneumonia.1

Coordinating the Clinic and Ward

Sande: Then maybe the patient would be admitted to 5A or 5B, and they'd
get started on therapy. This allowed us to do a lot of clinical
trials on new drugs for Pneumocystis. Patients would be picked up
by the AIDS service; they then would be discharged and followed
over on Ward 86, in the AIDS Clinic.

Hughes: Did patients also flow the other way?

Sande: Sure. A patient would come into the AIDS Clinic. One of the
things that was interesting was that we hired a number of
physicians to see just AIDS patients. The clinic started working
a little bit too independently, so when they wanted to admit
somebody, the communication between the outpatient service and the
inpatient service was terrible for a while.

I hired this fellow from Portland by the name of Michael
Clement, who was just a genius at interpersonal skills. He's a
gay physician, a wonderful guy, and he solved that in spades. So
then we realized it was important to have a clinician who was
always associated with the AIDS ward. We don't have a specific
housestaff team working on the wards, but we had an attending who
was always around to help facilitate communication. That one
issue focusing on communication was incredibly important to making
it work. That solved a lot of the problems, so then communication
between the ward and the AIDS Clinic became really good.

Hughes: Are you talking about communication along the lines of, are there
beds to accommodate the people that are referred to the ward?

1 For more on the management of Pneumocystis. see the oral history in
this series with Constance Wofsy, M.D.

147

Sande: Yes. As we talked about earlier, there was a time when there was
a lot of fear about taking care of AIDS patients, and there was a
stigma that the AIDS patient, just like the gay waiter, might be
transmitting some awful thing. So initially we put the ward
together as sort of an isolated unit, initially twelve beds, and
then a couple of years later, twenty beds. These beds are
reserved just for AIDS patients.

The AIDS Ward

Sande: Around the country, they were having trouble getting people to

take care of AIDS patients. We left ward staffing open. It was a
volunteer service. The staff got paid for it, but they
volunteered to work on the AIDS ward. We always had a list of
people who wanted to work on the AIDS ward. Because it was
volunteer, they developed an incredible esprit de corps. There is
a wonderful spirit.

It actually was a cause of some concern to other wards,
because these people had a special spirit about them. As a
result, they probably got more resources. And then every Sunday
some gal from the community would bring in food, and then
Elizabeth Taylor gave us a great big television set. Actually,
she made rounds with me a couple of times here on the service. So
they were special.

Phil Sowa, who was hospital director when we started this,
was really a very supportive person with this. He and I thought
one day we probably should start doubling up patients. One
patient per room was the way we started, but we started it for the
other reason [fear of infection]. So later we said, "It's not
infectious between people; let's double up." So we had a meeting
with the nurses, and the nurses said, "Absolutely not." We looked
at each other and we said, "You know, this is not a fight worth
having. You win."1 [laughter]

Hughes: Why didn't they want doubling up?

Sande: Because they had developed a way of caring for the patients. For
example, a family could come and stay in the room; they had cots
in patients' rooms. It was a tradition, and [the staff was] proud
of it, and they had taught it. They weren't going to let a couple

1 See letter, The Staff of 5A to Merle A. Sande, MD, April 15, 1987.
(Ward 5A archives, unlabelled off-white file box.)

148

of yo-yos like Sowa and myself come in there and tell them they
couldn't do it. It was very interesting. They won, and they
deserved to win. It was a nice way also of letting them know that
that's their ward.

Hughes: What happened to patients who needed to be admitted and yet there
weren't beds?

Sande: They got put in the other wards. We have patients with AIDS all
over the hospital.

Hughes: And that never caused a problem?

Sande: Occasionally, people who weren't gay, who had AIDS from blood

transfusion, did not want to be on the ward. There was a stigma
associated with it, but it was very unusual to have that happen.
Usually there was such a nice spirit [on the ward] that they
enjoyed it. It was very good care, and it made us famous. Famous
beyond all imagination. You just couldn't quite believe it.

It's true what I said about politicians: They've all come
through here, and to have their picture taken--guy who's head of
social service in England, the secretary of state of Scotland, a
whole group from the German congress. All through Europe, they
all come over here to look at the ward. Jesse Jackson, all the
presidential candidates, came through here. We got sick and tired
of them after a while.

Hughes: Do they go home and, in some cases, establish something similar in
their countries?

Sande: They did in England, very much so. They took a lot of the

concepts. Yes, we've exported a lot of technology for disease
care, for a lot of the San Francisco model, community involvement.

Holistic Treatment of AIDS Patients

Hughes: What could be done for an AIDS patient in the early days?

Sande: Well, even today, what can we provide? The AIDS patient is a very
complex individual. It became known pretty soon that if you had
Pneumocystis. you had a disease from which you were going to die
in the next year or so. So there was tremendous emotional
concern, emotional upheaval, in the individual, his family, and
his friends.

149

The other confounding variable was oftentimes his family
would not know that he was homosexual. So they not only would now
find out that their son was going to die, but that he was gay. I
remember an air force general who just could not accept it. So
learning to deal with those issues was equally important as
learning to deal with the medical issues.

Hughes: Who did have to deal with those issues?

Sande: We did.

Hughes: Everybody? Physicians and nurses--

Sande: Yes. The housestaff, and the nurses, and the attendings, and the
social workers.

Now, I have always said, and I firmly believe, that AIDS for
us medically has been an incredibly humbling experience, and we
certainly learned the limitations of our technical medical
abilities in this disease. But it's been a real positive in re-
teaching us the art of medicine—very important, I think. We have
learned to deal with death and dying. We have learned to deal
with code orders. We have learned to appreciate much more than
ever before the quality of life endpoints in our therapeutic
interventions.

We've also learned, I think, and very importantly, to
orchestrate a good death, which is a characteristic that is
extremely important. My philosophical approach to teaching is
that if you can orchestrate a good death, it is a tremendous
success. If you can allow somebody to die with dignity, to die
without pain, to die without being alone, and you as a house
officer, as an attending, have been able to do that, you should be
congratulated for it. You should be rewarded for it. It's not a
failure to have somebody with this disease die. It's a success to
have them die in a setting that you would appreciate dying in.
Ten, fifteen years ago, you'd never hear us say that. It's "keep
them alive at all costs."

Hughes: How much did this new attitude or approach originate from the
patients themselves?

Sande: A lot of it did.

Hughes: You mean that they were demanding a pleasant death? Pleasant
isn't the right adjective.

Sande: Yes. As pleasant as a death can be.

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Hughes: In the early days, the very informed and articulate patient

population must have influenced the course of medical practice.

Sande: Yes. Very well-informed. Usually excellent teachers for our

housestaff. They knew a lot more about the disease and the drugs
than a lot of us did. You learn to listen to your patients.

More on the AIDS Clinical Research Forum

[Interview 2: September 23, 1993]

Formation and Membership

Hughes: Dr. Sande, I believe you want to say more about the AIDS Clinical
Research Forum.

Sande: Yes. This was a group that we established because Steve Morin,

who was Representative Nancy Pelosi's person on health, very early
in her term, or maybe before she even was in Congress, told us —
actually told us through Rudi Schmid, who was dean of medicine at
UCSF at that time—that there was a gap that we had not recognized
between the activists, who were very powerful nationally, and our
own investigators, a gap in communication and a gap in knowledge
of what each group was doing. So I established this group that
included Martin Delaney and John Jones and Jesse Dobson, who was
the head of the ACT-UP group here. There were representatives
from BAPHR [Bay Area Physicians for Human Rights], the Hispanic
AIDS group, and the African American AIDS group.

We met for a number of years, and we presented to this group
drug trial protocols that were in the process of being developed,
so they had a chance to react to them before they went into
action. Then we also reviewed results of drug studies that we
were doing at the time, and got feedback. It was often an
explosive meeting—it was a meeting that I just didn't want to go
to, but we did. I just felt like there was always a lot of things
to talk about.

[tape interruption]

It started in March of '88, and it went through '91.
Hughes: Why didn't you like to go?

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Sande: Well, it's one I worried about, because you could never predict
the issues and you could never predict the temperament.
Occasionally it was a very hostile group which was frustrated and
wanted us to do more. We talked a lot about issues of informed
consent, the use of placebos, fast tracking, why aren't you doing
more, why don't you get more patients, why are you slow on this?
But it was good for us to hear it. The end result of it, I think,
was a very positive thing—much closer relationships—and they did
not feel excluded from the process.

Hughes: Did they cause you to change process, protocol?

Sande: Oh, yes, sure. Lots of things would be brought up about how you
get an informed consent, and what should be the placebo. So
hearing it from people outside of the system was actually very
beneficial. You didn't like to admit it, but it was very
beneficial.

Hughes: Give me an example of some of the things you changed as a result
of those interactions.

Sande: It's hard for me to remember specifically.

Compound Q

Hughes: Was Compound Q an issue?

Sande: Yes, well, Compound Q was an issue during the entire time, because
Project Inform with Martin Delaney was doing its own clinical
studies. Actually, we were a little upset with him for not being
very forthcoming with the data in those meetings.

Hughes: About their results?
Sande: About their results.
Hughes: Why would that be?

Sande: Oh, probably because he anticipated us being critical of the way
the studies were being performed. We had minutes of those
meetings, and I'm sure they're still available.

Hughes: I know that Michael McGrath was doing research here on Compound Q,
and there was research going on under Delaney.

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Sande: I don't have much hope now that Compound Q is going to offer any
great advance in the treatment of AIDS. However, when Mike made
his first observations in the test tube, it looked promising. I'm
afraid this happens a lot; things that work in vitro don't
necessarily make drugs that work in people. That's Q.

Hughes: What did the Delaney group think?

Sande: I don't know what's happened to them. We haven't heard much more
about it in the last couple of years . I remember when the
international AIDS conference was here [1990], I ran a panel with
Martin Delaney, who presented some of his data, and Dr. Arnold
Relman, who was editor of the New England Journal of Medicine at
that time. There was a very hostile interaction between the two
as to what made up good research and what didn't.

NIH Visitors

Sande: After about a year, I told Tony Fauci, who's been a very close

friend of mine for thirty years, that we were holding this meeting
with the community to discuss clinical trials and other issues of
common importance. He got very excited and flew himself, Dan
Hoth, Jack Killen, Peggy Johnston, and about three or four other
people from NIAID [National Institute or Allergy and Infectious
Disease] at the NIH out here for a single meeting with this group.
Tony held court for about two or three hours, answering questions,
because he was also interested in trying to establish
communication with the activists. We had really the only
functioning group that I knew about in which investigators and
activists were working together in a single group.

Hughes: How was that meeting in terms of atmosphere?

Sande: I think Tony got what he wanted. He got a dialogue. I know as a
result of that meeting, some of the people in this group had
direct access to him, which nobody else did. So he established
what he wanted to establish, and I think it worked out very well.
That actually was, when I think about it, one of the more
interesting things that happened organizationally.

Hughes: Was this the only place that such a group existed?

Sande: I'll bet it was, because our investigators are all members of the
UCSF faculty. Now, there were people from the VA [Veterans
Administration Medical Center] --John Ziegler; people from the
Moffitt [Hospital] --John Greenspan, Jay Levy, Harry Hollander.

153

They would attend some of these meetings with us and our
investigators here—Mark Jacobson, Sharon Saffron, Jim Kahn,
Lorrie Kaplan, Connie Wofsy, Don Abrams, Paul Volberding.

We would have an agenda; we would have the studies listed
that we were going to talk about; the activists would come
prepared to criticize them and react to them. I think it worked
out quite well, even though, as I said, it wasn't a meeting I
looked forward to.

Defining AIDS

Hughes: Well, let's go back to the early years. I want to talk about how
the disease was initially framed, which as you well know was as a
gay disease. What difference did that initial definition make in
the sorts of questions that you asked? What might you have asked
if it had not been framed as a disease of gays?

Sande: It's an interesting question. The gay association for us I think
was a positive, in that it polarized a very vibrant,
intellectually stimulating, intelligent group of men to a disease
that they took on as their own. The negative impact was obviously
that homophobia, hidden or latent, became expressed. It unearthed
that in areas around the city, but not nearly as much here as it
did in other parts of the country. All the pent-up fears of
homosexuality and latent homosexuality. "So now not only does
this group of people have sexual practices that are difficult to
understand, but now they're also potentially dangerous, now they
have a virus that I can potentially get." This brought out a lot
of pent-up emotions.

Hughes: Which you saw expressed here?

Sande: Not much. Much more from friends outside. Well, I guess for some
groups in the city and city government, of business people, people
who may have had a homophobic orientation to begin with, it became
perhaps easier to express that prejudicial attitude. But for
people like myself, who never had much interaction or experience
with the gay community before I came here, the epidemic quickly
forced me into the position of having to interact very actively
with the gay community- -which was a learning experience, and
didn't always come easily.

We talked yesterday about some of the bathhouse activities
and actions that we took. It seems to me that today we, the old
boys of academic medicine and the heterosexual community, are much

154

more comfortable with homosexuality and the gay community, much
more comfortable, to the point of it never enters your mind any
more. Many of my faculty are gay; many of our housestaff are gay.

Michael Clement, who I mentioned yesterday was the person
Paul and I recruited from Oregon, had talked many times of writing
an article about the importance of having a visibly gay attending
physician as part of your department, somebody who is a role model
for gay housestaff and gay students, and somebody who is visibly
proud to be gay.

Michael really was that, and was very visible and very proud
to be able to help people. So I learned a lot from him, as I have
from many of my other faculty.

Hughes: Did you sense that gay patients were also more comfortable if

there was an attending or somebody on the housestaff who was gay?

Sande: I don't know; I'm sure it did. One of the reasons I'm sure that

we were so successful in providing care to the population was that
we had gay nurses and gay physicians who were part of the program.
The interaction was never worth discussing, because it became very
natural. It wasn't forced; it was just sort of a natural
interaction. I feel that way today, that it's very much that way
now.

Hughes: Are you aware of other institutions that had an atmosphere that
was comfortable for a gay patient, and presumably also for a gay
physician?

Sande: I bet it was unique. I think it was one of the things that

allowed us to be so successful. It's really quite remarkable that
a city hospital like San Francisco General that has always had a
reputation for good care of the sick, but we're just a little city
hospital, and yet we have emerged as the number one AIDS hospital
in the world. That is remarkable, when you think about it. And I
think all the things we've been talking about: the support from
the administration, the support from our chancellor and [chief of
medicine and] dean [Julius] Krevans, and Holly Smith and Joe
Martin—the impact of the gay population, and the impact of the
gay physicians and support of the gay community have been
remarkable.

Hughes: How fully did you buy into the early framing of the disease as a
gay disease? When did you begin to think that maybe that wasn't
broad enough?

Sande: I don't think we ever consciously made this a gay disease, because
the transfusion cases and some IV drug-using cases came after

155

that. It never was important to us that it was or wasn't a gay
disease. We knew that the gay community was very supportive of
our efforts, and very supportive of the gay population with HIV.
That was important to us. But framing it as a gay or non-gay
disease wasn't really relevant to our operation at all. Most of
the patients were gay; some of them weren't.

There was a feeling in the community that it didn't want this
as a gay disease. You certainly heard that. And I remember when
David Durack at Duke, who was a good friend, suggested in the New
England Journal that they call it GRID,1 which is gay-related
immunodeficiency syndrome, there was an outcry, and it's a good
thing that didn't go through.

By the way, do you know who named the virus HIV?

Hughes: A subcommittee of the International Committee on the Taxonomy of
Viruses .

Sande: Do you know who chaired that committee?
Hughes: [Harold] Varmus.

Sande: Yes. I said that in my talk. The HIV of V, the human
immunodeficiency virus of Varmus.

Hughes: [laughs] I never thought of the V business. But the gay

orientation must have been important to some people, because look
at the early theories. The immune overload theory, for example--

Sande: But theories came and went every day. Before the virus was

identified, new ideas emerged all the time about why this epidemic
was happening. Let's say that we thought it was overload theory- -
too many antigens from previous exposures to sexually transmitted
diseases. Well, too many antigens rectally or intravenously,
there are still too many antigens. So the theory still was
possible.

Hughes: The only one I can think of at the moment that wouldn't be
plausible is the popper idea.

Sande: Yes, that didn't last long.

1 D. Durack. Editorial: Opportunistic infections and Kaposi's sarcoma
in homosexual men. New England Journal of Medicine 1981, 305:1465-1467.

156
CDC Epidemiology

Political Pressure

Hughes: Well, I understand that CDC spent a fair amount of time trying to
track that one down.

Sande: Well, the CDC was under political pressure to track everything

down. Some of them were false starts, and some of them were good
starts, which is what you'd expect.

Hughes: Political pressure from whom?

Sande: From everybody. Certainly political pressure from the right wing;
political pressure from the gay population to track things down
and try to find quick answers to complex questions.

Hughes: Are you saying that CDC was under pressure to explore every

possible cause regardless of whether it was on the surface valid?

Sande: The CDC was under incredible pressure throughout, particularly in
those early days, but even as recently as the outbreak from the
infected dentist. But I think they've done a remarkably good job
on essentially everything else.

More on the Acer Case

Hughes: How did the CDC handle the dentist case?

Sande: This is a personal bias, but it's shared by a lot of us, that
while the CDC did a superb job in working up the epidemic, the
final word, the final perception, about the dentist epidemic was
incorrect. It's a very complex issue. First of all, we don't
know the truth. We suspect that five and possibly six patients of
the dentist became infected with the same virus the dentist had.

Hughes: I thought that was sure, that they'd done the nucleotide
sequencing and it was the same sequence in all cases.

Sande: The sequencing is not a sure thing, but it's probably correct.
The image that was created by the investigation and the early
publications from this was that probably the dentist stuck his
finger with a needle or something sharp, bled through his gloves
into the patient's mouth, and transmitted the disease. Therefore,

157

all health care workers that do procedures that could possibly
nick themselves should be tested and benched if they are positive.
That ' s what came out of this .

Hughes: And that was the CDC line?

Sande: They were careful not to specifically say that, but that was the
implication. And then there was a call for a list of invasive
procedures that HIV-infected people could not perform. There was
direct implication that this dentist had done that (transmitted
HIV) , therefore all HIV-infected health care workers should be
considered a risk.

The premise is probably incorrect. If the dentist
transmitted the virus to his patients, he probably did it by
infected instruments, by contaminated instruments. We do know
that he had Kaposi's sarcoma in his mouth. We also are led to
believe now that he used the instruments in his office on his own
mouth, he or his dental assistant, and that those instruments were
not cleaned well. Now, rational people looking at the data are
much more likely to feel that that was the mechanism of spread
rather than accidental nicking of his finger.

The other hypothesis which has actually gained more
popularity recently is that this was an angry individual who did
it purposely. Now, nobody's going to be able to tell that. But
this one incident led to more confusion, to more hysteria, to more
prejudicial reactions, to more witch-hunting, particularly in less
informed regions of the country, than anything else. Now, I'm not
sure the CDC could have predicted that, but there were also, as I
understand it, very strong political—not interventions, but
fooling around with this thing by the politicians.

And as I understand it, (which is all hearsay), it was John
Sununu, who was assistant to the president, Jesse Helms [senator
from North Carolina], and Orrin Hatch, senator from Utah, who were
the three big ones who interfered with the CDC's publications,
made them shred one of their documents because it didn't go far
enough, and tried to instill the right-wing version, which is that
health care workers who are infected are bad, and are potentially
dangerous. Therefore everybody should be screened and benched if
infected. The CDC never recommended screening. But the
politicians certainly had that in mind. So this was a very
uncomfortable, unnecessary, and hysterically motivated part of the
AIDS epidemic that will be a black mark on all of us. I think the
CDC did their job but the politicians blew it.

158

Hughes: I think it doubtless had repercussions for what you were doing
concerning infected health care workers in the UCSF AIDS Task
Force. Am I right?

Sande: Yes. We fought with letters and media presentations that the data
did not support the recommendations.

UCSF's Attitude Towards AIDS

Hughes: Although I have read, and my information comes predominantly from
Randy Shilts' book,1 that in the early days of the epidemic, the
campus on Parnassus [UCSF] was pleased to move the bulk of AIDS
activities over here [SFGH].

Sande: I don't know where Randy got all this. I am really flabbergasted
by his perception of reality. I'm sure we all have our own
perception of reality. As far as I remember—and I was the single
person who was more involved in UC politics than anybody else in
the state--! never once perceived that there was an attempt by
Parnassus to unload AIDS patients here. In fact, if anything, it
was just the opposite; they developed an AIDS clinic [Adult
Immunodeficiency Clinic] under Harry Hollander, who was one of my
chief residents. And I never sensed that there was any attempt,
even early, to downplay AIDS, to export AIDS, because of the fear
of developing the reputation of becoming an AIDS hospital. So
much of this came out of the figments of people's imagination, and
that was a low blow. I don't agree with that at all. I think
probably I am the single person that has the most access to that
information because I ran all those committees. It was an earnest
attempt on all of our parts, including the administration at
Moffitt, to find a compassionate, user-friendly system for caring
for AIDS patients. That's just a bunch of baloney, and it
permeates a lot of what came out of that communication [And the
Band Played On] , as far as I'm concerned.

The Kaposi's Sarcoma Clinic

Hughes: The KS Clinic at UCSF preceded the AIDS Clinic at San Francisco
General by probably a good six months. The KS Clinic was up and

'Randy Shilts, And the Band Played On: Politics, People, and the AIDS
Epidemic. New York: St. Martin's Press, 1987. (Hereafter: Shilts.)

159

running by the summer of 1982. The outpatient clinic got going
here officially in January 1983. '

Did the KS Clinic remain strictly a KS clinic? Did it see
other problems associated with AIDS?

Sande: You know, I'm not really sure. You should talk to Paul Volberding
because he was really involved in that clinic. The KS Clinic
continued to function under Marcus Conant. Marcus Conant is a
clinical professor of dermatology; he has a private practice
clinic across the street and down a little bit from Moffitt
Hospital, and he saw KS patients.

Hughes: Did it make a difference that he wasn't mainstream academic UCSF?

Sande: Well, Marcus Conant is in private practice. He was very

influential in gaining attention for and sounding the alarm,
probably more than anyone else, in terms of, "AIDS is a big
problem, and you guys have got to get off your duff and do
something about it . " He ' s the one who went to Willie Brown and
said, "Listen, Willie, we need money for research," and got it.
Then he was the head of our center.2 He donates his time to UC to
do things like that.

Hughes: You're talking about the AIDS Clinical Research Center?

Sande: Yes, that the statewide task force [Universitywide Task Force on
AIDS] funds.

Hughes: Did the KS Clinic die when the AIDS Clinical Research Center came
into being?

1 A combined dermatology-oncology clinic, called the KS clinic, was
established at UCSF in September 1981 for the evaluation and treatment of
patients with Kaposi's sarcoma. (Marcus Conant to William Epstein et al.,
September 2, 1981. Conant's KS Notebook, 1981-2/82.) A formal AIDS clinic
was established at SFGH in January 1983, although patients with KS and /or
opportunistic infections had been seen previously in the oncology clinic
and, beginning in November 1982, in a combined KS and 01 clinic. For
further information, see the oral history in this series with Paul
Volberding, M.D.

2 Conant was the first director [1983-1985] of the AIDS Clinical
Research Center at UCSF. For more on these subjects, see the oral history
with Marcus A. Conant, M.D.

160

Sande: See, I don't know that. I think the KS Clinic continued for a
long period of time. Once the flood hit, the KS Clinic was no
longer able to handle any more patients than they were handling.

SFGH and the Competition with UCSF

Sande: You have to understand one other thing which I think is very

important about the difference between San Francisco General and
Moffitt, and that is, we here are incredibly competitive. We saw
AIDS, and we grabbed it.

Hughes: Competitive with whom?

Sande: With Moffitt. Now, this is one thing that I've been accused of,

and probably correctly, that I was looking for something to really
make this place [SFGH] great. AIDS came along, and here I was an
infectious disease-oriented person. I had Paul Volberding, who
was a wonderful facilitator, communicator, organizer. We just
went with it. We tried very hard to develop the resources
necessary through the city, through other agencies, to build,
build, build the program down here, make it the best in the world,
and we did. We were jealous of --we were not interested in giving
a lot of what we had built to Moffitt Hospital. Even though we're
part of the same group at UCSF, we live by our own family here.

Hughes: Were there people at Moffitt who would have been very pleased to
have taken a piece of the pie?

Sande: Probably. Jay Levy was there; Harry Hollander was there; Diane
Wara was there. They had their own programs. But we had
resources; we had space; we had patients; we attracted more
patients. So I'm saying this not to be self-serving, but to
explain a little bit and react a little bit to what Randy Shilts
was saying.

Hughes: That's why I asked.

Sande: We wanted this. So we went for it. And I do not think in any
way, shape, and form, there was an aversion to it at Moffitt.

Hughes: Conant had been first on the scene, in terms of organization

anyway- -he got the KS Clinic going and then invited Volberding to
come in. Do you have any sense that he felt left in the dust, so
to speak, when AIDS activities became centered at SFGH? Certainly
by 1983, that's the case.

161

Sande: Well, I don't know how Marcus feels. When I gave the lecture for
Krevans1 retirement, I named Conant as one of the real heroes.1
He is one of the real heroes. I was in the process of describing
my perception of how he interacts with the academic community, and
he doesn't interact a lot with the academic community. He's in
private practice, and he has a lot of obligations at the state
level; he was co-chairman of the AIDS leadership conference that
the governor appointed, and he's been very active in lecturing and
teaching around the world about AIDS.

But it's not really his thing to run a center. He doesn't
get paid for running the center. He donates his time. And so
after a period of getting it started, it passed over to John
Ziegler. Now, that center has never come to San Francisco
General. That is still administered at Moffitt and the VA, and
we're part of it, and Paul is part of it.

Hughes: Is that just history? It was started there and it's never been
moved?

Sande: It is history because it went there first, and it actually went to
Conant first. The center funded initially an AIDS tissue bank
that John Greenspan kept at Moffitt2. It's been very successful.
It accumulated serum and tissue from the very beginning, and it is
available to all investigators throughout the country, and it's
been very well used and well managed. It also supported some
clinical studies. It has a little granting cycle where it
provides $10,000 and $20,000 grants for investigators with new,
creative ideas. It just has always been administered there, and
it stayed there.

Community AIDS Physicians

Hughes: Has cooperation within the local medical profession been the

tradition in San Francisco? Is it a place where there is less
physician infighting than elsewhere?

1 Symposium in Honor of Chancellor Julius Krevans, M.D., on his
Retirement, UCSF, May 19, 1993. For a draft of Sande 's talk, see "Sande
Presentation: Symposium in Honor of Chancellor Krevans." (Binder: AIDS
Coordinating Council: Historical Report, AIDS Coordinating Council Office,
UCSF Faculty Club.)

2 For more information on the tissue bank, see the oral history in
this series with John S. Greenspan, Ph.D.

162

Sande: That's a difficult question, because I don't really know. I think
there has historically been here a certain degree of town-gown
conflicts between the practicing physician, the academic
physician, and the medical center. There certainly is competition
between hospitals in San Francisco, a city that has too many
hospital beds. There's always a battle for patients and for
referrals.

I do think that because AIDS was not a disease that
practicing physicians initially or even somewhat today felt
comfortable dealing with, there was initially less competition for
AIDS patients. Why didn't physicians feel comfortable dealing
with AIDS? There have been a lot of theories. One of them is,
that it's a brand-new disease with a lot of peculiarities that
they were not trained to handle. So it was ignorance that was the
first deterrent. There was a deterrent for a while, which I think
is less obvious today, that the AIDS patient was dangerous to take
care of because of the possibility of infection. And then there
was the possibility that if they took many AIDS patients, they
wouldn't acquire referrals of other patients because they didn't
want to be associated with AIDS patients. I think that's markedly
decreased.

But because of that, I think very early in the epidemic there
was a cadre of young physicians, many of them our own trainees,
and gay physicians, who were immediately thrown into the hopper to
be the AIDS doctors, and then increasingly it spread out to many
of the practicing internists and other physicians. This group, I
think, cooperated very well. They all knew each other; they were
friends. I think Donald Abrams did a wonderful job in developing
the San Francisco County Community Consortium, which I think has
sixty or seventy doctors in it. These are the people who take
care of most of the AIDS patients. They have a monthly meeting;
they have rounds; they do clinical studies together. They have
been funded by a large grant from the NIH. So the disease
certainly brought this group together, and they have worked
wonderfully together.

Hughes: Had there been any precedent in San Francisco for close

interaction between physicians in private practice and academic
physicians?

Sande: Not that I know of.
Hughes: Were there tensions?

163

Sande: You know, I don't know that. You should talk to Don Abrams.1 I'm
sure that there's competition. One of the real problems has been
that for a doctor who sees primarily AIDS patients, it's been
suggested that if you get up to sixty or eighty AIDS patients in
your practice, you go "psychotic." Because they're so demanding,
require so much time, and are emotionally draining, you burn out.
You need to spend so much time with them. And if they don't have
insurance and are on Medi-Cal... Medi-Cal I remember at one time
was paying something like thirteen dollars an office visit, which
is probably 30 or 40 percent of overhead. So not only were the
patients time-consuming, complicated, required a lot of energy and
resources, there was essentially a negative incentive financially
to care for them.

And yet, Bill Owen is one of these heroes who at great
personal expense took on a large number of AIDS patients, and just
worked with them, worked with them, worked with them.2 I haven't
been as close to that group as Donald would be. I've heard
recently that the number of AIDS patients is decreasing for a lot
of these practitioners, and that the epidemic is moving more
towards the intravenous drug using population, which tends not to
be as rewarding a patient population to care for.

AIDS Demographics

Hughes: Well, you said last time that the number of cases with AIDS is
dropping. Did you mean overall, or in the gay population?

Sande: Well, in the middle-class gay population, it seems to be dropping.
In the IV drug-using population, it tends to be staying the same,
maybe a slight increase. And in the heterosexual population,
particularly in the African-American, Hispanic group, increasing.

Hughes: The net effect is a decrease?
Sande: Probably flat right now.
Hughes: Is the change due to education?

1 See the oral history in this series with Donald I. Abrams, M.D.

2 See the oral history with William F. Owen, Jr., M.D., in The AIDS
Epidemic in San Francisco: The Response of Community Physicians (in
process) .

164

Sande: Well, no. I think I understand it. About 50 percent of the gay
male population in San Francisco was infected before 1983, if the
studies are correct, and I think they probably are. And there has
not been a lot of transmission since 1982. So now that's
thirteen, fourteen years, and the incubation period is about ten
years. So half of them would be six to ten to ten and a half
years after infection. So now, 60, 70 percent of them are
developing symptoms, if they haven't died already. Now, that's
the population that education clearly worked for, because
transmission of AIDS dropped way down.

But since that time, the proportion of cases in the
intravenous drug-abusing community, the crack-smoking community,
has started drifting up, particularly in women. It's becoming
more of a problem now than it was before. Ninety percent of our
patients are still gay males, or gay males who are also
intravenous drug users.

Early San Francisco AIDS Investigators

Hughes: You mentioned that the early AIDS investigators were by and large
young people, in many cases beginning their careers, which was
certainly the case with Volberding and Abrams and a number of
other people. Why did Paul Volberding rise to the top of the
heap?

Sande: I think Paul did very well, and I think his skills are
communication and organization.

When you say AIDS investigator, you have to define what that
means, because there are clinical investigators, of which
certainly Paul has been very prominent, and you could name the
other ones: it would be Margaret Fischl, Henry Masur, Doug
Richmond, Marty Hirsch--! think that's the group. Then working
with Paul, Donald Abrams did other things, Jim Kahn, Lorrie
Kaplan, and more recently Mike Jacobson. John Mills was involved
with AIDS for a while when he was here.

Clinical investigator as opposed to basic science
investigator, and in that latter area, Jay Levy was one of the
first. We recently recruited Warner Greene here [as head of the
Gladstone Institute of Virology and Immunology] , who is probably
one of the best basic science investigators in AIDS in the world
right now.

165

Paul was recruited to do something else [oncology], but I
gave him complete flexibility to run with the AIDS thing, and
supported him fully with resources and time and people. He also
had an immediate patient population, and a very supportive
administration, both at UC and the hospital [SFGH] and in the
city. So I think he really fell into a wonderful situation, for
which he was able to utilize his talents and skills of
communication and organization. So I think it was a perfect mix
for him in that setting.

Hughes: John Ziegler came here in 1981 with more of a reputation, because
of research experience, than Paul Volberding had.1 And then of
course , there was Marcus Conant .

Sande: But Marcus was never trained as an investigator. Ziegler had
developed a wonderful reputation in Uganda with the Burkitt's
lymphoma program. But Ziegler wasn't here. Ziegler was at the
VA.

Hughes: And that made a big difference?

Sande: Made a big difference, made an incredible difference, because the
VA didn't have the resources, didn't have the AIDS population,
didn't have the organization that we had.

Hughes: What made you think that this epidemic was going to be important?

Sande: There was never a conscious decision to say it was important. It
just was there. It was there, and it was there in spades. We
were opportunists. We said, "We've got to do something with
this." It clicked. That's how you build a department; that's how
you build an organization. But I don't think we ever sat down and
craftily planned any of this. It was there to grab, and we
grabbed it and ran with it. And the more we ran, the more
success, the more accolades, and gee, after a while, we were on a
roll. [laughs] Nobody was going to stop us.

Hughes: Have we said enough about who was making AIDS policy in San
Francisco in these first four years of the epidemic?

Sande: Well, we talked about when Merv Silverman was head of the health
department, the bathhouse issue. And we talked about the mayor's
task force, which I think was very influential on all AIDS policy,
once that became established. I think the health department here
in San Francisco did a very good job in quelling hysterical fears
and in charting a fairly rational course, and people followed.

See the oral history in this series with John L. Ziegler, M.D.

166

What's really interesting is that the things that the health
department, the mayor, the mayor's task force, did in San
Francisco led the world. I mean, everything emanated from San
Francisco. We were always the first in everything, and everybody
else sort of followed behind. It's a generality, but I think it's
very, very true.

We could see that when we went elsewhere. I used to run the
Infectious Disease Society of America [IDSA] symposium on AIDS.
Most of the people we got to talk were from here, on almost all
the issues. San Francisco has been very, very powerful,
influential.

AIDS Activities at San Francisco General

Hughes: As AIDS activities expanded at San Francisco General, was there

any resistance from other hospital services to what must have been
a drain on staff and finances?

Sande: I think the finances actually were increased because of AIDS.
Hughes: In general?

Sande: Yes. We attracted political attention and as a result attracted

resources. I'm sure there were some jealousies, and probably some
concerns that we were getting too much publicity. There's a lot
of other good things at San Francisco General. I guess one of the
things we were reacting to was, for years the trauma service was
held up as the most visible part of the organization, and we (in
medicine) were sort of proud to have something of our own [AIDS
activities] that matched them for visibility. And pretty soon,
all the divisions of medicine were somehow involved in AIDS, and
also the other departments—certainly OB/GYN, pediatrics,
ophthalmology, psychiatry, and surgery.

I think one of the real heroes of the AIDS epidemic is Bill
Schecter, who is our chief of surgery. Bill Schecter, working
with Julie Gerberding, really did a lot to quell the fears of
surgeons operating on AIDS patients. Bill was always a very, very
articulate presence, scholarly presence in the surgical world on
responsibility of surgeons to care for AIDS patients, and took a
passionate look at the data relative to risks, innovative ways for
reducing risks, i.e., double-gloving. He really is a wonderful
guy, and a wonderful speaker. He did a lot to quell the hysteria
that Lorraine Day had whipped up.

167

And before Bill, Frank Lewis was also very good. Actually,
most of his time Frank Lewis was head of surgery, and he was also
a very strong believer in the rational approach and a surgeon's
responsibility to operate. Both those guys did a great job. So
it wasn't just the AIDS division in medicine that was doing this.

The Multidisciplinary Approach

Hughes: A multidisciplinary approach to a disease is not unique to AIDS,

but is the wide spectrum of the specialties focused on one disease
something new?

Sande: Sure. Not focused, but a part of. See, the specialties all had
their own arenas, and AIDS was a small part of most of those
arenas for the other services. But it was a vital part, and they
certainly participated in it.

Hughes: Can you think of any disease that called upon such a diverse
approach?

Sande: Trauma.

Hughes: But not another infectious disease.

Sande: No.

Hughes: So of course, that forced cooperation and collaboration, didn't
it? Because of the very nature of the disease itself, one
specialty couldn't cover it adequately.

Sande: Right.

Hughes: So the disease itself--

Sande: Was a unifying force.

Hughes: Interesting. Were there non-San Francisco General physicians
seeing AIDS patients here at the hospital?

Sande: Yes, people in private practice who have clinical appointments

come and work in the AIDS Clinic. There were a number of those.
Steve Follansbee, who has a big practice in town.1 Mike McCune,

1 See the oral history series in the AIDS community physicians series
with Stephen E. Follansbee, M.D.

168

who is the inventor of the SCID [severe combined immunodeficiency]
mouse model, is a very, very prominent scientist worldwide, comes
up every Monday morning and sees patients in the clinic. Yes,
there's a lot of volunteer help that still goes on.

Hughes: Does a private practitioner lose his patient when he is admitted
to SFGH?

Sande: Most private practitioners admit their patients to their own
hospitals.

Hughes: Even when the best treatment for AIDS is here?

Sande: I don't know the answer to that. I think there were some patients
admitted here who would go back to their private practitioner, but
usually they were admitted to the private hospital. But a lot of
those private practitioners were also working in the AIDS Clinic.
So there was some connection. If the patient was admitted SFGH,
it probably was the result of their private physician's
relationship with the AIDS program at SFGH.

In terms of best care, that's a tough one. I'm not sure
there's a best care. Certainly this was really good care.

Sande: Patients elsewhere didn't have as much access to the clinical

trials and the new drugs as they did here. But I would be very
careful not to say that other hospitals didn't provide good care.

Hughes: When I asked that question, I was thinking in a broader sense than
just the medical. I was thinking of what we had talked about last
time--

Sande: Access to the resources, access to the community placement, and
things like that.

Hughes: Right, and the atmosphere of the inpatient ward.

Sande: That was a real plus. That's what we had to sell. That also
helped to attract a lot of private patients to San Francisco
General.

169
Projecting the Need for Hospital Beds for AIDS

Hughes: I understand that one of the responsibilities of the mayor's
advisory committee was to try to project future need for AIDS
beds.1 How did you go about that?

Sande: Well, it was two- fold. One of my agendas, which I didn't speak
about a lot, but I did speak about occasionally, was that I was
adamantly opposed to making San Francisco General an AIDS
hospital. We have here probably the best, if not the best, one of
the real top training programs in internal medicine in the
country. It's a training program that includes the VA, Moffitt
Hospital, and SFGH. I was concerned when we saw this tremendous
onslaught of AIDS patients that the AIDS population would crowd
out everything else, and that our teaching program would suffer.
There would be very good caring for AIDS patients, but trainees
would lose a lot of the other important aspects of the training.

So one of my agendas was to be sure we never got more than a
third of our medical patient population in AIDS. We had made
potential arrangements once it got to that point to divert
patients to other hospitals. We would still maintain some care of
those patients, but we would unload the patients if it came to
that point.

Hughes: So you had essentially a quota.

Sande: It never went into effect, because the market forces and the

expertise of others started to take over, and if anything now, we
can take more AIDS patients. So it never became a problem, but I
was very concerned about that.

Now, in terms of projecting hospital beds and how many were
going to be needed, that's where Phil Lee, who was a very
important part of the mayor's advisory task force, and the people
that worked with him, and Ann Sikowsky from Palo Alto, and some of
the health planners, were helpful in looking at the data, as was
Andrew Moss. But there was a lot of guessing, although there were
mathematical modeling that could project that.

Hughes: Was the projection fairly accurate, as it turned out?

1 See for example, Meeting Minutes, Mayor's Advisory Committee on
AIDS, October 22, 1984. (AIDS History Project Archives, Special
collections, UCSF Library, Ward 86 papers, carton 1, folder: to PV [Paul
Volberding] Oct. -Dec. '84.)

170

Sande: It was for a while. The increases were certainly projected, and
the increases were seen. Yes, I guess it was pretty accurate.
But then also other factors were at work, such as increasingly we
were able to make diagnoses and initiate therapy in the outpatient
arena, which didn't require a hospital bed. We reduced our length
of hospital stay.

The other thing, by the way, that was very important to the
training program and to the hospital is that our length of stay
got down to around seven days, where in New York it was fifty
days.

Hughes: I saw some figures for 1986 for the considerably lower cost for

the average care of an AIDS patient in San Francisco, as compared
to elsewhere, and it was something like $29,000 per patient.

Sande: Yes, and a lot of that was Ann Sikowsky's data.

Hughes: Was the lower cost largely based on shorter hospital stay?

Sande: Yes. It was the San Francisco model: treat the patient at home,
in the community.

Hughes: Well, I saw in the minutes of a meeting of the mayor's advisory

committee of November 5, 1984 that twenty to twenty-three patients
could be accommodated in 5A.1

Sande: We started with 5B in July '83, and then expanded from twelve
patients to twenty to twenty-two patients.

Hughes: Anyway, the mayor's advisory committee projected 150 AIDS cases

per day needing hospitalization in San Francisco by the summer of
1985.

Sande: That's probably about right, because we always had about a third
of them.

Hughes: That number didn't worry you?

Sande: I didn't want them all to come to San Francisco General, for
strictly personal purposes relative to the training program.
Kaiser [Permanente Medical Care Program] was real good with AIDS;
they always had about a third of the patients, too. They were
second behind us .

1 Minutes, Mayor's Advisory Committee on AIDS, November 5, 1984.
(AIDS Resource Program Archives, UCSF, AR92-20, carton 2, folder: Mayor1!
Task Force on AIDS.)

171

Hughes: Aren't you being overly complimentary? They didn't have a choice
if somebody had Kaiser coverage, right?

Sande: No. I'm being positive about their response, because they didn't
shrink from taking them. They developed good patient care
activities. George Matula over at Kaiser in San Francisco became
a real leader in the area. They were proactive. You didn't get
the sense that Kaiser was trying to shirk its responsibility at
all. At least, that was my perception.

Hughes: So that 150 cases, which is considerably over the twenty-three
maximum that the General felt it could accommodate on 5A--

Sande: Well, no, we never really said twenty-three maximum. We usually
probably had thirty to forty.

Hughes: But scattered around the hospital.

Sande: Scattered, yes, and the twenty-three on the AIDS ward.

Hughes: Okay, even if you took forty, you still had 110 patients that you
had to hospitalize elsewhere. Was the committee pretty sure that
it could find beds elsewhere?

Sande: We were worried about it. That's when I was very concerned about
us becoming an AIDS hospital.

UCSF Task Force on AIDS and Mayor's Advisory Committee on AIDS

[Interview 3: January 3, 1994]

Formation of the Mayor's Advisory Committee

Hughes: Dr. Sande, could you talk about the interrelationship of the UCSF
Task Force on AIDS and the Mayor's Advisory Committee on AIDS?

Sande: Okay. The UCSF Task Force on AIDS was the committee appointed [in
March 1983] by Julie [Julius] Krevans, who was then dean, to deal
with infection control. The group was large and included members
of the health department, including Merv Silverman, and members of
the hospital; Geoff Lang was the SFGH administrator at that time.
This in '83 and '84 was the group at the health department and in
the hospitals that talked about AIDS.

172

We then gradually merged into a consulting body for Mayor
Feinstein. They were the same players, and we then formed what
was called a mayor's advisory committee on AIDS, that I suspect
started in the fall of 1984.

Hughes: Do you remember what the impetus was?

Sande: As 1 remember, at this time there had been a long, drawn-out

process and a group of people independent of this body that was
dealing with the bathhouse closure issue. I recall numerous
evening meetings would go far into the night discussing that
issue. Paul Volberding and I were on it; Merv Silverman was
reporting to the mayor. I think the mayor realized that she would
benefit from a more structured organization whose purpose was to
keep her informed and advise her on the extent of the epidemic,
the direction of the epidemic, new problems of the epidemic,
political responses to the epidemic, political statements that
needed to be made about the epidemic.

So while a small group of us were meeting with Merv Silverman
to talk about closing the bathhouses, this large group of the UCSF
AIDS Task Force, which included health department officials, sort
of became, or many members of this group became, the mayor's
advisory board.

Hughes: She officially appointed you to that committee?

Sande: She appointed me, and she would make recommendations about who
should be on it, and then I would essentially invite whomever I
wanted. What was neat about it is that we would bring her up to
date about not only issues in the city and the state, but also
around the world. We had people visiting who were up to date on
this because they were the people doing the research, and finally
Nathan Clumeck, when he first described AIDS in Africa. And they
all met with Feinstein. As they came to town, we would bring them
to see the mayor, and she would open her arms to them, because she
was the mayor who knew more about AIDS than any other mayor in the
country at that time. That would have been '84 to '88 [January
17, 1988]. '

1 Information courtesy of Sally Osaki, Office of the Executive
Assistant to the Director of Health, San Francisco Department of Public
Health.

173
Advising the Mayor

Sande: During the last months of her tenure, we were meeting with her
almost once a month. She had this insatiable thirst for
information about the epidemic.

Hughes: Which might or might not be specifically applicable to San
Francisco?

Sande: It was much broader than San Francisco.

Hughes: Yes, if she was interested in Africa, it must have been.

Sande: I think I said this last time: It was a wonderful way for a

politician to use her academic resources to educate herself and
help decide policy. I think that's without precedent. And boy,
if I were running a city or a state or a country, I would really
have this independent body with no political aspiration, nobody
vying for attention. In fact, all this stuff was secret. We
never mentioned a word about it to the press or anybody else,
because we only had one agenda, and that was to educate her. She
appreciated it, and she respected it, and we did too. It was a
remarkably nonpolitical body.

But when Silverman finally decided to close the bathhouses in
the early fall of 1984,' then Feinstein became obsessed with the
delay, delay, delay, and felt he should have made a stronger
statement earlier. Then I was appointed, because of this body
[UCSF Task Force on AIDS], to chair her advisory committee.

Hughes: You mean because you were chairman of the UCSF Task Force on AIDS?

Sande: It naturally followed, because the same people became part of her
group. Now, she added a few others, like Jim Foster, who was on
the board of the health commission. He was a gay man who actually
died of AIDS a number of years ago. Phil Lee, who became head of
the city's health committee [San Francisco Health Commission],
joined; we appointed him. And then when Silverman was replaced by
Werdegar as health department director [1984], David Werdegar
became a member of that committee. Actually, I think he was a
little threatened by it, because it was a direct link to the mayor
on health that didn't go through the health director, so there was
a natural potential for conflict. We actually worked it out

1 Silverman closed the bathhouses and private sex clubs in San
Francisco on October 9, 1984.

174

fairly well. I was sensitive to that potential conflict, and he
was sensitive to what we were trying to do.

Hughes: You said a few minutes ago that you had leeway in appointing

people to the committee. Now, did you really mean that, or did
you mean that you invited speakers on specific topics?

Sande: As I remember it, I also appointed people. I think I appointed
Julie Gerberding. I think I appointed Connie Wofsy. Paul
Volberding was always part of it. I think I appointed Andrew Moss
to be part of that. I'm not sure how the dynamics worked, but it
was a heterogenous group, and I think the mayor appointed some and
I appointed some.

Hughes: Where did the group meet?

Sande: In the mayor's office. We discussed many issues. We were very
concerned about who would care for the growing numbers of AIDS
patients, how they would be cared for. This was a time when there
was a tremendous stigma and fear of the private hospitals being
branded AIDS hospitals. Besides, it was a new disease, and people
didn't understand it, didn't know how to care for it, so there was
a lot of uncertainty. So we were concerned about where people
with AIDS were going to be taken care of, where they were going to
be hospitalized, really concerned about who was going to pay for
it, because the reimbursement was not very good for this disease,
and a lot of these people required governmental support.

So we would meet, look at the data, and we would always have
an update at these meetings by whoever the AIDS epidemiologist
was. Dean Echenberg, and then George Rutherford of the health
department's Bureau of Infectious Disease Control would update us
on the number of cases that month or the month before, trends, new
things. And then we would crystalize, distill all the
information, look at the national scene, look at the international
scene, and then we would have a program to present to the mayor.

Hughes: It makes sense to you that the committee was organized as late as
fall of 1984?

Sande: This part of it did. I think we had met with the mayor several

times before when Silverman was chair of the committee. You see,
when he was the driving force as head of the health department at
the same time he was trying to close the bathhouses, we would meet
with the mayor to give her updates on this process. I would give
her updates on what was happening at the UCSF meetings about
infection control and risk to health care workers, which was
always a big, big concern.

175

And then when Silvennan fell from favor, she put me in as the
chairman of the committee, and then we started having these other
meetings to talk about preparation. But our group continued until
the very last day of her tenure in office, and meetings increased
in frequency as she reached the end of her term.

Mayors Art Agnos and Frank Jordan

Hughes: And then died with--

Sande: Agnos. He didn't want anything to do with us.

Hughes: Why was that?

Sande: I don't know. We met with him twice, offered our services, and
didn't hear from him again.

I met with [Mayor] Frank Jordan and said, "We had this really
positive body of knowledgeable people whose only job was to keep
the mayor informed on what was happening." I said we would be
more than happy, I'm sure, if he was interested, to do it again.
He said, "Oh, well, of course," and he never did it.

Recognizing AIDS as a Sexually Transmitted Viral Disease

Hughes: Moss says in his oral history that he put data on the board at

what he called the Mayor's Advisory Committee on AIDS.1 He didn't
give a date, but I suspect it might have been 1983, because he was
working from his census tract study. His point was that he had to
convince you, the group, that AIDS was a sexually transmitted
disease. He maintains in the oral history that it was his data
that convinced you that it was a sexually transmitted disease.
You couldn't have been doubting that as late as fall of 1984 after
the discovery of the virus.

Sande: I remember Andrew being particularly prophetic about intravenous

drug use, and it's the second demographic wave of the epidemic. I
don't specifically remember him trying to convince us that it was

1 See the oral history in this series with Andrew R. Moss, session 1,
September 30, 1992.

176

a sexually transmitted disease, but that wouldn't be surprising
that I wouldn't remember that point.

Hughes: Do you remember ever having doubts about that?

Sande: No, I don't remember having doubts about it. I certainly had
doubts about where the virus was, or how it was transmitted
sexually. But once it was occurring in just gay males, it had to
be a sexually transmitted disease. But why it was particularly
gay males, we didn't know.

Hughes: And it had to be a virus?

Sande: That was the most logical thing. Everybody thought it was
probably a virus.

Stigma

Hughes: At the first official meeting of this mayor's advisory committee
in October of '84, you introduced the idea of equitable
distribution of AIDS patients.1 Do you remember how the committee
set about to try to allocate AIDS cases throughout the city?

Sande: As I said before, nobody was anxious to jump in and care for

patients. I shouldn't say nobody, but there was a general sense
that the private hospitals would look very bad if they were known
as an AIDS hospital. At that time, there was a concern that these
individuals were infectious to other people. So the hospitals
were concerned that if they had AIDS patients, other patients
wouldn't want to come there. They were concerned that if they had
AIDS patients, that they wouldn't be able to recruit good
housestaff to their programs.

Hughes: What about homophobia?

Sande: I always thought that was over-sensationalized. I didn't have a
good understanding of homophobia. I didn't think that any
hospital in San Francisco would be penalized, or a physician would
be penalized, for taking care of homosexual males. I didn't feel
doctors had an aversion to taking care of homosexual patients. I
thought it was much more the fear of infection and fear of the

1 Minutes, Mayor's Advisory Committee on AIDS, November 5, 1984.
(AIDS Resource Program Archives, Ward 5A, SFGH, carton 2, folder: Mayor's
Task Force on AIDS.)

177

unknown. Now, this has been studied and written about a lot-
maybe that fear brought out homophobic responses in people.

But I always thought there was more of an aversion to
intravenous drug users, because of their crime-associated
behavior, than there ever was for gay males. Now, I know a lot of
gay physicians and gay people don't think that's true, but I
didn't think homophobia was a big problem, particularly in San
Francisco.

Hughes: I think San Francisco is a special case, but to this day there are
people who consider homosexuality a crime, at least a crime
against nature, and in some states it is a crime.

Sande: Oh, yes. I'm only talking about San Francisco. I'm not talking
about outside the San Francisco area. I bet it was '83, I made a
tour through the Bible Belt, and lectured in Spartansburg, South
Carolina, where Bob Jones University is. There were some places
that were really totally homophobic.

Hughes: You were lecturing on AIDS?

Sande: Yes. And the response was, "Good God, God's finally awakened and
found a way to get rid of these people." But of course, I didn't
find it at San Francisco General, and I certainly didn't find it
at UCSF, and I didn't find it in the city. But the fear of
contagion and the fear of the unknown I think was a definite fear
and a realistic fear. That's why we felt that if every hospital
took AIDS patients, the stigma would be neutralized. And I think
that's what eventually happened. I don't think it was anything we
did. I think it just happened.

Hughes: Because it became known that AIDS could not be transmitted

casually? That there was not a great danger of infection? Was it
as simple as that?

Sande: I think that may have helped, but I think it was happening

regardless. Hospital boards were afraid, but it turned out that
the decision to admit or not admit AIDS patients isn't controlled
by hospital boards or hospital administrators; it's controlled by
the physicians. So through the medical society and through the
educational programs that we all put on, physicians assumed their
natural Hippocratic responsibility to care for all patients. So
all the hospitals eventually had AIDS patients. But I don't think
it was anything we did politically, or did using the mayor's
office, to make that happen. I think it just happened. And
certainly, once it looked like AIDS was not disseminated by casual
contagion, that helped an awful lot in easing the fears of the
health care workers.

178

Hughes: What about easing your fear of San Francisco General becoming
labeled as an AIDS hospital?

Sande: We were not concerned about our patient population, because we're
the hospital of last resort. We don't have a lot of private
patients. So we were never concerned that if we had lots of AIDS
patients, other patients wouldn't come here, because they come
here anyway. We were concerned that it would destroy the training
programs, that if we became nothing but an AIDS hospital, then
where do you learn about diabetes, and where do you learn about
heart disease and other things? That was one of my personal and
selfish concerns, and it's reflected in that document in '83 and
'84, describing the hospital's response.1 We actually got the
mayor to propose that we could cut off the number of AIDS patients
at San Francisco General and distribute them if we had to. We
never had to, but we worked hard to get that feeling that we would
not just let San Francisco General become an AIDS hospital.

Hughes: There was talk in that same set of minutes about generating a list
of physicians throughout the city who maintained that they would
be willing to treat AIDS patients.

Sande: Yes. There was a concern that initially physicians wouldn't do
it. Today, a small group of physicians see the vast majority of
the AIDS patients. But I don't think that it any more is fear of
contagion. I don't think it's homophobia. I think it's just that
the disease has become complicated, and certain internists,
infectious disease specialists, oncologists, and some family
practitioners who have mastered the art and have kept up with the
changing scene of AIDS are the ones who do most of the work.
Which is not unusual, and it has no negative connotation.

Consultant on AIDS to the San Francisco Medical Society. 1985-
Present

Hughes: You said off -tape that you didn't play much of a role as a

consultant to the AIDS task force of the San Francisco Medical
Society. But another thing I learned from those minutes was that
the mayor's advisory committee decided that the society would be
the one which sought the list of physicians.

1 Sande, Merle A., "The AIDS epidemic: Blueprint of a hospital's
response." Transactions of the American Clinical and Climatological
Association. 1987:99.

179

Sande: Yes. The president of the medical society was also on our UCSF
task force, and then on the mayor's advisory body.

Hughes: [Glenn] Molyneaux?

Sande: Yes. He was a very loyal member of that group who came to all the
meetings and was very supportive. A wonderful, wonderful human
being.

Hughes: Did the society indeed help to solicit AIDS physicians?

Sande: I don't remember how far that went, or if it was ever really

necessary to do it. But there was an active process of engaging
physicians to the need for it, and as I remember, it was a pretty
positive response.

I do think it's important that we get Sally Osaki, if she has
minutes of those meetings, to make them available to us.1

Obtaining Funds from the State of California, 1983

Hughes: The UC Systemwide Task Force on AIDS, as I understand it, was
fallout from the money that came from the state of California
through [Assembly Speaker] Willie Brown, for AIDS research.

Sande: Right. In '81, Mike Gottlieb from UCLA reported five cases of
Pneumocystis pneumonia in gay males.2 Shortly thereafter, we
started seeing- -Marcus Conant was one of the first ones here in
San Francisco who started seeing Kaposi's sarcoma in homosexual
males. Then we started seeing here at San Francisco General a
number of homosexual males with strange diseases, with
toxoplasmosis, cryptococcal meningitis, toxoplasmic encephalitis,
Pneumocystis. Kaposi's sarcoma, et cetera.

So stimulated by this explosion of bizarre findings, a group
of our investigators, which included Marcus Conant and Jay Levy, I
think John Ziegler, maybe Paul Volberding, and a number from UCLA

1 Sally Osaki, now retired as Executive Assistant to the Director of
Health, was approached in March 1994 but did not possess minutes. However,
she graciously supplied copies of various documents relating to ex-Mayor
Dianne Feinstein's AIDS activities.

2 M. Gottlieb. Pneumocystis pneumonia- -Los Angeles. Morbidity and
Mortality Weekly Report. June 5, 1981, 30:250-252.

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--Mike Gottlieb was the leader of that group, and I think it
included Ron Mitsuyasu and a few other people—met with Willie
Brown at the airport in Los Angeles and said, "This epidemic is
scary, we need money." Willie answered, "How much?" They said,
"Jeez, we hadn't thought of that." So they came up with maybe a
million or something, and he said, "I'll give you two," and it
ended up with being $1.9 million, if I remember correctly.

Hughes: $2.9 million, I think.1
Sande: Was it? Could be.

Anyway, so Willie went back and got a bill passed in the
legislature—yes, I guess it was $2.9, because it was $3.1 the
next year; I remember that. So that's all fine and good, but the
state of California is not really a granting agency for medical
research. So now you have money to give, who do you give it to
and how do you decide who to give it to, because immediately
you're going to have a lot of people who want it.

The Universitywide Task Force on AIDS

Formation

Sande: So they gave it to the University of California, systemwide, as a
line item in the UC budget. The university said, "Well, we're not
a granting agency. What are we going to do with this money?" So
[UC President] David Gardner, at the suggestion of Julie Krevans,
who was chancellor then, appointed a task force, and I was the
chairman.

Hughes: Why?

Sande: Why? I was in a position of responsibility in the UC system as

head of the Department of Medicine at this hospital, and I was an
infectious disease specialist. Those are probably the reasons
why. I certainly had done nothing to build a reputation that had
anything to do with what we were talking about, although I was
leading the UC effort on AIDS. See, the UCSF Task Force on AIDS
was started before the systemwide task force, and I was the
chairman of that. Krevans, because I was an infectious diseases
specialist, had appointed me to that, so then I'm sure he

1 Shilts, p. 281.

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influenced Gardner to appoint me to the other committee. I
imagine that's what happened.

It was a small group. The first meeting included Mike
Bishop, who immediately resigned, because he saw it as a political
body, not a scientific body. Ira Goldstein took his place.

Hughes: Is that typical of Bishop?

Sande: I don't know. I think Mike saw it as perhaps not a way he wanted
to spend his time.

Then Larry Freedman [M.D.] from UCLA who was head of medicine
at Wadsworth, VA; Jack Stevens [D.V.M., Ph.D.], who was chairman
of microbiology at UCLA- -he's a vet, a wonderful guy--; Abe Braude
[M.D.], who was head of infectious disease at University of
California San Diego; Tom Cesario [M.D.], who is now chairman of
medicine at UC Irvine but was then head of infectious diseases;
and Bob Cardiff [M.D.], who was a pathologist at UC Davis; and
then Dr. Reeves-
Hughes: William.

Sande: Bill Reeves [Ph.D.], yes, who was from Berkeley, an old virologist
who worked on mosquitoes.

Hughes: Encephalitis.1

Sande: Yes. So that was our group.

Hughes: Do you know why those particular people were chosen?

Sande: Because they all had interest in infectious diseases and viruses.
So they felt like they would be able to identify good science.

So we met, and then Bishop resigned, and we appointed
Goldstein as the other member from UCSF other than myself. So we
had two from UCLA, two from UCSF, and one from the other schools.

Hughes: Was this money to go just to UC campuses?

Sande: Originally, it did, because it came to UC. Then after the first
session, we said, "Well, this isn't fair." Actually we never got

1 William C. Reeves, Abrovirologist and Professor. UC Berkeley School
of Health, an oral history conducted in 1990 and 1991 by Sally Smith
Hughes, Regional Oral History Office, The Bancroft Library, University of
California, Berkeley, 1993.

182

credit for this. This is the most amazing, frustrating thing. We
as a group decided that the RFA [Request for Application] should
go out to the other campuses, and specifically to the medical
schools at USC [University of Southern California] and Stanford,
but also Cal Tech, I think.

Hughes: Regardless of whether they were doing AIDS research or not?

Sande: Well, no. All of this money was to go to AIDS research. This was
wonderful money, because it was used to stimulate bright young
people to think about this new disease.

Sande: So it was used to entice people into looking at the problem, good,
young scientists. And it worked; it really worked.

So we then decided to open this up to other campuses, and
recommended to the president to let us do this. The UC
administrator here was Cornelius L. Hopper, from systemwide, a
very nice person who I got to be very good friends with. Well,
the next year when we went to the legislature and made our report
--let me see. The first time I went [1984], I reported on our
progress to Willie Brown in Willie Brown's office with [State
Assemblyman] John Vasconcellos, [Senator] Dave Roberti, [State
Assemblyman Tom] Campbell, and [Assemblyman] Art Torres.

Senator Roberti 's from Hollywood, John Vasconcellos is
chairman of the [California] Assembly Ways and Means Committee and
from Santa Clara, Art Torres is from L.A., and Willie is from
here. I'm not sure if [State Assemblyman William] Filante was
there or not. Anyway, I made this report, and they criticized it.

But then I got in front of the Assembly Ways and Means
Committee, I guess, and Torres lit into me because we kept all the
money at UC. Why were we so stingy and self-serving that we would
just give the money to ourselves? And I said, "Well, Senator, we
have just recommended to the UC president that we open this up as
a statewide competition among all the universities." And he said,
"That's a bunch of baloney. We know you're not doing it."

Anyway, we never got credit for doing it on our own. But he
accused us of only doing it after political pressure was brought
to bear, and that's not correct. But that's the way that it was
written. I got very angry and very flustered at that, my
inability to make him see, but he was a real politician. He was
staging this, I guess. Phil Lee said I behaved very badly at that
meeting. [laughs]

183

Hughes: Because you showed your temper?
Sande: Yes.

Delay in Fund Distribution

Hughes: But there was controversy even before that, I believe. Randy

Shilts wrote about the delay, as he and apparently others saw it,
in the distribution of those Willie Brown funds.1 The bill was
passed in July [1983], and I think the task force first met in
October.

Sande: And we had money going out the next spring. That's the natural
reaction of reporters — it seems so simple to give money away.
It's very difficult to give money away and to be accountable for
the way you decide and how much you give. We thought it was very
important that it was not a political process, but it was a
scientific process. Well, we had money available, and then we had
to send out the announcement; we had to say what it was for; we
had to develop a form; we had to develop a study section to review
the grants when they came in; we had to have a way of deciding
priority scores and who the money should be awarded to and who it
shouldn't.

The criticism came because of course the people who met with
Willie Brown thought they should get the money. But we couldn't
give them the money. That would have been absolutely untenable.
They had to show that they deserved the money, and there had to be
a competition.

Hughes: Would it have made any difference if these had been really senior
people?

Sande: No. They still wouldn't have gotten it. UC was given the

responsibility of being sure this money was spent as well as
possible. It was remarkably speedy. It was the most rapid
process I've ever been associated with, in terms of putting an
organization together, getting out requests for grants, getting
the grants in, reading them, evaluating them outside the political
system, and then awarding them. That that should happen within
eight months was absolutely remarkable, as far as I'm concerned.

1 Randy Shilts, "University Assailed for Delay on AIDS Funds." San
Francisco Chronicle. August 25, 1983, p. A10; Randy Shilts, And the Band
Played On. pp. 357-358.

184

Hughes: The Chronicle quoted Rudi Schmid as saying that the delays and the
university administration's review of requirements were "totally
unacceptable" and "ludicrous".1

Sande: [laughs] Good for Rudi.

Hughes: The article is dated August 25, 1983--before the task force had

met .

Sande: Well, I think the process was a very good one. We actually were

very proud of that process, because it worked very quickly and has
been remarkably free from political influence. What turned Mike
[Bishop] off I think was he felt like his time was going to be
totally wasted, and that political pressure would be very strong
to award the politically astute investigators, and it never was.

Hughes: Did you feel any pressure from Sacramento?

Sande: I didn't. I don't work for them. I'm not dependent upon them. I
think David Gardner did, and I think UC did.

Hughes: How was that expressed?

Sande: Well, the legislature determines the university's budget.

Hughes: Be a little more specific. What would Sacramento have had Gardner
do?

Sande: There were examples where investigators didn't get funded, and
they would go to their legislator, and the legislator would
investigate why, when people are dying of AIDS, didn't we take
every bright idea and fund it. Then if you don't, we'll certainly
be sure that the university's budget is affected by this. Rumors
were perpetuated. The legislature enjoyed looking at distribution
of grants- -who was getting the grants, why weren't more grants
going to Stanford. Actually, that's where I got in trouble,
because when we did open it up, we opened it up late, and Stanford
and USC investigators didn't have very much time to respond to it.
As a result, their grants were not very good, and they didn't get
what some thought was their fair share.

What we tried to point out is that there wasn't such a thing
as a "fair share." It was based upon the quality of the grant
application, bringing in outside reviewers from around the country

1 Randy Shilts, "UC assailed for delay on AIDS funds." San Francisco
Chronicle. August 25, 1983, p.AlO.

185

to review these grants. We had no influence on them ourselves,
because we got other people to review the grants.

Hughes: Leaders in AIDS research were doing the reviews?

Sande: Yes.

Hughes: Was it like an NIH study section?

Sande: It was a study section, and it grew increasingly large and complex
as some more money came in. I'll bet it's up to $100 million now
that the group has given out. I was chairman for five years
[1983-1988]. We put a process into place that I think stood up
very well under political scrutiny. I think that there were
people who were very mad that we just didn't give a lot of money
to certain people who had helped get the money in the first place,
and there will always be some sour grapes over that. But I think
the process worked very well in terms of getting quality science.

Facilitating AIDS Research

Hughes: I saw a letter written in January 1985, which was signed by you

and Robert Cardiff, announcing Jay Levy's virus, and the fact that
it was available to researchers. It struck me as an unusual thing
for a committee to do, which I thought was strictly a funds-
distributing unit.

Sande: Our job was to facilitate research on AIDS, any way we could. So
we did a couple of very creative things. First of all, we created
tissue banks- -John Greenspan runs the one up here at UCSF. There
was one down south at UCLA. We created a central laboratory for
routine assays at Davis, and first of all, it was just the ELISAs
[enzyme -linked immunosorbent assays] for HIV. Then it was more
and more sophisticated assays.

Hughes: Where was the central lab?
Sande: Jim Carlson ran it at UC Davis.

Actually, the task force had complete power. We didn't have
to answer to anybody. In the charter or in the law we had to
report to the Assembly Ways and Means Committee once a year or
something. So we created a tissue bank, created a central
laboratory with Carlson, finally got tremendous fights from
southern California, so we created another lab down there. Then,
we funded two centers, one at UCSF and one at UCLA. We gave

186

blocks of money to these centers to create small grants, local
interest in studying HIV--clinical, basic, whatever.

Hughes: Now, those are the AIDS clinical research centers?
Sande: Yes.

I think our most successful investment was developing a
consortium in southern California that [John A.] McCutchan ran
from San Diego, and it included San Diego, Irvine, USC, and
Stanford. This group of four institutions had been incredibly
productive in doing clinical trials of treatments of AIDS-related
conditions. Unbelievably successful.

Hughes: In what sense?

Sande: Well, they were the first ones to demonstrate that we should use
steroids for Pneumocystis pneumonia. They were the first ones to
test trim [ethoprim] sulfa versus pentamidine and show trim sulfa
was better for prophylaxis—a whole series of very important
observations done with the state money that beat any of the ACTG
[AIDS Clinical Trial Group] or national investments of much more
money. This was a very creative thing.

And then we made reagents available, one of which was Jay
Levy's virus, because Jay was heavily funded by this task force-
never enough, according to Jay.

Hughes: Was it a significant advantage to have a local virus, so to speak?

Sande: I think it was used. All of these things were significant

advantages, I think. The central lab, the tissue banks were
extremely effective. People were encouraged to share, and
basically they did. Some didn't, but most did. There had been a
real problem with Bob Gallo in sharing. That's why we didn't want
to have to face that issue. I actually think we put it in the RFP
that your reagents, after given proper identification and
acknowledgement, could be used by other investigators who were
funded by the statewide task force.

Hughes: But not others?

Sande: Priority was given to funded investigators.

Hughes: My understanding is that by being reluctant to share, Gallo
diverted from the code, that this sharing of reagents and

187

organisms was considered part of the etiquette of science, long
before the AIDS epidemic.1

Sande: Not necessarily. There's no etiquette in science, I don't think.
Basically people are pretty good people, and if you're in it to
push back the frontiers of science, you certainly will share.

Hughes: There was no code that said scientists should share? I don't mean
a written code necessarily, just an understanding among scientists
that you shared.

Sande: I'm not sure.

Hughes: The reason I think that there must have been some sort of

understanding is that Crewdson, the Chicago Tribune journalist who
did an expose of Gallo, contended that Gallo required a form to be
signed before the virus was released from the laboratory. In
fact, in the case of Jay Levy, he just didn't release it, and Don
Francis had trouble obtaining an NIH virus.2

Sande: That's probably hyperbole. What would Francis have done with the
virus anyway?

Hughes: Well, he was working on it.

Sande: He's not a bench scientist.

Hughes: He had been collaborating with the Pasteur Institute.

Sande: But he was an epidemiologist.

Hughes: Yes, but he was also a virologist. He has a D.Sc. in virology.
He worked with Max Essex at Harvard, so he did have some
virological background. One of the things amongst many that CDC
was doing was working on the isolation of the virus.

Sande: Well, among good people, people usually share. But this gave us
an opportunity to make it an official thing. And in general, it
worked out very well.

By the way, the other thing that the task force did that was
creative was every year we had a meeting, and had the research

1 John Crewdson, "The great AIDS quest." Chicago Tribune. November
19, 1989, section 5, p. 9.

2 Crewdson, p. 9; also see the oral histories in this series with
Donald P. Francis and Jay A. Levy.

188

presented. It was really a neat club that was developed to
present the science, to have long discussions, to talk about what
was going on. I thought that was also a big plus. So we
solidified and enticed people into studying HIV in California,
with the money, with the science, with the fraternity, the
camaraderie that developed, the sharing of ideas, the sharing of
reagents. And I think it really worked; it really did.

Hughes: So the annual meeting was a forum for explaining, describing, what
research the state money had supported?

Sande: In a way. But see, nobody else was doing this. Nobody in the

country was doing this. We were already having meetings, showing
that many observations had been made during the last year. So
that went very well. It went very fast. It was way ahead of the
federal government.

Political Clout

Hughes: It seems to me that you were in a position of considerable power
as chairman of the systemwide committee, an advisor to the mayor,
and also head of the UCSF Task Force on AIDS. Did these positions
give you political clout?

Sande: I don't know. I certainly think that we had a direct line to
plead our case for resources for AIDS care at San Francisco
General. And Feinstein was always quite supportive of our needs
to care for AIDS patients. So if political clout is reflected in
terms of resource distribution, I'm sure that did help us. But in
terms of personal power, I don't really know what that means in
this sort of arena. Visibility. We certainly became very famous.
But I'm not sure fame has been followed by fortune. [laughter]
We're still here, we're still doing the same thing we were doing
before. None of us ever tried to use it for political advancement
in any way, shape, or form. I don't think that was ever our
agendas.

Gladstone Institute of Virology and Immunology, San Francisco
General Hospital

Sande: We became very visible nationally. I became president last year

[1992] of the Infectious Disease Society of America, and certainly

189

have had a big influence, I think, on the political process in
AIDS nationally and internationally.

1 guess the one place where my being at a certain place as
chairman of the statewide task force may have influenced something
is when we got the Gladstone building. In a casual conversation
with John Vasconcellos we said, "In looking at how you really
approach a complex problem like HIV, if you get a group of highly
talented, brilliant young scientists who are working in the same
arena, working on the same area, there is synergy between
scientists. So what would make a lot of sense would be to have an
institute basically focused on AIDS research."

At that time, Vasconcellos was chairman of the Assembly Ways
and Means Committee. I was actually chairman of a subcommittee on
research of the Assembly Ways and Means Committee; there was a
small group of us. So I proposed that what they should do is
build a building for basic AIDS research. That's what was needed.
And then I half-kiddingly said, "And I think San Francisco General
would be a great place to have that."

Well, Vasconcellos said that was a big joke, but he would put
it on his wish list. That year he had, I think, twenty-one things
that came out of the Assembly Ways and Means Committee for
Deukmejian, the governor, to either approve or disapprove.
Historically, Deukmejian had vetoed all of them. So there was a
wish list of twenty-one things, and mine was on the bottom.

Julie Krevans got David Gardner to call the governor's
office, saying that for the city of San Francisco, not the
university, to build a building for AIDS research was a great
idea.

Hughes: Why are you emphasizing the city?

Sande: Because if the money had gone to UC, it would have been on the UC
priority list, where there are probably thirty different
priorities for buildings in the whole UC system. It would have
been a difficult task to work that through this priority list of
capital projects. But by going directly to the city to build at
San Francisco General, the university could run it, and the city
could build it, and the building could be a city building.

So we got Feinstein to politic Willie Brown; we got Krevans
and Gardner to politic the governor; I politicked Vasconcellos--
convinced him it was a good idea. To the surprise of many in
Sacramento, the governor signed it. [laughter] And that's how I
think we got this building. We forgot to ask for operating

190

expenses. Well, we wouldn't have gotten them. We promised not to
ask for them when we testified before one of the other committees.

Then Mary Pitman, who's an absolute genius—she was president
of the California Public Health Hospital Association, and now is
back working at the national level in Chicago—sort of was
responsible for seeing once the bill was signed that it didn't get
clobbered by staff in these various places.

Hughes: What was her position then?

Sande: She was with the health department here in San Francisco. So now
it became a health department issue, because they got the money.

Hughes: I was going to ask why a basic science institute was located at
San Francisco General. There was never a chance of it going to
Parnassus [UCSF]?

Sande: Oh, no.

Hughes: Which is a big thing!

Sande: Incredibly important for this institution, absolutely. Then to
have hired Warner Greene to run it was absolutely phenomenal.

Hughes: UCSF is the basic science campus, and SFGH is the applied clinical
science campus.

Sande: Not any more. I don't think so. I think we have built basic
science down here now to a position of really international
eminence. We have the Rice Liver Laboratories, the Lung Biology
Center, the Gallo Research Center for Neurology. We have the
Infectious Disease Laboratories, we have the two Gladstone
institutes— it ' s an absolutely incredible institute now.

Hughes: Does this cause tensions with UCSF?

Sande: Sure. Well, we are UCSF. Parnassus is a part of UCSF, just like
we're a part of UCSF.

Hughes: [laughs] They'd love to hear you put it that way.
Sande: I do it all the time.

191

Delayed Federal Funding

Hughes: Do you want to say something on the subject of federal money?

Sande: Not really. [laughter] I didn't have much to do with it until I
got put on the council of NIAID [National Institute of Allergy and
Infectious Diseases].1

Hughes: I was thinking of the earlier period when some people contend that
federal money for AIDS research was very slow in coming. Did you
feel that, and if so, why?

Sande: I don't know why it was. It was slow in coming. And when it

came, because of the state investment in AIDS research here, our
investigators were right at the front edge of being competitive
for those grants. They still are. I mean, everybody out here
really were in a strong negotiating position.

The San Francisco Model of AIDS Care

Hughes: Well, let's turn to the so-called San Francisco model of AIDS
care. Could you define it in your own words?

Sande: [laughs] I don't even know what it is any more. I think that

what is unique about San Francisco is the gay community, and the
incredible outreach—reaching out—that went on between members of
the community. This led to an awful lot of unsolicited support
systems that emerged and developed: the Shanti Project, the AIDS
Foundation, hospice care, and everything. So when you're faced
with treating a lethal disease like a malignancy, where would you
want that care to take place? You'd like to have that care take
place where there's a minimum of trauma, where there's a maximum
of comfort for the patient.

So using community-based support systems, using the
outpatient department as the major generator of delivery of acute
medical care, minimizing inpatient stays, only putting patients in
the hospital when they can't function in these areas--

1 Sande was a member of the National Advisory Allergy and Infectious
Diseases Council from 1987 to 1991.

192

Sande: --became the San Francisco model. And it was sort of a marriage
between the mayor, the city department of health, with their
resources, our inpatient ward, our outpatient clinic, and these
multiple support systems. It also allowed a lot of clinical
investigation to occur. In a disease where you don't know the
answers, where there is no obvious cure, there's a tremendous
incentive for patients to want to go where they're doing clinical
trials, because one of those things that they're studying might be
the cure, might be the answer. So that made us very attractive
for patient care. So that's my explanation.

Hughes: How successfully has the model been translated elsewhere?

Sande: Well, where there are resources and where there are good community
services, it has been successful. But not very well in New York.
Not very well in the big cities where this is a different disease
completely.

Hughes: If the gay community is an important ingredient of this model, it
has implications for other cities, but maybe also for San
Francisco eventually, since the face of the epidemic is changing.

Sande: We're seeing that here, too.

Hughes: Do you have any predictions about how the model would translate as
the risk groups change?

Sande: Not as well.

Hughes: Is there anything that you can do about that now?

Sande: I'm not sure what's being done on that, because I'm not quite as
close to it as I used to be. But as AIDS goes into the
underserved portions of the population, I think we're doing a
fairly good job in our primary care networks, in the city clinics,
at reaching out to those people. But the problem is then, you
don't have the manpower, the personpower, that you have when you
have this whole group of people committing large blocks of their
daily life to caring for others. And that's what the gay
community really does, and did, maybe even more than they do now;
it's been fairly decimated. But there's really just an outpouring
of commitment. That's what probably made it more possible than
resource allocation or clinics that you pay people to work in. It
was the volunteer work that was particularly important.

193
Burnout

Hughes: I've detected a similar commitment amongst the physicians, that

the rest of life was put on hold, so to speak. Does that fit what
you remember of those early years?

Sande: Yes. That's why there's a lot of burnout.

Hughes: Why was there such willingness to turn personal lives upside down?

Sande: Well, a lot of the physicians involved were, and still are, gay

physicians, and a large number of these highly committed- -but not
all of them. Others were just committed because they were caught
up in an incredibly depressing situation.

Hughes: Was there also a feeling of "us against the epidemic," that a
battle was being waged, and they had to stick with it?

Sande: I think so. And I think that helps to explain the [County)
Community Consortium, which Donald Abrams runs. He brought
together seventy to 100 physicians in San Francisco who cared for
AIDS patients to do clinical trials. I think there is a
tremendous sense of camaraderie and esprit de corps among that
group. And these are guys who are doing most of the AIDS care in
the city, and who do have a lot of burnout. So this consortium
has been a resource for them to share their miseries and share
their successes, and help bond together to do clinical trials, or
help solve the epidemic, in a little way, shape, or form.

Hughes: Are there also more formal ways of dealing with burnout,
specifically here at the hospital?

Sande: Here, there are support groups. They meet on a weekly basis to
talk about patients, talk about their own problems. That's been
handled quite well. I think Paul has done a great job in
organizing the clinic, and he's had really good people to run it-
Michael Clement, who's gone into practice over in Oakland, and now
John Stansell.

More on the Relationship between the AIDS Clinic and Ward. SFGH

Hughes: Talk more about the relationship between the clinic and the ward,
and the tensions that must have arisen, and probably still do.

194

Sande: There were tensions because there was a lack of communication.

Typically, the clinic would start running down at four-thirty on a
Friday afternoon, and they'd have all these really pretty sick
people who hadn't been seen. So the natural tendency was to want
to admit them over the weekend to tune them up a little bit. And
initially there was not much communication between the providers
in the clinic and housestaff, and the attendings here on the
wards. It was really because of that need that Paul and I hired
Michael Clement.

Hughes: Who was to serve as a liaison?

Sande: He was the communicator. His job was to communicate between the

clinic and the ward, to bridge the gap, and he did it beautifully,
just beautifully. He is a gay physician who came from Portland
[Oregon] with training in internal medicine, and has an absolutely
winning personality. I wonder what year we hired him? I would
think '86 or '87. Then he became head of the clinic after that,
and then he gave it up to John Stansell.

We get consultations on all the AIDS patients by this
"service," in quotes, of AIDS docs who are on 5A, who are the link
to the outpatient clinic. That was a very important thing, to do
that, because that really dissolved the tensions that we had
because of lack of communication. That worked beautifully; one of
the few things that's really worked well.

Patient Care

Hughes: Is there anything to be said about the evolution of patient care?
How did patients experience their suffering and how did the staff
respond?

Sande: I don't think I am close enough to say now. I'm probably the
wrong person to ask.

Hughes: I'll ask Connie Wofsy.

Sande: Connie might be good. Maybe people like Lorrie Kaplan, John
Stansell.

Hughes: You used to deal routinely with AIDS patients?

Sande: I have never had an outpatient practice in the clinics here. I've
always dealt with them on the wards. So on a daily basis, I have
not been as close to the actual care of AIDS patients as the

195

people that work for me . I hear about it here every morning at
report, when inpatients are presented to the other residents, the
assistant chief, and myself. I see them on the wards. I attend
like I am doing right now in infectious disease when I take care
of them. But that's why it's just great when I get up in front of
a large group of people and say, "This is the way we treat these
things," and all the people in the audience who really know sort
of snicker and say, "Baloney." [laughter] So that's my true
confession.

The Epidemic's Effect on Medical Education

Hughes: How has the epidemic changed American medicine?

Sande: That's too broad a question, but let me focus on one part of it
that I am particularly involved in or sensitive to, and that is
how it has changed medical education. I think it's actually been
very good for the focus and the way we train young doctors. I
have a perception, beginning when I was in training, that we got
increasingly enamored with technology, with our ability to put in
pacemakers and EKGs all the time in the wards, and document the
pathophysiology of the arrhythmia and all these sorts of things.
We worked very, very hard for our patients, and a death was a
terrible failure.

And what's happened with AIDS is we [physicians] have come to
realize that this is a dying population, this is a dying patient.
But then we're all in the process of dying. So I think we have
become much more sensitive to quality-of-life issues, of dealing
with the human part of the patient. I think it's brought the art
of medicine back into our medical education process. The idea of
orchestrating a good death, which would have been an oxymoron in
my days of training, has now become a real endpoint. And if we
can teach our physicians to consider a death of a patient who is
at peace, whose estate has been handled, who dies without pain,
who dies without loneliness, as a major success, as an A+, then we
have made a tremendous impact and a positive statement. And I
think that's what AIDS has done to us.

I think it's brought us face to face with our own personal--
that's not the right word- -we are very mortal. We are able to do
only so much. It has, I think, helped our reality testing and how
much we can do and how well we can do it . I think that ' s very
important. I think we've become more sensitive, more concerned
about the patient as a patient and not as a test tube. I think
that's good. So I think AIDS has had a major impact on that.

196

Hughes: You're speaking in a broader sense than impact strictly on AIDS
medicine?

Sande: Yes. I think it spills over to everything. That's why I think
taking care of AIDS patients for housestaff is a very, very
important and rewarding experience from that standpoint.

Hughes: Is it a hard orientation for a medical student or an intern or

resident to adopt, because that isn't, as you've been saying, the
thrust of medical education?

Sande: I think it's happened. No, I don't think it's difficult. I think
from the very beginning they are learning the limitations of their
own abilities to positively alter these processes.

Physician-Patient Relationships

Hughes: Do you want to say anything specifically about the impact of the
epidemic on the physician-patient relationship?

Sande: I think there are tremendous personal rewards for physicians who
care for AIDS patients. This is not what the general perception
has been. But I think if you have the attitude that you can
significantly affect the quality of life of the AIDS patient, and
that you focus on that, that there will be tremendous rewards for
the individual physician.

Now, this is where it gets very tricky in terms of the
changing patient population. In this hospital, when we took a
survey about four or five years ago, "What are the patients you
most like taking care of?," it was the AIDS patient as number one.
Not what you would have predicted, but that's true. Because in
our hospital it tended to be an intelligent, communicative,
thankful patient population that brought that feeling of thanks to
the house officer.

Now—this might sound bad—because of the nature of the
intravenous drug user, the hardened addict who contracts AIDS,
that population tends not to be as thankful, pass along those
feelings to the house officer. Now, that's a generalization, and
they're always dangerous, but in general, I think that's probably
true. So that may alter the dynamics to a certain extent.

Hughes: Has your engagement in the epidemic meant more than just a series
of medical and scientific problems?

197

Sande: Yes, I think I've just articulated that. I think it's made us

better doctors in the traditional sense of the word. That is an
area that has not received enough play, enough visibility, enough
publicity. This maturity, this learning one's limitations and
learning one's mortality has been a very important issue.

Failure to Move AIDS Science to the Bedside

Sande: 1 think it's done another thing. I recently chaired a consensus

committee back in the NIH in Washington on antiretroviral therapy,
which was published in JAMA a couple of weeks ago.1

Hughes: Yes, I saw that.

Sande: This is hard to say correctly—but among basic scientists who are
really good, who are really creative and tough, hard-nosed
scientists, there is an obvious arrogance. And you know what I
mean.

Hughes: Yes.

Sande: If there has ever been a disease that should destroy that

arrogance, it's AIDS. Because while we have gained incredible
insight into how the virus works, incredible insight into the
molecular biology and how the regulatory genes create, and how the
immune system turns on, how the signalling happens, that has
essentially in no way, shape, or form, been translated to the
bedside. There is a tremendous gap.

In fact, I was just quoted in the New York Times about three
or four weeks ago by a fellow who died of AIDS who was the
reporter for the New York Times . He interviewed me last summer,
and I was talking about this. He said- -that was my quote, and I
loved it, because it's so true—that we're in an in-between phase
between the generation of the scientific information and the
translation to the benefit of the patients. Vaccines haven't
worked; therapy hasn't worked very well.

1 M. A. Sande, C. C. J. Carpenter, et al. Antiretroviral therapy for
adult HIV-infected patients. Recommendations from a state-of-the-art
conference. Journal of the American Medical Association 1983, 270, 121,
2583-2589. See also: Lawrence K. Altman, Government panel on H.I.V. finds
the prospect for treatment bleak. New York Times. June 29, 1995, p. 63.

198

The most important single observation is one that Margaret
Fischl made where she started using trimethoprim sulfa
prophylactically against Pneumocystis . That's probably given more
prolongation of life than any of the multi-millions of dollars
that have been spent on AIDS. So there should be an honest self-
evaluation by these brilliant people.

Hughes: Humility, maybe.

Sande: Humility! Humility was the word I was looking for. That was the
word I used. There should be a tremendous humility emerging in
our basic science community in terms of their inability to make
significant progress in translating the basic science information
to the clinical arena.

Hughes: Has there ever been an instance in the history of infectious
disease where so much of the science was known and so little
clinical application?

Sande: That's an interesting question. I guess one area might be
malaria. There's been a series of failures in vaccine
development. I think polio worked, but polio is a simple virus.

The Media

Hughes: Do you want to say something about the media's role in this
epidemic?

Sande: There were the good guys and the bad guys. [laughter] My hero

and very close friend is Larry Altman, who I talk to a lot. He's
got his hangups, like peer review, but he really has handled
himself very admirably and some day should be rewarded for his
reporting of this epidemic.

Hughes: In terms of what qualities?

Sande: Interesting question. He is precise and accurate to a fault, very
thorough, very searching comments, searching journalism. Why is
it, why doesn't this work? He was so taken by the observation
that three drugs in a test tube worked, killed the virus, because
the final mutation necessary for emergence of resistance to the
last drug was a lethal one. This was the thing that Marty Hirsch
reported. Larry was so taken by that, and then he started to hear
rumors that there was problems with it. And then other people
couldn't confirm it.

199

And then it turned out that they didn't use the right
controls. Larry kept probing: "What happened? Why did this
happen?" They finally admitted that they just didn't use the
right control. Marty came across and said, "I'm sorry; I made a
mistake." And it was dropped.

Hughes: Did Altman speed that process along?

Sande: I think so. He is a hero of mine because he is totally honest, to
a fault, as I read him. I've known him since 1969, I guess.

Hughes: What do you mean by "honest to a fault"?

Sande: He's a guy who I think has no other ambition in life than to be a
reporter and to seek the truth. He traveled through Africa before
any of the African nations would agree they had AIDS, and he
reported on it. He became persona non grata, at some great
personal risk to his own life. He just pushed, pushed, probing,
probing, probing. I just love him. I read him all the time.

Hughes: You're saying that he does not bend stories for political ends?
He reports as he sees it?

Sande: As he sees it. And he doesn't exploit the sensationalism, like
others do. What I admire about him is his honesty, the way he
probes.

Hughes: You have been pulled into the political process in a disease which
probably is the most political that has ever existed. How do you
feel about that politicization?

Sande: Well, I guess it's a two-edged sword. The money to study the

disease comes from the political process. Without the advocate
groups, without the political pressures put on, there never would
have been this much money this quickly, even though we all say it
was too slow. So in a way, the political process has been a very
positive process for trying to find solutions to a very
complicated problem. I was amazed at the testimony by the
advocacy groups before this committee that I ran in Washington.
They just flip-flopped totally, 180 degrees, about placebo
controls. What they're saying now is that, "We want the truth.
Do the drugs work or don't they work? We want the truth."

Before, they were saying, "Study all the drugs. We want to
be part of your studies. We want to get the drugs. We don't want
placebos; we just want the drugs." There's been a total change in
that mentality. Now they realize that uncontrolled trials have
given—bad science gives bad results, gives bad answers, gives
inconclusive answers. What we were faced with in writing this

200

consensus report is that a lot of the trials didn't answer the
questions. Now they're saying, "We want the answers." But you
can't fault the advocacy groups, because particularly back then,
they were hoping for a quick cure, a quick solution.

Hughes: One of the main messages of that paper was that there aren't any

fixed answers. It's not even certain when treatment should begin,
if at all.

Sande: That's true.

Hughes: So that's an evolution in medical thinking about AIDS therapy,
right? AIDS physicians as a group used to be quite doctrinaire
about early intervention.

Sande: We wanted simple answers to complex problems.

Sande ' s Contributions ##

Hughes: What do you consider your greatest contribution to the epidemic?

Sande: Hmm. I guess as the facilitator of development of this

institution to the national prominence that we've achieved. Which
is what my job is. I mean, that's what I was hired to do, to try
to bring this place into national prominence. I don't think I
could have done it without AIDS. I think that AIDS was a vehicle
--it's a crass way of saying it--it was an opportunity for
somebody with my background in infectious diseases to take hold of
it and run with it. I didn't do any of these things myself. I
was the facilitator. I was the person who made it happen through
other people.

My own contribution in a more personal way is as a
communicator, as a person who tried to produce for the practicing
physician or for the public, a comprehensive view and
understanding of what the scientists were saying. So I look at
myself as an interpreter of the science for the clinician. That's
why our AIDS book has done well.1 We felt it was important that
doctors knew how to care for AIDS patients, and if we were able to
show them what the real pros were doing, communicate that to them,
that they would feel comfortable in caring for AIDS patients and

1 The Medical management of AIDS. M. A. Sande and P. A. Volberding,
eds. Philadelphia: W. B. Sanders Co., 3rd Ed., 1992.

201

they wouldn't fear them. So I guess those two things I consider
to be my contributions.

I've enjoyed writing papers on new clinical descriptions of
AIDS with my chief residents over the years. We had a lot of good
publications in the New England Journal [of Medicine] . Some have
been greatly criticized. We've had this incredible patient
population, and I think we have maximized the use of it for
scientific development.

Hughes: Do you look upon the hospital's standing as the leading AIDS

hospital in the country as an affirmation of your ambitions for
the institution?

Sande: Yes, I think so. I think that it took a lot of people to do that,
and I was only part of the picture. I hired good people and I
supported them. I hope that I let them grow and develop without
any hindrance, which I think is tough to do sometimes. I would
hope one of my personality traits that has allowed me to do that
is that I'm secure enough that I don't need to get in the way. So
I can derive tremendous personal satisfaction in seeing people
develop and emerge, and in helping them and guiding them and
supporting them when they need support, and thrashing them when
they need to be thrashed.

That's what the role of chairman of medicine should be, I
think. I try to emulate other people that have trained me and
I've worked with. What I think I'm proudest of is to see these
people develop. That's why I love this course [Clinical Care of
the AIDS Patient] that we just had in December, three days, 600
physicians from all over the country come to hear our people.
Ninety percent of the program was [made up of] people from San
Francisco General Hospital and UC. It's really neat. It's a
showcase of our accomplishments.

Hughes: Well, I thank you.

Transcribed and Final Typed by Shannon Page

Regional Oral History Office University of California

The Bancroft Library Berkeley, California

The San Francisco AIDS Oral History Series

THE AIDS EPIDEMIC IN SAN FRANCISCO: THE MEDICAL RESPONSE, 1981-1984

Volume IV

John L. Ziegler, M.D., Ph.D.

ONCOLOGIST: KAPOSI'S SARCOMA AND AIDS RESEARCH IN
SAN FRANCISCO AND GLOBALLY

Interviews Conducted by

Sally Smith Hughes

in 1994

John L. Ziegler, 1988,

Photograph by David Powers

Interview History—by Sally Smith Hughes, Ph.D.

John Ziegler, a physician and oncologist, was the most senior clinical
scientist of the faculty members at UCSF and San Francisco General Hospital
[SFGH] who in the summer of 1981 became involved in the epidemic of immune
deficiency, later christened AIDS, which was just being recognized in gay
men in San Francisco, Los Angeles, and New York City. Ziegler arrived in
San Francisco in August 1981 to assume positions as Associate Chief of Staff
at the Veterans Affairs Medical Center in San Francisco and as Professor of
Medicine at UCSF. By then, he had accumulated almost fifteen years of
experience in cancer research and treatment at the National Cancer Institute
[NCI] of the National Institutes of Health. Ziegler 's career-long interest
was in the lymphomas and Kaposi's sarcoma, forms of cancer which he had
studied not only at the NCI but also on a five-year sojourn in Africa as an
NCI Senior Investigator.

As Ziegler recounts in his oral history, within days of his arrival in
San Francisco, he heard of cases of Kaposi's sarcoma occurring in young
patients being treated at the university. He was immediately interested,
especially since Kaposi's in the West is usually found in elderly men or
patients immunosuppressed by chemo- or radiotherapy. These patients fell
into neither category. He consulted Paul Volberding and Marcus Conant,
physicians seeing these patients, and attended the first meeting of the
Kaposi's Sarcoma Study Group at UCSF, which the two physicians co-directed.
As Ziegler explains in his oral history:

We put our heads together and we first of all figured out that
we needed some funds to get started studying this epidemic of
Kaposi's sarcoma. There was no money, and the university really
wasn't coming up with anything at that time, because nobody knew
what [the epidemic] was and whether it was worth pursuing.

With the advantage of his reputation and professional contacts in the
cancer field, Ziegler orchestrated what most likely was the first grant
awarded anywhere for AIDS activities. The $50,000 received from the
American Cancer Society on November 1, 1981 supported a nurse-coordinator
for the Kaposi's Sarcoma Clinic at UCSF.

Six months into the epidemic, Ziegler began to notice the occurrence
in AIDS patients of a second type of cancer. In 1982, he and his San
Francisco colleagues published a paper on "Burkitt ' s-like lymphoma in
homosexual men," which constituted the first report of the association of
malignant lymphoma with AIDS. However, it took two years, a more extensive
study (which Ziegler coordinated), and a publication in the prestigious New
England Journal of Medicine to persuade the CDC to include lymphoma on its
list of AIDS-defining conditions.

Among the other topics which Ziegler discusses are the many hypotheses
about AIDS etiology circulating in the early days, speculation that was more
or less settled in 1984 when the U.S. Secretary of Health officially
announced the isolation of a virus, later named the human immunodeficiency
virus or HIV.

The Oral History Process

Two interviews were conducted with Dr. Ziegler, a man distinguished in
appearance and address, on January 28 and February 16, 1994, in his
unpretentious office in the Nursing Home at the Veterans Administration
Medical Center. The sessions were hastily scheduled so that they could be
concluded before Dr. Ziegler 's departure for sabbatical leave in Africa,
where he was returning to pursue a new theory about the cause of an
indigenous form of Kaposi's sarcoma. The interviews were abetted by
research in Ziegler 's papers, which have since been transferred from the VA
to the AIDS History Project Archives at UCSF Library. A short telephone
interview conducted with Ziegler in 1990 by the NIH Historical Office served
as orientation to some of the features of Ziegler 's AIDS efforts.1
Articulate and thoughtful, Dr. Ziegler was an apt and engaged subject. The
edited transcripts were sent to Africa for his review and returned with
minor corrections and additions.

This is the oral history of a man who because of his position as a
full professor and his long experience and solid reputation in academic
oncology—he is a recipient of the prestigious Lasker Award ( 1972) --added
weight and substance to the initial group of UC AIDS researchers. Young,
inexperienced, and handicapped by the stigma associated with AIDS, they
benefited from Ziegler 's standing in the eyes of colleagues and funding
agencies.

But AIDS work also changed Ziegler. He describes how as co-chairman
of the Sixth International Conference on AIDS, meeting in San Francisco in
1990, he joined the activists in protesting the Bush administration's dictum
that conference attendees from abroad be tested for HIV. "In the end, when
we joined hands with the AIDS activists and walked down Market Street [in
downtown San Francisco], it was the first time in my life I had ever taken
to the streets for a cause. And I must say, my heart was in it by that
point."

Sally Smith Hughes, Ph.D.
Research Historian

Regional Oral History Office
April 1997

1 I thank Victoria Harden, Ph.D., director of the NIH Historical Office,
for arranging to send the transcript of the telephone interview conducted with
Ziegler on January 5, 1990.

Regional Oral History Office University of California

Room 486 The Bancroft Library Berkeley, California 94720

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202

I EDUCATION AND EARLY CAREER
[Interview 1: January 28, 1994] II1
Medical Training. 1960-1966

Hughes: Dr. Ziegler, please start with your education and early career.

Ziegler: All right. My involvement with the AIDS epidemic really does

begin way back. I went to Cornell Medical School [1960-1964] and
Bellevue Hospital [New York, 1964-1966], where I did my training.
I think training in Bellevue Hospital gives you a taste of what
third-world medicine must be like, because of the deprivation and
the poverty and the problems with indigent patients. Then I went
to the NIH, the National Cancer Institute, where I was inducted
in 1966 with many other doctors who wanted to do research and not
go to Vietnam. So I ended up in the Public Health Service.

I had encountered a patient with Burkitt's lymphoma when I
was training at Memorial Hospital in New York. Burkitt's
lymphoma is an unusual childhood cancer that was reported by
Denis Burkitt in Africa in the early sixties, and it was a
fascinating problem from many points of view, but one of the most
interesting facets was that this tumor could be cured by
chemotherapy.

'If This symbol indicates that a tape or tape segment has begun or
ended. A guide to the tapes follows the transcript.

203

Clinical Associate. Medicine Branch. National Cancer Institute.
1966-1967

Ziegler: So when I arrived at the National Cancer Institute as a young
associate in 1966, they asked me if I had special interests in
certain kinds of cancer, and my response was that I was very
interested in Burkitt's lymphoma, because of the unusual cure
rates and the fact that I had encountered a patient at Memorial
Hospital. So one thing led to another, and I was asked to look
into the possibility of setting up a small cancer treatment unit
in Uganda, funded by the National Cancer Institute. The first
year, I worked with Dr. Paul Carbone, Dr. [Vincent] Devita, and
Dr. Zubrod at NIH, and Dr. Burchenal from Memorial Hospital. All
of these men were pioneers in cancer chemotherapy. They were all
very interested in why Burkitt's lymphoma was curable.

Director, Uganda Cancer Institute, Makerere University Medical
School, Kampala, Uganda. 1967-1972

Ziegler: To make a long story short, the project was approved, I went to

Uganda in 1967 with my family, and worked there for five years on
Burkitt's lymphoma (this childhood tumor that is curable). Along
the way I became interested in another indigenous African tumor
called Kaposi's sarcoma. Now, this is a tumor that's exceedingly
rare in developed countries and the West, but in Uganda comprised
nearly 8 or 9 percent of the adult malignancies. So it was a
very common tumor. For the five years from "67 to "72, I and
many colleagues from the National Cancer Institute and elsewhere
worked on these indigenous African tumors. Other tumors that
were interesting there were liver cancer, melanoma, malignant
melanoma, and other childhood cancers.

Hughes: In much greater prevalence than here?

Ziegler: Much greater prevalence, yes. Liver cancer, for example,

accounts for half of the malignancies in many African countries.

The other interesting thing about this group of malignancies
was that they were becoming more and more related to viruses.
Burkitt's lymphoma was linked with the Epstein-Barr virus, a
virus that we now know causes infectious mononucleosis. It's
also linked with several other forms of cancer. And liver
cancer, of course, is linked with the hepatitis viruses. And we
thought Kaposi's sarcoma [KS] at the time might be linked with a
virus, but nobody could figure out which one. There was some

204

suggestion that it might be cytomegalovirus, one of the other
[herpes] viruses.

Hughes: Why did you think that in the first place?

Ziegler: Well, because Kaposi's sarcoma is clustered in certain parts of
Africa. It occurs in generally high, wet areas, not in low, dry
areas. It was spotty in the country where I was working, for
example; more than two-thirds of the cases came from the western
side of Uganda. So there were some geographical peculiarities
which we couldn't figure out. But in the end, after five years
in Africa, my career had really centered on the indigenous tumors
of tropical countries, and I wrote quite a few papers about that.

Then I left. Idi Amin came to power in Uganda in 1971, and
he was, as everybody I think knows, a real tyrant and plunged the
country into a desperate economic situation which resulted in a
civil war lasting all the way up until 1986. After I left
Africa, I kept up with my colleagues there. Fortunately, we had
trained a number of Ugandans who took over and kept up the
research that we had started in an institute called the Uganda
Cancer Institute, which is still running today.

Return to the National Cancer Institute. 1972-1980

Ziegler: I went back to the National Institutes of Health, to the National
Cancer Institute, took several positions there leading various
groups--f irst , pediatric oncology [1972-1975] and later clinical
oncology [1975-1980].

Associate Chief of Staff for Education, Veterans Administration
Medical Center, and Professor of Medicine. University of
California, San Francisco, 1981-present

Ziegler: In 1981, I was invited out to San Francisco to take over a job as
associate chief of staff for education here at the VA, and also
to become professor of medicine at UCSF.

Hughes: How did that come about?

Ziegler: I had been at the NIH for about fifteen years, and I was ready
for a career change. My former professor of medicine, Marvin
Schlesinger, who's still here, found me and invited me to come

205

out and look at a job here at the VA.
down.

It was too good to turn

Hughes: Did they want a research-oriented person?

Ziegler: Well, they were starting an oncology division here; they wanted
some help with oncology. I had a great interest in medical
education. I had doubled my salary, and there were a lot of good
reasons for coming here. I had remarried, and my wife [Rue] also
was very interested in coming to the Bay Area, where her children
were. So there were personal and professional reasons for
coming .

206

II THE AIDS EPIDEMIC

Kaposi's Sarcoma in Gay Men

Ziegler: In the end, I arrived here in August of 1981, and I hadn't been

on the campus but maybe a day when I got a call from somebody who
said, "You know, there's a doctor down at San Francisco General
[Hospital, SFGH] who's seeing a lot of cases of Kaposi's sarcoma,
and we know you've done some work in it. Maybe you could get
together." So I got together with Paul Volberding and Marcus
Conant. Within weeks of my arriving, we had figured out that
Kaposi's sarcoma was appearing in gay men for unexplained
reasons, and that there was an associated immune defect in these
patients. We put our heads together, along with John Greenspan
and Donald Abrams and Art Ammann and quite a few other UC people.

Hughes: Had you seen the article in the MMWR [Morbidity and Mortality
Weekly Report]?1

Ziegler: Yes, 1 had known about that. In fact, the first I knew about it
was in the New York Times,2 which had published a small piece
about Kaposi's sarcoma in gay men.

1 Centers for Disease Control. Kaposi's sarcoma and Pneumocystis
pneumonia among homosexual men- -New York City and California. Morbidity
and Mortality Weekly Report 1981, 30, #25:305-307 (July 3, 1981).

2 L. K. Altman. Rare cancer seen in 41 homosexuals. New York Times .
July 3, 1981, p. A20.

207
NCI and CDC Workshop on Kaposi's Sarcoma, September 15, 1981

Ziegler: About a week after that, I was called by Bruce Chabner who was
then the head of the Division of Cancer Treatment [at the
National Cancer Institute], because he knew I had known about
Kaposi's sarcoma, and said, "We're having a meeting at the
National Cancer Institute in September [1981], could you come?
We want to have discussions about this thing." This was probably
the first multidisciplinary workshop on what was to become the
AIDS epidemic.

Hughes: Did it make any difference that the cancer aspect of the disease
seemed to come to the attention of NIH first? Was the epidemic
at first under the auspices of NCI?

Ziegler: Yes. In fact, one of the things in my CV, you may have noticed,
is a report of that workshop, which is in The Journal of the
National Cancer Institute.' That piece shows how naive we were
at the end of the workshop; we hadn't a clue what was going on,
not a clue. There were all kinds of guesses as to what Kaposi's
was about. But you're right: The cancer caught people's
attention. Then the infectious disease people quickly came in
when they saw the Pneumocystis cases rising, and the cryptococcal
disease and toxoplasmosis and all of the other opportunists.

Hughes: I remember from that paper that you came up with a staging

system. But something else I read of yours gave me the idea that
it was very difficult to stage KS.

Ziegler: It was, and it still is very difficult. It doesn't behave like
the usual cancers in stage I, II, to III because it occurs in
many places simultaneously. Most cancers start, for example, in
the breast; they move to the lymph node; they move to the bone
and the brain. So they march along in an orderly way. Kaposi's
doesn't. And it doesn't necessarily spread in a particular way.

Hughes: Didn't you say everything telescoped in AIDS patients? That
everything was moving much faster?

Ziegler: Yes, that's exactly right.

Hughes: How useful was the staging system that you came up with at the
end of the workshop?

1 J. L. Ziegler. Kaposi's sarcoma in homosexual men. Journal of the
National Cancer Institute 1982, 68:337-338.

208

Ziegler: Well, probably no less helpful than it is now. [laughs] There
have been about eight different staging systems since then. But
I think it all comes down to a couple of things: where Kaposi's
appears and how it is spread is probably more a matter of what
causes Kaposi's rather than any kind of intrinsic nature of the
tumor. And also, of course, the host immune defense; people who
have very bad immunity can have very widespread disease.

Raising Funds

Kaposi's Sarcoma Study Group

Hughes: Tell me about the Kaposi's Sarcoma Study Group which met at UCSF.

Ziegler: We started right away getting together and meeting in September
[1981].

Hughes: Were you at the first meeting?

Ziegler: Oh, yes. Marcus Conant, I think, was probably the main leader,

and Paul Volberding at the General [SFGH], and myself here at the
VA, were the three principals. We put our heads together, and we
first of all figured out we needed some funds to get started
studying this epidemic of Kaposi's sarcoma. There was no money,
and the university really wasn't coming up with anything at that
time, because nobody knew what [the epidemic] was and whether it
was worth pursuing.

The American Cancer Society Grant, November 1, 1981

Hughes: Had you explored getting university funds?

Ziegler: No, we actually hadn't at that time, because the university

didn't have any particular pot of money with which to do this. I
called an old friend of mine, the late Dick [Frank J.] Rauscher,
[Jr.] who was the senior vice president for research in the
American Cancer Society. I explained to him that we were seeing
a kind of epidemic of Kaposi's sarcoma here in gay men, and could
we apply for what they call a research development award, which

209

would have a very quick turnaround, and would award money for
research in a matter of weeks.1

So Marcus and myself and others put together a protocol with
myself as the principal investigator. We sent it to Dick
Rauscher, and within a week he called to say, "$50,000 for a
Kaposi's sarcoma clinic." And I think I would have to say,
unquestionably, that's the first grant for AIDS in the United
States, because the grant was awarded I think November 1, 1981.

So with that $50,000, we immediately hired a research nurse.
Hughes: Was that Helen Schietinger?

Ziegler: Yes, Helen Schietinger. Who's still in the business, and is an
AIDS consultant now in Washington.

The National Cancer Institute Grant, May, 1983

Ziegler: So we started the clinic. Helen immediately saw the magnitude of
the problem. We began to look elsewhere to see if we could get
additional funding, and we approached the National Cancer
Institute, and they responded.2 We put in for a grant that would
cover the expenses of the clinic plus some additional research.
By that time, Andrew Moss had joined the team, and was very
interested in looking at the epidemiology.

See Ziegler to Rauscher, September 23, 1981. (Ziegler papers

folder: AIDS-NCS grant, library, AIDS Resources Program Archives, UCSF.)

2 Request for Cooperative Agreements Applications: RFA. Studies of
acquired immune-deficiency syndrome (Kaposi's sarcoma and opportunistic
infections), National Cancer Institute. NIH Guide for Grants and
Contracts, vol. 11, no. 9, August 13, 1982. (John S. Greenspan
Correspondence, 89-011, carton 2, folder: Conant, MA: JG/Beckstead etc.
1982); Marcus A. Conant to Kaposi's Sarcoma Study Group, August 20, 1982,
(Courtesy of Evelyne Lennette.)

210

Scientific and Medical Resistance to AIDS Research

Ziegler: I have to say that as we progressed, there were a lot of

skeptics. People were saying, "You guys are barking up a funny
tree with all this—what's going on?"

Hughes: What was behind that remark?

Ziegler: One of the interesting things about the early part of the
epidemic was that many of the mainstream scientists in the
university were reluctant to see this either as a major public
health crisis, or even as a scientific paradigm and curiosity
that was really worth going after. There were some very good
scientists who did. There were also some very good scientists
who simply ignored the epidemic altogether.

Hughes: Why was that?

Ziegler: I'll never know to this day exactly why that was. I think it was
a combination of things. I think part of it was clearly the fact
that in San Francisco it was almost 100 percent a gay disease. I
think that there was a reluctance to get involved in gay
diseases, for whatever reason. I just don't know what the other
reasons might be. Obviously, many scientists were totally
absorbed in their own fields and just didn't want to divert
themselves.

Hughes: And it was always just a natural for you?

Ziegler: Well, it was an obvious thing for me, because it just fell right
straight into my career path. I had already been interested in
cancer and viruses, and now here's a cancer epidemic with yet
another virus.

Cancer and Viruses

Hughes :
Ziegler:

What was the status of the viral theory of cancer?
credible hypothesis?

Was that a

Very much so. By that time, there were at least four viruses
linked with cancer. There was the Epstein-Barr virus and
Burkitt's lymphoma, which was probably the first, followed by
liver cancer and hepatitis virus. By that time, there was some
pretty good evidence that cervical cancer and ano-genital cancers
were linked with the human papilloma virus. There was the

211

discovery of the HTLV, the human T-cell leukemia virus, in the
late seventies by Bernie Poiesz and [Robert] Gallo. That was
another tumor virus, although it didn't pan out to be causing as
many tumors as people thought it might. It was responsible
primarily for a rare form of adult leukemia.

So there were four viruses linked with tumors, and there was
always Kaposi's sort of hanging out there--Kaposi's and a vague
association with cytomegalovirus , although many people were
skeptical about the data.1 Of these virus-associated tumors,
four of them are common in Africa. And with the association of
immunodeficiency--! 've always been interested in immunology and
cancer anyway--A!DS was a natural for me.

Lymphoma Associated with AIDS

Ziegler: Within the first year of the epidemic, we noticed a number of

cases of lymphoma in gay men who were mirroring the same kind of
clinical features that we saw with Kaposi's sarcoma—usually a
high-grade lymphoma, very often in gay men who had other
immunological defects.

Six months into the San Francisco epidemic, it was clear we
were getting another outbreak of another kind of tumor in gay
men. Still at this time we had no idea that this was an
immunodeficiency caused by a virus, but there were suspicions.
So again, our group wrote up that experience, called an outbreak
of Burkitt's lymphoma in gay men in San Francisco, which was
really the first report of the association of malignant lymphomas
with AIDS.2

Hughes: Now, when you say the group, are you talking about the KS Study
Group?

Ziegler: Well, members of this KS Study Group: Donald Abrams and Paul

Volberding, and I think that John Greenspan was a co-author on
that. And a group of people from Mt. Zion [Medical Center] were

1 See the paper to which Ziegler contributed: W. L. Drew, M. A.
Conant, et al. Cytomegalovirus and Kaposi's sarcoma in young homosexual
men. Lancet. July 17, 1982, 125-127.

2 J. L. Ziegler, W. L. Drew, et al. Outbreak of Burkitt's-like
lymphoma in homosexual men. Lancet 1982, 2:631-633. John Greenspan was
one of twelve co-authors.

212

getting involved- -Larry Drew and others. That was the sort of
mix and match of the original group.

Hughes: As I remember, Burkitt's lymphoma was not part of the original
CDC definition of AIDS.

Ziegler: No, it was not. And when we reported this outbreak, the CDC

didn't really pay too much attention to it. In November of '83,
I was in Houston, Texas. I had just gotten an award [Heath
Award] there at the M. D. Anderson Hospital. It was a big
meeting on lymphoma. There I met up with Ben Koziner from
Memorial [Hospital in New York City], with Alexandra Levine from
USC [University of Southern California] , with the doctors from M.
D. Anderson Hospital, and a group from New York University, Linda
Laubenstein and others. I said, "Look, are you seeing a lot of
lymphomas as well in these gay men?" And they said, "Yes, we all
are." I said, "How many do you see?" And they said, "Oh, we
have fifteen or twenty cases."

So I said, "Well, now, look. Let's put it all together in
one article. I'll coordinate all the responses; I'll send out
kind of a questionnaire; you send me your clinical information."
So we did that, and within a month, we had ninety cases
accumulated from five big centers.

So I wrote that up, and sent that to the New England
Journal.1 Immediately before that was published, the CDC called
me and they said, "Yes, we'll put high-grade lymphoma on the list
of AIDS-defining conditions." So that was the next step after
Kaposi's, as far as cancer and AIDS was concerned.

I guess the main contribution that I made in the early years
was the Kaposi's sarcoma work,2 and also the recognition of
lymphoma as an AIDS-defining condition.

1 J. L. Ziegler, J. A. Beckstead, et al. Non-Hodgkin's lymphoma in 90
homosexual men. Relation to generalized lymphadenopathy and the acquired
immunodeficiency syndrome. New England Journal of Medicine 1984, 311:565-
570.

2 See, for example: J. L. Ziegler, C. L. Vogel, A. C. Templeton.
Kaposi's sarcoma: A comparison of classical, endemic and epidemic forms.
Seminars in Oncology 1984, 11:47-52.

213

The Expanded Definition of AIDS. 1993

Ziegler:

Hughes:
Ziegler:

Although they have now added, in the 1993 expanded surveillance
case definition of AIDS, invasive carcinoma of the cervix, I
don't know if there are going to be any cases. That's sort of
anticipatory.

Why was it added if it is anticipatory?

My guess is that it was partly political. I think it had to do a
lot with the fact that women in general were being ignored in the
epidemic, that human papilloma virus and cervical carcinoma were
closely linked, and it was clear that women with AIDS certainly
had higher risk of cervical dysplasia, which is a precursor for
carcinoma. So I think they felt comfortable in putting in
cervical cancer as a potential AIDS-defining condition. But it
takes many, many years to get cervical cancer, and so I think
that anybody who would survive long enough to get it would be
pretty unusual.

Is that the only condition in the case definition which is linked
exclusively with women?

You know, I don't know the answer to that. I'd have to look it
up. But the CDC definition is pretty generic, and I think that
is the only gender-specific one. But I couldn't swear to it.

One of the cries of the women activists was that they were being
ignored. '

Yes. But that is now being remedied.

The Kaposi's Sarcoma Clinic and Study Group. UCSF

Hughes: Well, go back to the KS Clinic. I understand there was quite a
protocol for taking patient histories. The CDC also had a long
questionnaire that it was using for epidemiological studies?

Ziegler: Yes.

1 See, for example: Gena Corea, The Invisible Epidemic: The Story of
Women and AIDS. New York: Harper Collins Publishers, 1992.

214

Hughes: Were these two sets of questions independent, or did you
incorporate the CDC questionnaire?

Ziegler: Well, before we started registering patients, we had just an

informal group meeting every week, and it was pretty much Donald
Abrams and Paul and Marcus and John Greenspan and Andrew Moss and
myself. Art Ammann was a regular attender.

Hughes: Did Jay Levy come early on?

Ziegler: Yes, Jay was an early person. And then others came and went over
the years.

Hughes: How unusual was it to have so many disciplines represented?

Ziegler: I think it was pretty unusual in that respect. I think we all

came together because all of us had an interest in immunology. I
think that was the one drawing card for everybody, and of course,
immunology does cross many disciplines.

Hughes: What becomes of the KS Clinic? Does it die out?

Ziegler: Well, here's what happened. The KS Clinic was funded first by
the American Cancer Society, later by the National Cancer
Institute, and then still later Paul and I were co-principal
investigators of a program project grant that got funded by NIA1D
[National Institute for Allergy and Infectious Diseases] . So we
were able to sustain the, quote, "KS Clinic" at Moffitt
[Hospital, UCSF] for a number of years. But obviously, AIDS
clinics needed help in other parts of the institution that were
not supported.

When we applied and got some NIH funds for the KS Clinic,
they were clearly inadequate. The NIH team had come out, they
had cut the budget way back, so we were kind of bereft. That's
when Marcus Conant did a remarkable thing. He went to
[California State Assembly Speaker] Willie Brown, and he said,
"Look, we've got an epidemic here in San Francisco. We need
special earmarked funds. This is a crisis. We have no way of
coping with this crisis, because none of the established
institutions are really addressing it." Frankly, I think the
federal government--"too little, too late" was well applied. I
just don't think they got on top of it until the latter half of
the 1980s.

Hughes: What were the reasons for the delay?

Ziegler: I think turf and disinterest and disbelief and too little direct
contact. The AIDS epidemic in Washington, D.C., for example,

215

didn't really accelerate until about '83, '84. So the geography
wasn't there.

Characterizing AIDS

Hughes: But wasn't it also that what you were seeing demanded input from
all these different specialties, and touched on them?

Ziegler: Well, yes, it did. And I guess the thing was that the AIDS

diagnoses were anomalous. These were things that you don't see
in everyday clinical practice. You would wait a lifetime to see
one case of Kaposi's sarcoma, and now we had a clinic full of
them. Lymphomas in immunosuppressed people, yes, relatively
common, but only in kidney transplant clinics. So here we had
suddenly an outbreak of lymphoma.

Then these other opportunistic infections popped up:
Pneumocystis pneumonia, herpes, cryptococcal meningitis, and so
forth. It was pretty obvious within a few months that we were
dealing with a very serious immune deficiency.

Hughes: Did that realization come from the lab work?

Ziegler: Oh, yes. Art Ammann's group quickly showed, along with many
others almost simultaneously, that CD4, T4 helper lymphocytes
were low in these patients, and that something funny was going on
with these lymphocytes.

Then there were lots and lots of theories that cropped up,
and we were working with the CDC. I think the CDC was hot on the
trail of an acquired immunodeficiency that was spread from person
to person, and they did some very classic studies, really nice
studies, in Orange County and L.A. where they drew a lot of
connections between the different gay men who were getting the
disease, showing that there were many commonalities --not only
common partners, but common practices, and a great deal of
promiscuity that really characterized this huge cluster in L.A.1
And then Andrew Moss began to find the same things here in San

1 S. Fannin, M. S. Gottlieb, et al. A cluster of Kaposi's sarcoma and
Pneumocystis carinii pneumonia among homosexual male residents of Los
Angeles and Orange Counties, California. Morbidity and Mortality Weekly
Report 1982, 31, 12, 305-307 (June 18, 1982).

216

Francisco a little bit later.1 So we were pretty much convinced
that there must be some infectious agent.

And then in the fall of '83, [Luc] Montagnier wrote his
paper in the Lancet that showed that LAV [ lymphadenopathy-
associated virus] was the causative virus, and then Gallo's
papers six months later came out.2

The Baby with Transfusion AIDS, UCSF, December 1982

Hughes: Well, there was something else here at UCSF that convinced a lot
of people that it had to be a virus, and that was the baby with
transfusion AIDS.3 Remember?

Ziegler: Art Ammann's patient, right.

Hughes: And that was December of 1982, before Montagnier and Gallo
published.

Ziegler: Yes, that was a very important thing. Art and—who is that other
fellow in UC pediatrics?

Hughes: [Morton J.] Cowan?

Ziegler: Yes. And Diane Wara. But Art Ammann I would have thought was
the main UC person early on, and that baby was a classic. Then
the blood bank groups started noticing that there must be
something in the blood. And then everybody said, "Well, my god,
could this be hepatitis?" It was looking for all the world like
hepatitis—sexually transmitted, blood transmitted, vertically

1 A. R. Moss, P. Bacchetti, et al. AIDS in the "gay" areas of San
Francisco. Lancet April 23, 1983 (letter).

2 F. Barre-Sinoussi, L. Montagnier, et al. Isolation of a T-
lymphotropic retrovirus from a patient at risk for acquired immune
deficiency syndrome (ADS). Science 1983, 220:868-871; R. C. Gallo, S. Z.
Salahuddin, et al., Frequent detection and isolation of cytopathic
retrovirus (HTLV-III) from patients with AIDS and at risk for AIDS.
Science 1984, 224:500-503, and two additional papers by the Gallo group in
the same issue of Science.

3 R. O'Reilly, D. Kirkpatrick, et al. Unexplained immunodeficiency
and opportunistic infections in infants—New York, New Jersey, California.
Morbidity and Mortality Weekly Report 1982, 31:665-667 (December 17, 1982).

217

transmitted. Could it be hepatitis? And there was a flurry of
excitement when somebody in Girish Vyas's lab found hepatitis
virus in lymphocytes, but that completely fizzled out. But
anyway, those were the days in which we were all thinking
infection.

Hughes: How were you linking the lymphomas and KS with the opportunistic
infections and what you were learning from the epidemiology and
blood transmission?

Ziegler: Well, the biology was pretty straightforward, because we've known
for years that lymphomas and Kaposi's sarcoma prey on people who
are immunosuppressed. That was known before the AIDS epidemic.
In renal transplant cases and in patients who get lots of
corticosteroids, Kaposi's sarcoma occurs much more than you would
see ordinarily. That doesn't mean it's terribly common, but for
a very rare disease, when you see a lot of cases, it becomes
unusual. So we had always linked Kaposi's with some form of
immunosuppression.

The lymphomas had also been known to prey on people with
immunosuppression--renal transplants, and other organ
transplants, and so forth. So the cancer-AIDS connection, of
course, was through the immunodeficiency link. That was pretty
clear. The only question was whether the virus that was causing
the immunodeficiency had anything to do with the cancers. And
quickly after the virus was discovered, it was determined that
the virus was not in any way involved directly with the Kaposi's
sarcoma; they couldn't find the virus in the lesions. Nor could
they find it in the lymphomas. So it was obviously a two-step
process in the causal chain—the virus, immunosuppression,
lymphoma .

Immune Overload

Hughes: Did you ever give any credence to some of the other theories that
were floating around? Immune overload, for example?

Ziegler: Yes. Actually, Jay Levy and I wrote a paper before the virus was
discovered.1 It was a sort of accepted theory at the time that
somehow gay men, because of their immense promiscuity, were

1 J. A. Levy, J. L. Ziegler. Acquired immunodeficiency syndrome is an
opportunistic infection and Kaposi's sarcoma results from secondary immune
stimulation. Lancet. July 9, 1983, 78-81.

218

overloading their immune systems with viruses and amoebas and
various other things. Then we tried to explain the same thing by
saying that it was immune overload in hemophiliacs, and immune
overload in people with blood transfusions, and immune overload
in IV [intravenous] drug abusers who were continuing pushing
foreign antigens into their bloodstream.

But if immune overload were the case, why would the epidemic
start in 1981 when these people had been immune overloaded for
decades? So although immune overload was always held out as a
co-factor, and I think it probably is a co-factor, the
concatenation of all of those things simply didn't explain the
explosive rise of the epidemic.

Hughes: Did that worry you at the time when you and Dr. Levy put forward
the secondary immune stimulation theory?

Ziegler: Yes. I think we were all a little skeptical of it, and it was a
little too facile, because it didn't explain why it should occur
almost as a point-source of the epidemic.

Hughes: This was 1983 and public fear and health care worker fear of AIDS
was at a pretty high level. Was there an element behind the
theory of trying to pacify the public, because one of the points
your paper made was that if you were not immune suppressed, then
you didn't really have to worry about AIDS.

Ziegler: That wasn't even a tertiary concern of ours. We were trying to
guess at the scientific truth of the matter. I don't think that
had anything to do with it, frankly. In retrospect, it was a
very weak hypothesis, because it didn't explain the timing of the
epidemic very well. My contribution to that hypothesis was
really the Kaposi's part of it, and that I think has held up
pretty well.

Hughes: Well, explain that part of it.

Ziegler: Well, the article that Jay and I wrote had two parts to it. One
was Jay's idea that in fact you had to be immunosuppressed in
order to get the virus in the first place.

Ziegler: He proposed that a causative agent was also an opportunistic

infection, and that you had to have a suppressed immune system
already, and the virus would then prey on people who were already
immunologically weakened.

Hughes: Why did he think that?

219

Ziegler: Well, I think just looking at the epidemiology and at the patient
characteristics that we were seeing- -but we were only seeing one
small corner of the epidemic. We hadn't really picked up on the
global situation which was emerging, because the cases in Africa
were coming in late. There were just scattered reports here and
there. It was kind of hard to put it all together.

His theory didn't exclude an agent; in fact, we were
thinking that an infectious agent was most likely going to be
found. But I think his idea was that in order for the agent to
take hold, you had to be immunosuppressed to start with. And
there is still some evidence that that may well be the case.
Certainly in hemophiliacs and others, there is sort of synergism
between being infected and having a weakened immune system.

The Etiology of Kaposi's Sarcoma

Theory: Kaposi's as a Reactive Hyperplasia

Ziegler: But my contribution was more for the Kaposi's sarcoma, because we
were interested in why Kaposi's should appear in these patients.
We believed that it was sort of a reactive hyperplasia that then
went on to become malignant, and that it was biologically very
responsive to immune signals and probably cytokines and other
wound-healing kinds of events that were going on, that it was
almost like an endocrine tumor that would wax and wane in
response to certain biologicals.

Hughes: Now, was this theory based on your own research?

Ziegler: This was based on the work I had done on Kaposi's in Uganda. I
had been thinking about it for quite some time, and then trying
to figure out how to explain the biology of the disease. The
role of the immunosuppression was really what we set out to
explain. Jay was much more the virologist of the two of us, and
I was more interested in the cancer side. So that article simply
proposed that Kaposi's was like a reactive hyperplasia that was
hormone-responsive or responsive to other cytokines.

And I think that's been borne out by Gallo's work and
others, who showed there are many cytokines which can make
Kaposi's sarcoma cells grow. We tried in vain for years to get
Kaposi's growing in tissue culture, and failed. It was Gallo's
lab that succeeded simply because they were using conditioned

220

media from HIV- infected cells. They produce something in the
media that stimulates Kaposi's to grow.

Hughes: Well, go back to the KS Clinic. Could you follow a patient
through from the time he first presented?

Ziegler: Actually, the main proponent of the KS Clinic was Marcus Conant,
because they were mostly his private practice clinic patients--
they were coming to him for Kaposi's sarcoma. Later on, we were
instrumental in setting up the Adult Immunodeficiency Clinic [at
UCSF] which Harry Hollander now runs. In those days they were
all coming through Marcus1 clinic. Paul [Volberding] had a
clinic down at the San Francisco General, and I saw patients here
at the VA in the hematology-oncology clinic, and eventually we
developed an AIDS clinic there as well. So we had three clinics,
and we would come together and share our patient stories and try
and make sense of this as time went on.

Donald Abrams, in the meantime, was collecting a large group
of gay men who had lymphadenopathy syndrome, we called it. They
were just coming to him with nonspecific symptoms and fever, and
not feeling so hot, and weight loss, and night sweats, and these
large lymph nodes. Donald started collecting cases, and he very
soon collected several hundred, and wrote this up finally in the
Annals of Internal Medicine.' But we would get reports of his
group and his analysis.

An Hypothesis Associating Kaposi's Sarcoma and Volcanic
Soils

Hughes: Is there still not anything definitive known about etiology?

Ziegler: No. Kaposi's is really an interesting mystery. Before you go,
I ' 11 give you a paper that was in the Lancet about two months
ago.2

I explained to you that Kaposi's is one of these diseases
that comes up with immunosuppression. Well, when we were in

1 D. I. Abrams, B. J. Lewis, et al. Persistent diffuse
lymphadenopathy in homosexual men: Endpoint or prodrome? Annals of
Internal Medicine 1984, 100:801-808.

2 J. L. Ziegler. Hypothesis: Endemic Kaposi's sarcoma in Africa and
local volcanic soils. Lancet. November 27, 1993, 342(8883) : 1348-1351 .

221

Africa, we postulated that actually way back in 1967, not even
knowing that this was going to be a disease that was excessively
seen in immunosuppressed people. We did immunologic studies on
patients in Africa, fully expecting to find impaired immunity.
Not so; they were fine; they had good cell-mediated immunity;
they had good humoral immunity. We couldn't find any immune
defect in patients, but we were looking in the African patients
at general systemic immunity. And then there was their ability
totally to fight infection. And that was maybe self-evident;
they didn't get opportunistic infections; they weren't ill from
cryptococcal meningitis or any of these other things. They were
perfectly healthy people. They just had Kaposi's sarcoma.

So we could not for the life of us link the African Kaposi's
with immune suppression. And that's puzzled me for years; I've
never been able to figure out why it is. Because everywhere else
you find Kaposi's, for example, the classical Kaposi's in Europe,
it's almost always in very old people-
Hughes: Where you get a natural decline in immunity.

Ziegler: A natural decline, exactly. And these Africans were young,
robust peasants. These were farmers out in the fields.

This is a digression, but I think you'll find it
interesting. Last year, I spent the year on sabbatical at
Cambridge University, where my wife is doing some graduate work.
I was puzzling about Kaposi's sarcoma and working on a grant that
I hope will come through from the CDC to study this in Africa.
In my research, I've been trying to explain why Kaposi's in
Africa is so common there, and why it was not associated with
immune suppression. Those were anomalies of the disease that
never could be explained. You don't see it in South America; you
don't see it in India; you don't see it in Asia or in Eskimos.
But in certain parts of Africa, for example, in Rwanda, Kaposi's
sarcoma is almost 20 percent of the adult malignancies. Just
indigenous. Now, of course, with AIDS, in many countries it's 50
percent. Half of the tumors are Kaposi's sarcoma. But even
before AIDS, it was very common, and I couldn't figure it out.

I was riding on the train from Cambridge to King's Cross
[Station, London] with a colleague of mine, John Rickens, who's
just one of these brilliant Cambridgian types, who's a great
lateral thinker. I was showing him the maps. I said, "What on
earth could this be? What explains these distributions?" He
said, "Well, have you thought about the soil?" I said, "Yes, but
the soil all through Africa is pretty much the same. It's just
all laterite."

222

He said, "Well, there is a chap named Ernest Price who
worked in Ethiopia, and he discovered a relationship between soil
and elephantiasis." Elephantiasis in Africa has always been
ascribed to filaria, a small worm that gets into the lymphatics
and blocks them up. Price apparently found elephantiasis in the
highlands of Ethiopia, where there are no filaria, but he was
finding many, many villagers coming in with these huge, swollen
limbs. He traced it to soil which is of a very fine consistency,
like kaolin, like Kaopectate. It's clay soil with very slippery,
very tiny colloidal particles.

When Price began to study this, he realized that the people
who have elephantiasis live in areas where this kind of clay soil
is really common. In fact, they are all peasants. They all work
in the fields, and they stand in this soil up to their knees, and
then they get swollen legs, which also are burning and itching
and quite uncomfortable. If you put shoes on them and take them
out of the soil, protect them from it, the swelling generally
goes down and they're better again.

So he spent a lifetime studying this disease. He ended up
calling it podoconiosis--there' s a connection; I'll get to it in
a minute. Podoconiosis he explained as follows: these peasants
work in this soil with this particular consistency. They are
heavily exposed in the lower extremities to these tiny clay
particles. Clay particles get into the skin, under the skin, and
enter the lymphatics, and cause fibrosis of the lymphatics and
block them.

Price did enough epidemiology to convince many people that
this was true. He found particles of silica, of
aluminosilicates, in the skin and in the lymph nodes. He was
able to reproduce the disease in rabbits by injecting
aluminosilicates into their foot pads. He was able to find trace
minerals in the tissues of these patients. Perhaps the most
convincing thing was that he would sit in marketplaces with his
wife—this is a very eccentric Englishman- -and he and his wife
would sit down there at knee level and count swollen legs of
people who came in and out of marketplaces. They did it in many
different marketplaces in different parts of southern Ethiopia.

In the areas where these clay soils were dominant, they had
a 5 percent prevalence of swollen legs in the marketplace. In an
adjacent area where it's sandy soil or loam soil, totally
different consistencies, virtually no cases. So then Price said,
"Well, elephantiasis really isn't a filarial disease; it's a soil
disease." And he went around to different parts of Africa and
began to find more cases. Every time he found cases, he found
this kind of kaolin clay soil.

223

Well, where did he find it? He found it in Rwanda, Burundi,
western Uganda. He found it in Ethiopia, in parts of Kenya, in
parts of Tanzania. He linked it to volcanoes, and the reason he
linked it to volcanoes was that the volcanoes in these areas
produce a basalt which comprises the underlying rock. The soil
that forms on top of this basalt is very likely to be kaolin and
montmorillonite, very sticky soils, as opposed to the sandy soils
that are more characteristic of the desert areas. These volcanic
clay soils characterize the areas where he found elephantiasis
throughout Africa.

And the most extraordinary thing, Price jumped across the
whole continent of Africa to northwest Cameroon—that 's the place
where the lake exploded about five, seven years ago, and all that
C02 gas killed all those villagers. Well, that's a very heavily
volcanic area. In fact, a whole line of volcanoes runs straight
into the continent there. And sure enough, what did he find? A
lot of podoconiosis, elephantiasis, in that volcanic area. Now
then he had to explain, well, there are volcanoes all over the
world, why is it these African volcanoes are different? And he
could never explain that. I think the best explanation is that
the chemistry of the magma in these volcanic regions is quite
different from the chemistry of the magma in the Pacific islands,
like Hawaii and Japan, and along the continental volcanoes such
as Iceland, and there's volcanic activity in India and so forth.
The African, especially the east and west rift sections of
Africa, have a very alkaline basalt. It has to do with the
relatively recent eruption of the magma and the geochemistry and
weathering of the region.

Well, to get back to my train ride: This fellow [Rickens]
said, "Look up this Price and see if there's some relationship
between the distribution of KS and soil composition, because your
map looks a little bit like podoconiosis." So I looked up
everything Price had ever written. I then went to the FAO [Food
and Agriculture Organization] soil maps; got them out. Then I
realized I had to learn a little geochemistry, and had to learn
about volcanoes and crustal contamination, and then soil
formation and catenas (soil layers and weathering effects). I
got about ten books and sat down to study this for about three
months .

In the end, I was convinced that the Kaposi's and the
podoconiosis occupy the same geographical territory. The most
interesting part was this huge cluster of Kaposi's sarcoma in
south Nigeria and northeastern Cameroon, sitting right on top of
that volcano. Plus, when you look at it in its
microepidemiology, you find that Kaposi's sarcoma in Kenya, for
example, is not uniformly distributed across the country. It

224

clusters on the rainy side of Mount Kenya and on the rainy side
of Mount Elgon. When you look in Tanzania, you find that it's
not uniform across the country. Again, it's clustered near Mount
Kilimanjaro and then down in the Irunga plateau, which is a very
heavily volcanic area. The whole country of Malawi has a
relatively high rate of Kaposi's, and that lies along the whole
southern branch of the Rift Valley.

So putting all the geochemistry together, to make a long
story short, I came up with a hypothesis that in fact Kaposi's
sarcoma in Africa is related to clay soil exposure, and that the
clay gets into the skin and somehow disrupts the skin immunity to
make it susceptible to Kaposi's. When you think about it, 85
percent of the cases of African Kaposi's are on the feet or the
legs, and of the other, 10 percent are on the hands. So it has
something to do with hands and feet, and exposure of some kind.

It took me back to thinking, Well, if there's an infectious
agent involved here, it could come primarily from the soil. I
can't think of what it might be, because soil really harbors just
bacteria and fungi, and if either of those things were involved
in Kaposi's, we'd know it. We could see them under the
microscope. And I worked around that for a long time, and did a
lot of soil microbiology study, and I could not come with any
microbe linked with the soil.

Then I discussed it with a very bright scientist in Britain
named Robin Weiss, who does a lot of the work with HIV. He said,
"Maybe the soil is simply causing immunosuppression. " I thought,
Wow. That's something we never test. We never tested if there
is localized immunosuppression in the hands and the feet. We
were examining systemic immunosuppression and couldn't find it.
But what if there was some local immunosuppression?

Well, then it occurred to me, why not? The soil gets into
these tissues. One of the best ways to kill macrophages in
tissue culture is to dump in aluminosilicates, kaolin, diamond
dust. Immunologists love the stuff because they can completely
eradicate all their macrophages with this treatment.

So I came to the point of view that somehow the
immunosuppressive part of Kaposi's in Africa has to do with
immunosuppression of the hands and the feet, and that it probably
comes from exposure to this very fine clay soil, which you can
only find in certain parts of Africa.

Hughes: There's no way of actually testing that hypothesis?

225

Ziegler: Oh, yes. We've got several ideas of how to test it! First of

all i you have to find out if the skin of the hands and feet is in
fact immunosuppressed, and you can do that very easily by doing a
tuberculin test—positive here, negative here. That would be the
simple way to do it. Another way to test it would be to take the
tissues from the feet and the hands and see if they contain
aluminosilicates, like Price showed in the podoconiosis patients.
Another way would be to actually find the homes of patients with
a high prevalence of Kaposi's sarcoma, and test the soil in those
areas. On a grid, also test soil where there's no cases of
Kaposi's sarcoma, and compare the soil samples. I mean, there
are plenty of epidemiologic things you could do, none of which
have been done, so it's totally theoretical at the moment, but it
has geographical plausibility.

I gave the paper in a talk to the Geological Society in
London, and they thought it had geochemical plausibility. At
least, nobody shouted it down. It's consistent right now with
many of the observations.

Hughes: What do your oncologist colleagues think about it?

Ziegler: Oh, everybody thinks it's a good idea. Obviously, it needs to be
tested. Nobody's been able to explain the Kaposi's in Africa.
That's the curiosity. [tape interruption]

Hughes: Anything more you want to say on that subject?
Ziegler: No. [laughs]

More on Characterizing AIDS
A Gay Disease

Hughes: Well then, I'd like to go back to the earlier question of the

framing of the disease, and what implications that had, because
certainly in the two places where the epidemic hit first in this
country—California and New York—it was for a while very much
framed as a homosexual disease. What did that do to your
thinking?

Ziegler: Well, we were very puzzled by the high predominance in gay men,
and of course, all kinds of theories emerged having to do with
amebiasis and multiple infections and sperm, and immunologic
reactions to sperm, and all kinds of other curious hypotheses

226

that came out. I think when the other populations developed AIDS
a little bit later, such as [cases associated with] blood
transfusions, hemophilia, and IV drug abuse, it was clear that
this was just one generic problem that in the end turned out to
be a way that the virus could be very efficiently transmitted,
and that was through rectal sex.

Hughes: As early as August 1981, there were a number of heterosexual

cases reported.1 Nothing much seems to have been done with that
information. Was it because AIDS was seen as a gay disease?

Ziegler: Yes, and somebody wanted to call it GRID [gay-related immune

deficiency]. Well, I guess that's one of the lessons of science
history, and that is that you must treat anomalies with great
respect, because they're usually the ones that give you the
answers-- just like the code-breakers in Britain. I'm currently
reading about cryptoanalysis during the war at Bletchley Park.
Their reliance on these oddities, the anomalies, gave them the
words needed to break the code.

Hughes: You and other people relatively early on suspected that it had to
be an infectious agent. What would have been the rationale, if
it were an infectious agent of some kind, of confining it to one
population?

Ziegler: Yes, we couldn't understand that. By then, the epidemiologists
were telling us, Look, the ones who seem to be most susceptible
to this disease are people who had rectal intercourse one way or
another, who were recipients of rectal intercourse; they were the
most likely to be ill. So there were some practices that
suggested that trauma and possible sperm exposure, things like
that, might predispose a person to AIDS. And we puzzled quite a
lot over that, and couldn't quite reconcile it with the other
hypotheses except to say that whatever the agent was, it gets
into the bloodstream. And once it's in the bloodstream, it can
be passed to other people and also to infants. Hepatitis was the
best model.

Latency
Hughes: What about the evolution of thinking about the latency period?

1 S. M. Friedman, Y. M. Felman, et al. Follow-up on Kaposi's sarcoma
and Pneumocystis pneumonia. Morbidity and Mortality Weekly Report 1981,
30, 133, 409-410 (August 28, 1981).

227

Ziegler: That was another problem. I didn't engage too much in that

aspect, but it was obvious, I guess, that there was something
that happened to the gay population in the late seventies, early
eighties, that propelled this disease. And then only in
hindsight did we recognize that the virus was around, but was
spread very rapidly, and probably caused disease in a much more
accelerated way in the early part of the epidemic than it does
now.

I mmuno stimulation

Ziegler: Our explanation for that was that these patients were already

very immunostimulated. Again, I guess more or less in hindsight,
we always think of immunosuppression/immunostimulation as kind of
an on/off toggle switch, which is dead wrong. In point of fact,
what we should have known all along and which everybody is
rediscovering is that when somebody is immunostimulated, it
doesn't mean they have a strong immune system. In point of fact,
their immune system is probably diverted from what it should be
doing.

We learned that years ago when we were studying malaria in
Africa. Malaria is a disease that causes a very massive
stimulation of the immune system: Spleens get big,
immunoglobulins go up, these patients are very turned on
immunologically. But they're not necessarily healthier. In
fact, they're very unhealthy. If you have someone with acute
malaria and try to give him a tetanus shot, he won't develop
antibodies. He just doesn't respond to vaccines. If somebody
has bad malaria, he is more susceptible to getting bad pneumonia.
If you have malaria and measles together in children, you've got
a lethal combination--25 percent of them die of pneumonia.

So while we were thinking immune stimulation is a great
thing, gets the system revved up and that sort of thing, it's
totally wrong. A stimulated immune system causes a functional
immune suppression.

Ziegler: What Don Abrams was noticing in his men with lymphadenopathy

syndrome were patients who were massively immunostimulated. If
you take the lymph nodes out and slice them up, they are filled
with lymphocytes. Well, you would have thought, "Great, lots of
lymphocytes, lots of immunity." Wrong. Lots of lymphocytes, all
stimulated, not doing their job. And in fact, by getting

228

stimulated, the lymphocytes were putting out all these cytokines
and making people feel lousy, like they had the flu.

So that's sort of a sidebar, but it does help explain that
we were kind of on the wrong track when we were talking about
immunostimulation/immunosuppression. Basically,
immunostimulation equals immunosuppression.

Risk Groups

Hughes: The CDC identified risk groups for AIDS, the famous "four H's"--
homosexuals, hemophiliacs, Haitians, and heroin users. Was the
creation of risk groups standard CDC epidemiological practice?

Ziegler: Well, yes. No matter what you're studying, there will be some

groups at risk for disease and some groups which aren't. I think
that the epidemiologists used the term "risk ratio" and so forth
to try and characterize somebody who's going to get sick versus
somebody who isn't. I think it became a natural epidemiological
tool to use. Because the disease was so stigmatized anyway, it
quickly stigmatized the risk groups, and then there were a lot of
very unseemly jokes.

Hughes: It also, from a public education standpoint, may have diverted

attention from the message that I should think the CDC would have
been trying to get through, namely behavior, rather than just
what risk group you happened to be in, determines risk. If
you're a Haitian, that really is irrelevant; it's what you do as
a Haitian that should count. The other side of the coin was, if
you're not in a risk group, you are not at risk.

Ziegler: Well, I think you've found a real Achilles heel in the whole

process, and I don't know where the problem arose. I'm not sure
I would blame the CDC in any way. I think they tend to think in
terms of risk groups anyway, because it's an epidemiologic tool.

Fears about Heterosexual AIDS

Ziegler: I'm wondering if it isn't also the press. The press and the

media were trying to make sense of this at the same time, and the
thing that was really sensational was not a gay person who gets
AIDS, it's an actual straight person who gets it. I remember in
'84, '85, one of these magazines featured some heterosexual

I !

229

couple with their baby afflicted with AIDS, like this epidemic is
coming right into your living room. I think it caused a
tremendous sensation, just as much as Rock Hudson and the
basketball player "Magic" Johnson getting HIV.

Hughes: There was another incident like that, concerning a pediatrician
by the name of [James] Oleske- -

Ziegler: Oleske, yes, sure.

Hughes: --who had been seeing pediatric AIDS cases, and came to the

conclusion that AIDS could be transmitted through casual contact.
[Anthony] Fauci wrote an accompanying editorial, and the
combination of the two really raised anxieties.1 Do you remember
the time?

Ziegler: Yes, I do. I think there is a psychosocial side. There was a
certain amount of comfort among middle class, straight people,
thinking, This epidemic is not my problem. I'm not gay; I'm not
hemophiliac; I'm not Haitian. Therefore, no problem. And that
was a flawed message for sure. Of course, you don't want to
panic the entire world, but you also want to be prudent. So I
think that there were problems there.

Personal Risk

Hughes: Well, it leads me to a question. What were you thinking, before
the isolation of the virus, about personal risk? What was going
through your head when you were treating patients?

Ziegler: I think we knew that this was pretty much a sexually transmitted
disease, and as long as you were a monogamous couple, you were
not at risk.

Hughes: I guess you did up until December 1982, but then when you had
that baby with transfusion AIDS, how else could the disease in
that case be transmitted except through blood?

Ziegler: That's true. Paul and I and Marcus and the rest of us who were
dealing with AIDS patients, when we found out this was an
infectious agent, obviously we all got a little nervous because
we thought, Well, we've been drawing blood from these people and

1 J. Oleske, A. Minnefore, et al. Immune deficiency in children.
Journal of the American Medical Association 1983, 249:2345-2349.

230

so forth. Could we have gotten it? And there was a period of
anxiety there, I suspect, when everybody who was dealing with
AIDS patients wondered could they become infected by physical
contact with patients.

Hughes: Did you change any of your procedures?

Ziegler: I had always been very cautious. I had never stuck myself. I

think basically what we did here in the hospital eventually was

go to universal [infection control] precautions, which was the
prudent thing to do anyway.

Hughes: Were those the same pre- and post-epidemic?

Ziegler: No. Post-epidemic, the rules got much more stringent—gloves for
drawing blood, masks for coughing patients, and things like that.

Hughes: Were you involved with the committee at San Francisco General
which devised the first infection control guidelines for AIDS?
An article was published in the New England Journal . '

Ziegler: Yes, that was Merle Sande's committee. I was involved

peripherally in that, but I didn't sit on that committee. There
were a lot of committees in those days, and all these committees
made an impact, because they got the rules changed. It took a
while; it usually does with committees.

AIDS Activities at the VA

Hughes: Were you seeing considerable numbers of AIDS patients at the VA?

Ziegler: Here at the VA, we started seeing more and more patients. By

1982, we had about several dozen all together. By 1984, we were
up into the hundreds. Now we're way up, 800, 900, l,000--I'm not
sure.

Hughes: Was there anything that differentiated these patients from the
ones at San Francsco General and UCSF?

Ziegler: No. Just the geography of the hospitals. We were a veterans'
hospital, so we tend to see slightly older patients. Paul's

1 J. E. Conte, W. K. Hadley, et al. Infection-control guidelines for
patients with the acquired immunodeficiency syndrome (AIDS). New England
Journal of Medicine 1983, 309, 112:740-744.

231

hospital [San Francisco General] is very close to the Castro
[District], so he was seeing many gay men. And then a number of
IV drug abusers found their way into the VA.

Hughes: Well, tell me in more detail what was going on from the earliest
days in terms of AIDS activities at the VA.

Ziegler: I guess I'd have to say for quite awhile I was pretty much the
only person here who was interested in AIDS. I tried to get
other people interested, and there was a little bit of
investigative curiosity, but as the patients began to come in, I
guess the infectious disease clinic was the one that started
getting involved. There were two people there who were pretty
alert. One was Ira Tager, and the other was Peter Jensen. Peter
now runs the AIDS Clinic and is very active. They began to see,
as I did, the Pneumocystis pneumonia, and those infections which
were problematic.

Hughes: Did other physicians hesitate for reasons that we already
discussed in regard to UCSF?

Ziegler: Yes, I think so. I've always wanted to study that, Sally. I
always was curious why it was. I almost did a questionnaire,
because I was curious why it was that more faculty scientists
didn't get more interested in this disease sooner. I mean, here
is just an extraordinary new illness. You don't very often
encounter new diseases. This is sort of like [William] Osier
trying to figure out what typhoid was at the turn of the century
--just great opportunities. But there was really a disinterest
or apathy, and some scientists really wanted to distance
themselves. They just didn't want to have anything to do with
it, didn't want to serve on this committee, didn't want to
investigate or treat patients, and the like.

Anyway, the VA was slow, but I guess I did a lot of stirring
up. I got the hospital director, Larry Foye, to send in a
message to the Central Office saying, "Other VAs may be
encountering these patients; pay attention; we should get some
policies." And I served on a central committee [Steering
Committee on AIDS, 1987-1989] to set up policy, which eventually
created an AIDS office at the VA, and then they got their act
together.

Hughes: How early was that?

Ziegler: About 1985.

Hughes: So not terribly early.

232

Ziegler: Not terribly early, no. The VA was slow to get its act together.

AIDS Clinical Research Center. UCSF

Funding for AIDS Research

Hughes: Were you having trouble getting the necessary resources that you
needed?

Ziegler: Well, no, because what happened was that in those early years,

Marcus got to [Willie] Brown and they set up the [Universitywide
Task Force on AIDS], what they now call the Universitywide AIDS
Research Program. And Merle Sande headed that. They immediately
gave us a grant for the AIDS Clinical Research Center [at UCSF].
Marcus was the director of that grant for about a year or two,
and then I took over from him in 1985. I remained the director
right straight up to 1992.

Hughes: Why did Dr. Conant step down?

Ziegler: I never could understand that. I think he had a very, very busy
practice. He was not a keen administrator. Running the
practice, watching the budget, monitoring clinics, paying
employees, doing a whole lot of managerial things, I think he
just decided that he would rather spend his time with his
patients. He was also then on a campaign to try to launch [AIDS]
vaccine programs. He wanted to make sure that the vaccine
developers were free of liability, so he was introducing
legislation to cap liability for vaccine and things like that.
So he had other projects.

So Rudi Schmid, who was the [UCSF] dean, asked me to direct
the AIDS Clinical Research Center.

Hughes: Why did he choose you?

Ziegler: I think because I was probably, in the UC system, the most senior
physician working on AIDS. Merle Sande and Paul were setting up
a big program down at the General. There wasn't much going on at
the Moffitt Hospital [at UCSF], except in a small way.

233

AIDS Patients at Moffitt Hospital

Hughes: Well, that brings up a question: Why bother with Moffitt at all?
Why not refer AIDS patients to the General [SFGH], where there
was already so much going on?

Ziegler: I think the General had its hands full, for one thing. The

Moffitt already had patients going through the system. I don't
think it was in any position to ship anybody- -the General
generally takes care of the indigent of San Francisco.

Hughes: But there had been exceptions made already, because Don Abrams '
lymphadenopathy patients moved from Moffitt down to the General.

Ziegler: Yes. Well, that happened when Abrams went down to work with

Paul, that's true. He took a lot of his patients with him. But
I think that was a special circumstance, because Don was one of
the few gay physicians who was really looking after such a large
cohort of gay men, and I think they all just decided they would
stick with him.1

Hughes: So what you're saying is that it was natural that there were two
university institutions dealing with AIDS patients; it didn't
make sense to have it all at the General?

Ziegler: We didn't think it was sensible at all to centralize it. In
fact, I think the collegiality of the group was such that we
could all call each other and communicate very freely without
need for any kind of hierarchy.

Ziegler as Director

Ziegler: I think I was chosen because I had a lot of experience, and
because I was pretty senior and I had already done a lot of
administrative work. Paul was quite young and new at the time.
Marcus was just overwhelmed with his practice and other things,
and I think he just wanted out. And there was nobody else. I
guess maybe another candidate might have been John Greenspan,

1 For more on this subject see the oral history conducted with Donald
I. Abrams, M.D. , in The AIDS Epidemic in San Francisco; The Medical
Response, 1981-1984. Volume II, Regional Oral History Office, The Bancroft
Library, University of California, Berkeley, 1996. Hereafter, this series,

234

because he was doing a lot of the oral biology and discovered
hairy leukoplakia.1 He is the current director after I stepped
down.

I had a lot of support from the administration here. Ralph
Goldsmith, chief of staff, everybody said, "This would be
wonderful for the VA. We'll bring you money; we'll give you an
office; we'll give you space. You hire Susie Hedberg and Layne
Ethington and you get started," so I set up the center here at
the VA.

Hughes: And that all came through UARP?

Ziegler: The AIDS Clinical Research Center gets about a million dollars a
year, and the center is still going strong. The program has
gotten rave reviews every year. It really worked well. And the
reason it did, I think, was, A, because of the collegiality of
the group, which really has been together right all the way
through—Paul, Marcus, John [Greenspan], Harry Hollander, and
many others. B, we had a very good administrative network; and
C, we had a good infrastructure that we were able to fund. So a
portion of those funds went to help pay for the AIDS clinics at
the UCSF hospitals.

We were also able to set aside some funds for quick
turnaround research projects, pretty much like the very first
grant we got. So people who had a good idea could submit their
idea in an abbreviated form, have a peer review, and get some
seed money right away to start to do whatever it was. They only
had to wait six weeks maximum.

Hughes: My heavens.

Ziegler: So we were able to fund lots of programs. I think the most

successful part of that enterprise was the fact that we could use
the resources of the AIDS Clinical Research Center, which had
ultimately quite a few components to it—you might have seen one
of the annual reports. But we basically had a very large network
of clinics and resources—the tissue bank, the serum bank, the
computer center, we had a lot of people involved, and we were
able to leverage funds.

But what we accomplished in this whole enterprise was the
ability to leverage funds. Our investigators used seed money to
do pilot studies, get data, and apply for grants. We leveraged

See the oral history in this series with John S. Greenspan, Ph.D.

235

maybe six or seven major centers in the UC area, NIH funded
centers on IV drug abuse and AIDS, and the Oral AIDS Center was
leveraged off of the ACRC start-up funds. The VA itself got a
grant from the VA central office of half a million dollars a year
for VA research, also facilitated by ACRC. So I figure that over
the years, we must have leveraged $30 or $40 million of research
funds from other granting organizations coming in to UCSF. It
was a big success from that point of view.

We were also able to support neglected groups: the women got
together, and Ruth Greenblatt and Diane Wara and others said,
"Okay, we need a consortium for women, research for women with
AIDS." So the AIDS Research Center gave them a $10,000 grant.
They were able to get secretarial help, get that organized, so
now that's a big going enterprise of its own. That was the sort
of thing that I enjoyed doing most when I was directing that
center.

Hughes : Have you stepped down now?

Ziegler: Yes, I stepped down in 1993. John Greenspan is running it now.
Marcus ran it for two years, and we were sort of co-running it.
I was on the executive committee, and we would meet periodically.

Founding the AIDS Clinical Research Centers [ACRCs]

Hughes: Why was the ACRC founded, in 1983?

Ziegler: Well, it got founded because Marcus went to [Willie] Brown to get
funds from the legislature. So they set up this universitywide
task force on AIDS [1983], put Merle Sande in charge, and then
the task force said, "Well, how are we going to spend this
money?" Merle and I talked, and others; we decided they would
set up two AIDS centers, one in southern California, one in
northern California. So UCLA got one and we got one. Later on,
UC San Diego got added in, so there were three centers. These
centers were going to be centers of excellence that would
coordinate and facilitate AIDS research in these different areas.

And then each one developed its own personality based on
what sort of leadership and guidance and needs it had. Ours took
on infrastructure by helping the clinics, setting up the mini-
grant program, helping to leverage the other grantees, and
coordinating research. And recently, the ACRC has been very much
involved in the community response as well.

236

Hughes: How is that manifested?

Community Outreach

Ziegler: Well, [laughs] back in '89, '90, [State Senator, who was State

Assmeblyman at that time] Tom Hayden held hearings to ask how the
university was responding to the community needs and AIDS. So
taking the cue from that, we began to look into the community to
see what more we could do to facilitate university-community
liaison. There are many nonprofit organizations looking at the
needs of AIDS patients. There was no clear link between the
research enterprise and the nonprofits' activities—the Shanti
Projects, the information services, and so forth.

We got diverted in 1990 because of the AIDS conference
[Sixth International Conference on AIDS] we had to put on in San
Francisco. But that experience taught us that community liaison
was essential for getting things done. In 1991 we sponsored
community forums to inform the community about our research
program. We created a community advisory board attached to our
AIDS center, and finally now at the ACRC we have a full-time
community liaison staff advisor who does nothing but work between
the university and the community.

Hughes: When did the community outreach start?

Ziegler: Well, it's been forming over the years. I guess I would say I

started it formally in 1991, and now 1994, it's going full steam.

Adult Immunodeficiencies Clinic. UCSF

Hughes: Is the Adult Immunodeficiencies Clinic at UCSF the functional
successor of the KS Clinic?

Ziegler: Yes. Marcus Conant started the KS Clinic, and then it began to
include AIDS patients with other conditions. Marcus had his own
private practice, and those patients who were not in his private
practice eventually found their way to what we called the Adult
Immunodeficiencies Clinic. That was founded by the AIDS Clinical
Research Center with funds from the center, and run by Harry
Hollander, who had just completed his chief residency at the VA.
Dick Root, who was the head of medicine at the time, Merle Sande,
I, and others sat down and said, "Let's start this clinic." The

237

AIDS Clinical Research Center put a large amount of funding in to
get it started, and then the funding slowly declined as the
clinic began to pay its way. Now it's a full-fledged, self-
supporting clinic with a big staff and many clients.

Hughes: The name implies that it's not strictly an AIDS clinic.
Ziegler: Well, it's sort of a euphemism; I think it's 99 percent AIDS.

Hughes: Is that part of the UCSF history of not really wanting AIDS
there?

Ziegler: Yes.

Hughes: Does it see other adult immunodeficiencies?

Ziegler: I suspect so, but I'm not sure there's anything that isn't AIDS,
[laughs] I mean, it's an AIDS clinic. In Uganda, they call an
AIDS clinic an immune suppressive syndrome clinic--ISS. They
will not say the "A" word. So it's universal. People don't like
the label.

Hughes: All right, let's stop.

Early Lymphoma Cases

[Interview 2: February 16, 1994] ##

Hughes: Dr. Ziegler, do you remember vividly your first AIDS patient?

Ziegler: Yes, I do. My first AIDS patient was a gentleman who came in
with the typical early manifestations of AIDS, with oral
candidiasis, fevers, lymphadenopathy , and just feeling pretty
punk--no energy. And as we followed him along, he developed a
very large lymph node in his neck, which we biopsied, and it
turned out to be a Burkitt's lymphoma, which is one of my great
interests. So we were quite astonished to find that lymphoma as
a manifestation of what we were regarding in those days as some
kind of gay syndrome of immunodeficiency, but cause unknown.

It seemed to remind us that we were dealing with an
immunodeficiency disease. Lymphomas of that type are very common
in Africa where I worked, but then very rarely do they appear in
young people in this country, except when they become severely

immunosuppressed,
and so forth.

238

as we know now through kidney transplant series

Hughes: Which hadn't been clear prior to that?

Ziegler: Hadn't been described before that. In fact, when we started

talking amongst ourselves — and I think one of the great virtues
of our little consortium, our Kaposi's sarcoma clinic, was that
we all got together practically every week and exchanged views.
Pretty soon, it was clear that there were a few other cases of
lymphoma in the San Francisco area that were occurring in gay
men, something that we hadn't anticipated.

So a few of us got together, pooled our resources, and
reported the first four cases of lymphoma as a kind of an
outbreak. That appeared in Lancet in 1982, l and was one of the
first reports. And then later, we accumulated a large series of
patients from many different medical centers around the country,
about ninety different cases, and that turned out to be the
definitive example of lymphoma as a diagnosis of AIDS.2 And
based on that paper, the CDC changed their AIDS-def ining
conditions .

Problems with Chemo- and Radiotherapy

Hughes: What did you do for lymphoma patients such as these in the early
days?

Ziegler: We obviously knew we were dealing with immunosuppressed people,
and when we started giving them standard chemotherapy and
standard radiation therapy, we got quite a surprise. They were
very fragile. They did not do well with chemotherapy or
radiation therapy. They got quite toxic. Their bone marrow
reserves were very limited, and when they got chemotherapy, their
white counts bottomed out, as we say. When they got radiation
therapy to the mucosal areas, they got very bad mucositis. So we
were clearly dealing with a group of people who were not normal
hosts, and that tied our hands with respect to therapy. We had
to back way off on the intensity of therapy.

1 J. L. Ziegler, W. L. Drew, et al. Outbreak of Burkitt's-like
lymphoma in homosexual men. Lancet 1982, 2:631-633.

2 J. L. Ziegler, J. A. Beckstead, et al. Non-Hodgkin1 s lymphoma in 90
homosexual men. New England Journal of Medicine 1984, 311:565-570.

239

Hughes: Wouldn't there have been a red flag in your mind when you knew

you were dealing with immunosuppressed people, and you knew that
radiation normally surpresses the immune response?

Ziegler: Well, there was no way to anticipate it, until the early

experience. We wouldn't have guessed that these patients would
have reacted to the chemotherapy in such a strong way. They just
don't tolerate it.

Hughes: Oh, you're saying chemotherapy; I'm thinking of radiation
therapy.

Ziegler: Well, even the radiation was pretty toxic, too. But

chemotherapy in healthy individuals is pretty well tolerated, and
some can be cured. But for these patients, you just couldn't get
away with the standard doses. They were just too toxic.

Hughes: These were drugs that you had used with success on other forms of
cancer?

Ziegler: Yes. Absolutely. KS and lymphoma both.

Hughes: Well then, when they didn't work, what did you do?

Treating Opportunistic Infections

Ziegler: Well, we began to realize that by the time people get lymphoma

and some of these other bad tumors, they also have a lot of other
problems as well. They were getting Pneumocystis pneumonia; they
were getting Mycobacterium avium, the tuberculosis condition;
they were getting cryptococcal meningitis. They were getting
other opportunistic infections that were very seriously
compromising their longevity. So we began to wonder if there
were certain circumstances in which we shouldn't treat them at
all, rather than really compromise them with chemotherapy and
then watch them die of some other opportunistic infection.

So for a number of years, there was a debate about whether
to treat, or if you were going to treat, how vigorously to treat.
Nowadays, I think we would treat, because we've got effective
ways of postponing some of those opportunistic infections with
prophylactic therapy. But in the early days, we really didn't
know what we were battling with.

240

Diagnostic Criteria

Hughes: What were the things that you were particularly looking for to
diagnose AIDS, in those very early days?

Ziegler: In the early days, before even the word AIDS came out, we didn't
give it a name. Somebody wanted to call it GRID [gay-related
immune deficiency], and that didn't seem to sit right, because we
knew it was not a totally gay-related disease; there were other
people who were susceptible. I guess I strayed off the question.

Hughes: What criteria were you using for diagnosis?

Ziegler: Well, we saw two different syndromes early on. Don Abrams was
following a group of men who had developed idiopathic
lymphadenopathy, called lymphadenopathy syndrome. In fact, Don
and I wrote an article for one of the very first textbooks on
AIDS by DeVita, Hellman, and Rosenberg that described that
lymphadenopathy syndrome,1 and then Don subsequently published
it.2 But what we were dealing with there was of course the
earliest manifestation of the AIDS epidemic, before individuals
got bad opportunistic infections.

Then what we noticed was that, as time went on, these lymph
nodes began to melt away, and then the patients started getting
thin, feverish, and quite miserable. They lost a lot of weight,
and they got very pale and fatigued. But we didn't have any
strict criteria. I think Pneumocystis pneumonia, any
opportunistic infection, and then Kaposi's sarcoma and the
lymphomas were diagnostic for AIDS. By that time, the CDC had
set up diagnostic criteria, and then as you know, when time went
on, things got added to it. But we were following CDC.

Hughes: Were some of those criteria set up at the KS meeting in September
1981?

1 J. L. Ziegler, D. I. Abrams. The lymphadenopathy syndrome and AIDS.
In: V. T. DeVita, S. Hellman, and S. Rosenberg. Acquired Immune Deficiency
Syndrome . New York: McGraw-Hill, New York, 1985, pp. 223-234.

2 D. I. Abrams, B. J. Lewis, et al. Persistent diffuse
lymphadenopathy in homosexual men: Endpoint or prodrome? Annals of
Internal Medicine 1984, 100:801-808.

241

Ziegler: No, I don't think so. I don't know when the CDC actually
published their early criteria for the syndrome,1 and they
certainly didn't call it AIDS until I think we were well into
1982 somewhere. So when their first criteria were published, I
think it had to do mainly with an acquired immune deficiency in
gay men--I can't remember quite how they characterized it. But
we used their criteria.

Epidemiology

Ziegler: The CDC people were out here all the time, of course. Jim
Curran, Harold Jaffe, and Don Francis and their group were
spending a lot of time in California trying to figure out what
was going on in San Francisco and L.A.

Hughes: Looking strictly at the epidemiology?

Ziegler: Yes. They were very interested in what was the network, how were
people passing the disease, was there a connection between the
different people who developed these conditions, what was the
connection.

Their early papers, I think, were really extremely good
examples of fairly complex epidemiology, because there were a lot
of cof actors here. For a while, everybody thought it might be
hepatitis, for example. Some hepatitis B [virus] was found in
lymphocytes, and the epidemiology behaved very much like
hepatitis — sexually transmitted, parentally transmitted, and so
forth. But you couldn't really believe that a liver virus was
causing a profound immunodeficiency, but it seemed to be
something like that. In fact, for a while, as you know, in the
blood banks, hepatitis was a surrogate marker [for HIV], until
they got hold of the [HIV] antibody.

1 CDC published the first case definition of AIDS in September, 1982:
Update on acquired immune deficiency syndrome (AIDS) --United States.
Morbidity and Mortality Weekly Report 1982, 31:507-514.

242
Virology

Hughes: Well, this sort of problem occurred with CMV [cytomegalovirus] as
well, did it not? Both viruses, from my understanding, are very
common in sexually active homosexuals.

Ziegler: Right.

Hughes: How does a virologist go about figuring out what actually is
causing-- [laughs]

Ziegler: With great difficulty, I would have to say! We had Larry Drew

right here in San Francisco, who was very active in CMV research,
and of course Jay Levy, who has done a tremendous amount in the
AIDS epidemic. Jay was looking at Kaposi's sarcoma, thinking
that some of the clues to identifying the AIDS virus might come
from growing Kaposi's sarcoma cells. This may be one of the
peculiarities of the disease.

As I mentoned earlier, Jay and I also believed at the time
that you had to be immunosuppressed in order to get the disease
in the first place.1 In other words, that AIDS was like an
opportunistic infection. To some extent that was right, but
epidemiologically, it didn't fit with all the subsequent data.

The virologists I think had a heck of a time trying to
figure it out. Jay was working on it, and Larry Drew, and Girish
Vyas was interested in the hepatitis side of things. He had his
own theories. In the '81- '82 era, there was a mad and somewhat
confused scramble for an etiologic agent. Obviously, by that
time it was clear that AIDS was caused by an infectious agent
that was spreading from person to person. This agent had a very
long incubation period, was predominantly sexually transmitted
but could be transmitted by blood and through the birth canal,
and just nobody had a clue what it might be. And then Luc
Montagnier published his LAV paper, I think in November of '83,
and I think that this discovery was the main breakthrough on the
path to discovery of HIV.

1 J. A. Levy, J. L. Ziegler. Hypothesis: Acquired immunodeficiency
syndrome is an opportunistic infection and Kaposi's sarcoma results from
secondary immune stimulation. Lancet 1983, 2:78-81.

243

Early Theories about Etiology

Hughes: Were you yourself fixing on any particular virus?

Ziegler: No. I went back and looked over my slides once, and my notes at
those Kaposi's Sarcoma [Clinic] Conferences, and we had all kinds
of models. We used to have lunch afterwards and try and figure
out what was going on; we had drawings on table napkins. There
were basically two theories: One was a sort of concatenation
theory, where everything seemed to be conspiring in these people
to suppress their immune system. We thought this might be a
cumulative effect of multiple exposures to sperm and to viruses
and to hepatitis and CMV, and that was sort of a major immune
overload. But nobody could really buy into that, including us,
because it never happened historically, that you would get a
whole lot of different agents conspiring at once in the same
person. And then it certainly didn't explain why other people
were getting AIDS from blood. So that theory quickly fizzled
out.

Then we realized that there was something profoundly wrong
with the immune system, that was obviously acquired from sexual
and other exposures, and that it was predominantly attacking the
T4 cells, the CDA helper lymphocytes. Art Ammann had a lot to do
with making that particular discovery. I would say by the spring
of "82, everyone was pretty much convinced we were dealing with
an infectious agent. CDC by that time had published their very
nice homosexual network paper, showing that in Orange County-
L.A., everybody was having sex with everybody else, and you could
see the network drawing of these multiple sexual contacts.1

Hughes: Which indicated an infectious agent?

Ziegler: Presumably, yes, that there was something moving through that

group in a very rapid fashion. And then the question was, just
what was it? I think the thing that Montagnier did, which was
correct, was to look at the lymph nodes. That seemed to be where
the virus was going to be, rather than in the bloodstream, where
as we know, it was very hard to find the virus.

Hughes: But that wasn't an obvious thing to do, was it?

1 S. Fannin, M. D. Gottlieb, et al. A cluster study of Kaposi's
sarcoma and Pneumocystis carinii pneumonia among homosexual male residents
of L.A. and Orange County. Morbidity and Mortality Weekly Report 1982,
31(23) :305-307 (June 18, 1982).

244

Ziegler: Well, I guess in retrospect it should have been, because we by
that time had pieced together the natural history, where people
start getting lymphadenopathy, swollen lymph glands. And then
after a while, the lymph glands begin to go away; then patients
start getting very seriously immunosuppressed. And during that
phase, they go from relatively mild opportunistic infections like
thrush and herpes zoster to really serious, big-time
opportunistic infections like cryptococcal disease and
Pneumocystis and TB. We had begun to see that shift, so if you
were going to go for a tissue, you should go for one of the lymph
nodes .

Hughes: What about the technology? From what I know about the work in

Gallo's lab, there were some technical problems growing the cell
lines.1

Ziegler: Right. We actually sent material to Gallo. I attended a very
interesting conference in April of 1982. In fact, it was the
American Cancer Society's annual meet-the-press conference, so
they invited people out to talk about what they were doing. They
were interested in my observation about lymphoma.

So I was on the same panel with Bob Gallo, who was actually
coming not to talk about AIDS at all, but about HTLV-I [human T-
cell lymphotropic virus-I]. We met on a number of occasions,
because I knew him from NIH; we go way back to early days. I was
saying, "Bob, you know, your lab ought to get interested in AIDS.
I bet you we're dealing with some kind of human lymphotropic
virus here. It probably isn't HTLV-I." I think most people had
figured out that HTLV-I antibodies and so forth weren't present
in these patients. So it wasn't that virus, but I said, "Gosh,
it could be a relative."

Hughes: Why would you think that?

Ziegler: Well, as I say, it was spring of '82, we were pretty convinced

that it was a transmissible agent, that it was lymphotropic, that
it was doing something to the CD4 cells, and that it was
spreading from one person to another sexually. So it had some
commonality with HTLV-I.

Hughes: Well, behaving like that in some ways, yes, but it was cytopathic
where the others were—what's the term?

Ziegler: Oh, the HTLV-I was latent, you mean?

1 Robert Gallo. Virus Hunting; AIDS. Cancer, and the Human
Retrovirus: A Story of Scientific Discovery. New York: Basic Books, 1991.

245

Hughes: No, I mean that it was tumorogenic; it caused a proliferation of
cells. And this virus was doing the opposite.

Overstimulation of the Immune System

Ziegler: Well, not necessarily. What we were seeing in the beginning was
a proliferation of lymph glands. It was lymphadenopathy
syndrome. If you take out the lymph node and slice it up, it was
filled with lymphocytes, huge, giant follicles. So these
lymphocytes and these lymph nodes were really switched on.
Something was stimulating them into overdrive.

One of the things we learned, as I told you, was that a
lymph node in overdrive is not necessarily a good situation. You
know, we always talk about lymphoid stimulation as being a good
thing; we want to stimulate, rev up your lymphocytes so that
they're all ready to fight infection. In point of fact, that's
not the way the system works. This system works because the
lymphocytes are quiescent, and they only wake up when there's an
alien invader. If they're all in a state of nonspecific
activity, then they don't recognize any aliens, because they're
all pre-empted; they're all stimulated. In fact, the lymphocytes
are turning out all these cytokines which make people feel lousy.
So the whole idea of immunosuppression and immunostimulation
needs to be defined. Stimulation is not necessarily a good
thing. Immunodepression is not necessarily a bad thing, if
you're talking about numbers of switched-on lymphocytes.

Hughes: Is it AIDS that has caused this conceptual reorientation?

Ziegler: I think so, yes. I think a lot of people were talking about that
in the earlier days, and then [Anthony] Fauci emphasized it in
some of his work, that in point of fact AIDS is a disease, at
least in its earliest stages, of lymphostimulation, and
lymphostimulation is a perfect hotbed for viral replication, and
a very unsatisfactory way for people to ward off infections. So
you get into a positive feedback here: You set up the patient
for infections; he gets infections; the infections stimulate the
lymphocytes; the lymphocytes, thus stimulated, make more virus;
more virus kills more CD4 cells. So each time you get a
stimulation- infection cycle, you've kind of notched yourself down
the ladder, immunologically speaking.

Which probably explains as the disease progresses why the
lymph glands eventually involute; they just die of exhaustion.
When you do an autopsy on an advanced AIDS patient, you can

246

hardly find the lymph glands, because they're all atrophied and
shrunken .

Hughes: And that was known very early on?

Ziegler: Yes, pretty much. Some of the autopsies showed that there were
different stages. Most of the autopsies, you see, were done on
patients who had been far advanced, so they couldn't find the
lymph nodes in the autopsies. Whereas, the biopsies that were
done in, say, Don Abrams' [lymphadenopathy] group, all showed
lymphoid stimulation.

I think a lot of the credit goes to the group at Stanford
for showing that. Ronald Dorfman, who's really one of the world-
class lymphologists, first described what he called follicular
lympholysis. He saw that these lymph nodes in the early stages
were very, very densely packed--follicular hyperplasia, as they
call it. As the disease progresses, it goes into what he calls
folliculysis — the lymph nodes just completely dry up and
involute.

Hughes: Which you don't see in other diseases?

Ziegler: No. That was the very first time that had ever been described as
a progressive thing. And I think Ron Dorfman and another
pathologist, Karl Racz from Germany, were the first really to do
excellent lymph node dissections. And Harry loachim too, in New
York. All three of them, and the group at NYU, began to show
that this involution was clearly what was happening in the lymph
nodes. So all the road signs pointed to lymph glands as the site
of infection. All the epidemiology pointed to an infectious
transmissible agent. And it was just, who was going to be the
first to find the virus? Montagnier, I think, gets the credit
for that.

Hughes: You talked about this AIDS network at UCSF, which included Mt.
Zion. How closely did Larry Drew interact?

Ziegler: Larry Drew was very much a part of it, yes.

Hughes: And of course, you here at the VA, and San Francisco General.

But what about physicians elsewhere? How regularly were you in
touch?

Ziegler: As time went on, a couple of things drew the community together.
First of all, Donald Abrams I think gets the mountain of credit
for mobilizing the community of private practitioners [the County
Community Consortium] , because clearly a lot of the gay men who
were getting AIDS were seeing private practitioners in the

247

community. I can't remember all their names, but Don Abrams was
contacted by many of them, because he was gay himself, of course,
and he began to see a much bigger pattern in the community.

We were all brought together, I think from a community
standpoint, by Merv Silverman, [director of the San Francisco
health department]. He formed a task force under Mayor [Dianne]
Feinstein in those early days to mobilize the city's response to
the epidemic. The first and most obvious thing that he wanted to
do was to close all the bathhouses, and that makes a whole
interesting political-medical story of its own, that you may or
may not want . '

Hughes: But he didn't want to close the bathhouses at first.

Ziegler: Well, actually, I think, to credit him, he wanted to close the
bathhouses when he realized that they were the seat of the
highest likelihood of transmission of whatever the agent was. 1
think Dianne was less interested in closing the bathhouses
because the gay men were saying, "Look, you can't legislate our
sex lives. This is a liberal community. If legislation is
needed, we'll take care of it ourselves, but don't start closing
down our fun houses."

In the end, it went to the courts, and they had to decide
whether the bathhouses created a public health hazard or not. So
they sent undercover investigators into the bathhouses with pads
and pencils, and they sat in there and they wrote down everything
they saw. And then they brought it back, and they published this
huge tome full of—really just gay pornography is what it was.
It's all on record down here in the City Hall. In the end, the
judge ruled yes, the bathhouses should be closed, and so they
closed them and there was an immediate appeal, and a week later
they opened. And that was the end of the bathhouse story, as far
as I remember. Eventually, the bathhouses kind of withered away,
or cleaned up their acts.

Mervyn Silverman' s Medical Advisory Committee on AIDS
Hughes: Did you have any role in closing the baths?

1 See the oral history in this series with Mervyn F. Silverman, M.D.

248

Ziegler: Well, more or less as a consultant.1 There were about a dozen of
us sitting around the table scratching our heads. There were gay
doctors from the community. There was one, Bob Bolan, who was
very active, who had a huge practice. And then Donald and Paul
and myself, and Merv, the epidemiologist George Rutherford was
there, and Andrew Moss2. We were all trying to say, "Look, we
don't know what's causing this, but obviously there's something
moving very swiftly through the gay community. This is a lethal
condition, and whatever steps should be taken to curb it should
be taken."

Hughes: And what was the forum for this discussion?

Ziegler: This was Merv Silverman's AIDS task force. It was commissioned
by the mayor. We met on about a biweekly basis for quite a long
time .

Hughes: Were you in touch with physicians outside the Bay Area?

Ziegler: Obviously the epidemic was spreading to other parts of the Bay
Area. Progress of AIDS [research] was slower on the peninsula,
because Stanford was behind us in research initiatives. It was
quite advanced at Highland Hospital [Oakland], in Sonoma
[County] , and up in the Russian River area, where a lot of gay
men go for their holidays. So where you found gay communities in
concentration, you found people having to deal with this disease
in the early days of the epidemic. But it clearly was not
concentrated [only] in the Castro [District of San Francisco].

AIDS in the Gay Community

Hughes: Why did the epidemic manifest itself in the gay community, when
there's no biological reason why an infectious agent couldn't
spread beyond the so-called risk groups?

Ziegler: Yes. Well, it's my understanding that the virus was probably
introduced into San Francisco in the late seventies, probably
some time after 1976, 1977, in there. Although I didn't live
here at the time, it was my understanding that the whole era of

1 See, in the Appendix, Ziegler 's declaration in support of a
temporary restraining order to close the bathhouses, October 10, 1984.

2 The AIDS series includes oral histories with all these individuals,
except Rutherford.

249

the seventies, particularly the end of the seventies, was a
period of massive influx of young gay men to the Bay Area because
of the enormous permissiveness of sexual freedom. The Castro
became alive with gay activities.

I remember interviewing a number of my patients, many of
whom were very forthcoming about their sex lives. They would go
into a bathhouse and have encounters with ten or twenty
individuals, all anonymous, all in the dark. They had these
grope rooms and orgy rooms , and an extraordinary number of
practices in which there's really ample opportunity for
transmission of just about every bodily fluid into every bodily
orifice among these men, in repeated fashion, with multiple
exchanges of partners.

It turned out in the end, with all of the epidemiology, that
receptive anal intercourse was the worst, the most dangerous
practice, because infected sperm landing in the traumatized
rectum found a ready entrance into the bloodstream, and I think
that's how most of the cases were transmitted. But there were
probably many other routes as well. But it's very hard to tease
out exactly which practice is the most risky, because many of
these men did everything. It was hard to find someone who was
just exclusively a receptive intercourse person, and somebody who
was exclusively another—they just switched back and forth.

I think from the point of view of transmission, though, San
Francisco, L.A., New York, probably some parts of Houston and
Miami, were areas where this degree of homosexual promiscuity was
totally permitted and occurred.

Physician Networks

Hughes: Were you in touch with investigators in each of those locations?

Ziegler: We knew a lot about what was going on in L.A. because with the
AIDS Clinical Research centers [at UCLA, UCSF, and UC, San
Diego], we could keep in touch with our colleagues in L.A. They
pretty much were seeing exactly the same pattern. The
epidemiology was a little different, because their gay men were
spread out all over Orange County, whereas ours were all focused
in the Castro.

I had colleagues in Houston whom I saw at meetings who were
seeing quite a lot of AIDS in Houston. And then of course in New
York, [Alvin] Friedman-Kien and Linda Laubenstein. I had known

250

all those people before because of various other common
interests. When I wrote the lymphoma paper,1 for example, I had
known before many of these people [who contributed lymphoma
cases] through the oncology circles—Linda Laubenstein in New
York, Sandy Levine in L.A., Ben Koziner at Memorial [Hospital in
New York] , and so forth. So we already had a network. So when
AIDS came in and all these lymphomas cropped up, the network just
kind of went into action. Each institution pooled ninety
lymphomas for publication.

Hughes: So the structure was already in place prior to the epidemic.

Ziegler: Yes. It was kind of a loose structure of oncologists who all
knew each other; we knew each other's work.

Hughes: Do you think the same thing occurred in other specialties, for
example dermatology?

Ziegler: Yes. Definitely dermatology was the other link. Al Friedman-
Kien and Marcus Conant and their colleagues in L.A. all noticed
the Kaposi's connection simultaneously.

Hughes: Were those informal networks the main way of transmitting
information?

Ziegler: Pretty much. I think you'd have to get all that first hand from
Marcus,2 but I would have thought yes. They had known each other
before the epidemic.

Hughes: You relied on the networks because publication takes a long time,
and you were having to deal with patients now.

Ziegler: Yes. I'm sure Al [Friedman-Kien] and Marcus talked with each

other many times on the phone, and then contacted other people,
because when a dermatologist sees an excessive number of an
unusual disease, they report it to each other.

1 J. L. Ziegler, J. A. Beckstead, et al. Non-Hodgkins lymphoma in 90
homosexual men. New England Journal of Medicine 1984, 311:565-570.

2 See the oral history in this series with Marcus A. Conant, M.D.

251

Ziegler: We got a publication in Lancet I think in the summer of '82,

which was that outbreak paper.1 Then I went to work and got the
ninety patients and that was sent in around February of '84, just
before the virus was actually announced by Gallo in the spring of
'84, but by that time, of course, it was clear from Montagnier
and from others that we were dealing with a transmissible agent.
So yes, there was a lot of networking going on.

Hughes: So oncologists in general were pretty much alerted to watch for
lymphoma?

Ziegler: Yes.

Multidisciplinarity

Hughes: AIDS was a new disease. What did that allow you to do that was
different from working in a well-established field?

Ziegler: I found it terribly challenging and interesting and exciting.

Obviously it was a devastating clinical problem too, which needed
solutions. But from the point of view of an academic
investigator, it opened just huge avenues of research
possibilities. And as you say, we were in completely new
territory, and there has never been, except for maybe measles and
a few other conditions, an acquired immunodeficiency of this
degree.

We were tremendously puzzled by what was going on, and we
started networking with other disciplines, because clearly this
was a multidisciplinary problem. First of all, you were seeing
it in adults and in children; it involved oncology; it involved
infectious disease and opportunistic infections; it involved the
immunologists, and particularly those who were dealing with
congenital immunodeficiencies; it involved dermatology; and most
importantly it involved the epidemiologists, because in those
days, what we needed was someone to come in and say, "Here's a
pattern; here's how we can study it; this is what we need to do."
And they started establishing the cohorts, these very important
groups of people that gave us the profile of the disease over
time.

1 W. L. Drew, M. A. Conant, et al. Cytomegalovirus and Kaposi's
sarcoma in young homosexual men. Lancet 1982, 2:125-127.

252

Ziegler: I found it a very exciting opportunity because of all these
different disciplines all tuning in to the same problem.
Virologists of course, like Jay, all did a lot of sharing of
information and ideas. Everybody put in their contribution.
It's sort of like the proverbial elephant: we described the piece
we could understand. But bit by bit, we began to see the whole
beast.

Hughes: Had you ever worked with a multidisciplinary team of this nature
before?

Ziegler: Well, cancer is by its nature multidisciplinary. Cancer involves
on the biological side, a lot of knowledge of enzymology and
pharmacology and immunology, and from the clinical side,
radiation and surgery and chemotherapy and hematology. So yes, I
think I'd have to say, if there was one breakthrough in oncology
in the last two decades, it's probably been the fact that it does
draw all the disciplines together. In the days when I was in
training, doctors of different disciplines didn't often talk to
each other. The surgeons didn't talk to the radiologists. There
was no such thing as chemotherapy, except in the back wards of
some of the big hospitals. There was virtually no communication
about cancer, least of all with the patient.

Now, it's a revolution. The patient is the most proactive
person, and all the disciplines now meet together in tumor wards,
and share their data. So yes, by nature, oncology was already
multidisciplinary .

Hughes: Is it fair to conclude from this that oncology in a sense set a
precedent for a multidisciplinary approach to AIDS?

Ziegler: Yes, I think oncology gets a lot of credit for doing that.

People like Paul Volberding, who'd already finished his training
in oncology, were well tuned in to organizing these kind of
multidisciplinary groups, and engaging the virologists and
immunologists. He got quite a lot of support for that in the end
through grants and various other centers that were forthcoming.

253
AIDS in Africa

AIDS and Civil Unrest

Hughes: You said last time that information about what was happening in
Africa in terms of AIDS came in only as time went on. Why was
that?

Ziegler: Well, AIDS arrived late in Africa. I'm not exactly sure why. I
think part of it had to do with the mobility of people across the
continent—truck drivers—and also had to do with civil unrest in
various countries. I think Uganda suffered the worst, because it
had a major civil war. I think it's not surprising that the very
earliest cases of AIDS in Africa appeared in Uganda and in
Zambia.

Hughes: Is that Idi Amin's uprising in the early 1970s that you're
talking about?

Ziegler: That's right. I left Uganda in 1972, when Idi Amin took over.
Then there was a series of really brutal killings and almost
tribal genocide under Amin's reign. The deposed president, whose
name was [Apollo M.] Obote, was sheltered in Tanzania. The
president of Tanzania, [Julius K.] Nyerere, had no love lost for
Amin. So he mobilized the Tanzanian army under Obote 's
instigation to overthrow Amin. And it took quite a while to do
that.

In the process, the Tanzanian army marched up around the
west side of Lake Victoria, and on their way, of course, they
consorted with many prostitutes who were coming east from Zaire.
So a lot of the epidemiology centers on that movement of troops
through a relatively pastoral, rural area, and the arrival of
many prostitutes from eastern Zaire and Rwanda looking for
business. And of course, there is a lot of trans-African traffic
in that general area anyway.

So the way it looks , the epidemic was picked up by the
Tanzanian army, brought into Uganda on the western side of
Uganda, and the biggest-hit area was in fact where that army
spent most of its time, which was in the so-called "Luwero
Triangle" and Rakai district. That's the district which they
always show on the TV- -where old women and children are the only
ones left in the village because everyone else has died of AIDS.
But that's where there was much civil unrest and troop movement.

254

When the civil war reached Kampala, HIV went along with the
soldiers. About five or six years later, up comes HIV, in those
very areas. People began dying of what they called "slim"
disease, which was just a name for wasting and tuberculosis and
diarrhea and other manifestations of AIDS.

Hughes: Are the manifestations of AIDS different?

Ziegler: Different in Africa. The biggest problem in Africa has to do
with TB, which comprises about half of the cases of AIDS, just
garden-variety TB, not the M. [Mycobacterium] avium that is
prevalent in the U.S. And a whole range of opportunistic
infections--toxoplasmosis and cryptosporidiosis, the usual
things, also affect Africans. What they call "slim" disease is a
gradual, progressive wasting disease with diarrhea, where victims
just get thin as skeletons, and then ultimately die. These are
the main manifestations of AIDS in Africa, plus Kaposi's sarcoma.

Heterosexual Transmission

Hughes: In Africa, AIDS is a heterosexual disease, yet here it is usually
not perceived that way.

Ziegler: In this country, there is clearly heterosexual transmission. But
it seems to be quite unbalanced. It's much harder for women to
give HIV to men than the other way around. Maybe at a ratio of
about ten to one. So in the early stages of the heterosexual
epidemic, you have a few women infected, with the men being
relatively less infected by the women. But when men have a huge
turnover of partners, this collection of women serves as a
"point" source of infection, and as the epidemic progresses,
eventually the men become infected. And then the men take it
home and give it to their wives, or their next partner. So it's
transmitted much more readily from men to women than from women
to men, simply because, I think, it's partly a matter of
topography. The area of exposed genital mucosa is totally
different between the sexes.

Hughes: Was that true in the early days of the African epidemic?

Ziegler: I think it was true in the early days there too, but there were
repositories of virus mainly in the bar girls and the
prostitutes. And when they were tested for HIV, clearly the
prevalence was much, much higher than in the general population.
And in Nairobi, where a very good study was done on a lot of
prostitutes, within three years the numbers went from 30 percent

255

to 90 percent—virtually every prostitute was infected by 1990.
They also found in those days that genital sores and ulcers
clearly were a risk factor. So obviously, any break in the
genital mucosa increased the chances of both spreading it and
getting it.

Recognizing a Global Epidemic

Hughes: As this information came in from Africa, did it change how you
approached the disease here?

Ziegler: 1 think we were just becoming cognizant of the fact that this was
a world-wide epidemic. What we were dealing with was a virus
that was spreading predominantly by a sexual route, and
secondarily by blood and maternal-child transmission. But
primarily sexually. In Africa, it was heterosexual, and in the
U.S. it was largely homosexual, but there was plenty of overlap.

How did it affect us? Well, I think the effect was delayed.
I don't think people really paid attention to the AIDS problem in
Africa until around 1984- '85, when it was clear that the epidemic
was widespread and expanding. The problem was, what can you do
about it in Africa, and what can you do to treat it, diagnose it,
and so forth?

And that's really where the World Health Organization came
in. They made a big effort to set up a global program in AIDS.
Jonathan Mann, of course, is legendary for his work in setting
that up. They went really worldwide, because there were
obviously problems in Brazil, in Thailand, now in India and
Burma. By 1985 the World Health Organization was getting into
high gear to try to bring this epidemic under control.

Hughes: Did it reinforce in a sense what you already knew, that the
problem was not confined to the so-called risk groups?

Ziegler: Yes. I think most definitely.

Physician Decisions Regarding Involvement in the Epidemic

Hughes: Well, going back to the UCSF scene, Dr. Conant said in his oral
history, and I quote, "John" --meaning you- -"was extremely

256

effective at bringing respectability to an epidemic that the
university didn't want anything to do with."1

Ziegler: [laughs]

Hughes: How were you bringing respectability to the epidemic?

Ziegler: Oh, I don't know what he meant by that. I think basically what
happened was that there was just a small group of us very
interested in an epidemic that was really highly stigmatized. I
think that there were some people who, while they recognized that
this was a devastating medical problem, were very uncomfortable
dealing with the homosexual community, dealing with a disease
that has so much stigma attached to it. I think some people just
found it not something they felt they could either deal with, or
be associated with. For whatever reasons, they just stayed away.

I guess Marcus just meant that he and I were probably the
most senior people in the academy, and I was a full professor in
residence, and I had a long career in academic oncology.

It was hard in those days to get some of the card-carrying,
best immunologists to give this disease some thought. Little by
little, they came on board. Dan Stites was one of the first
[immunologists] to really get involved, and Art Ammann.

More on AIDS Activities at the VA

Early Research and Clinical Work

Hughes: I read that a Kaposi's sarcoma follow-up clinic was founded at
the VA as early as 198 1.2 Were you behind that?

Ziegler: Yes. Well, I did most of the AIDS work here until Ira Tager and
Peter Jensen got involved in it in the mid-eighties. They are
both trained in infectious disease. In fact, their predecessor
was a retrovirologist named Ashley Haas. He was here in the
first year of the AIDS epidemic. We used to meet and talk about

1 Oral history in this series with Marcus A. Conant, M.D., p. 162.

2 Peter M. Elias, M.D. , to all dermatology residents and staff and
Bielan, R.N., October 12, 1981. Ziegler correspondence, AIDS History
Project, Department of Special Collections, UC San Francisco Library.

257

it, because one of the things he thought about was, gosh, could
this be a retrovirus? He worked in "slow viruses", and in fact
wrote a very good paper on it after he left. But he went off to
Minnesota in 1982, so we lost our only retrovirologist .

Hughes: Was it unusual to have an individual doing very specialized
research at the VA?

Ziegler: Well, it's not unusual here, because we have really world-class
investigators in every area. But he just happened to be a
retrovirologist, which was extraordinary, and I guess if history
had taken a slightly different turn, Ashley might have been the
person to discover HIV.

Hughes: What made him think that it could be a retrovirus?

Ziegler: Because the disease looked exactly like what he was familiar

with, the scrapie virus in sheep, and there's also a retrovirus
in goats and horses, and all showing manifestations of immune
deficiency and other disorders.

Hughes: The long latency--

Ziegler: Yes, long latency, the dementia, the immunodeficiency, all of

those things were very common in these diseases caused by animal
retroviruses.

AIDS Activities from 1985 On

Ziegler: But I don't think really much happened at the VA until we got the
AIDS Clinical Research Center set up in '85 at UCSF. Once that
was running and we had money available, then we started bringing
people into the VA for AIDS activites. We hired Sandy Charles as
a research nurse, got the clinic in better shape, and started
registering AIDS cases. Ira Tager got quite interested in it, as
the new chief of infectious disease, and he set up a larger AIDS
registry, and then things started moving along at a little faster
pace.

By 1988 we got very serious about AIDS investigation when we
were awarded our AIDS VACARE grant, the VA Center for AIDS
Research and Education, which I started with Martin Heyworth, who
now runs it. That primarily is an investigative center. We have
a very good track record now in new AIDS discoveries.

258
Seeing Patients

Hughes: In the early days, when it was pretty much you alone seeing AIDS
patients at the VA, how did you deal with opportunistic
infections? You presumably are not an expert on infectious
disease. How did you handle patients with problems that really
weren't in your territory?

Ziegler: Well, they were partly in my territory, insofar as a

chemotherapist renders people immunodepressed with cytotoxins.
So as a profession, we have to deal with opportunistic
infections. In fact, a lot of the early cases of Pneumocystis
pneumonia were seen in leukemia patients who were treated with
prednisone. So I was pretty familiar with the opportunistic
infections, and we just treated them as part of our daily
oncologic experience. But HIV disease obviously began to involve
many other specialties—pulmonary for PCP and the other
infections, neurology for dementia, dermatology clinics for
Kaposi's and other skin problems.

We started doing some clinical trials in Kaposi's here,
trying to figure out what was going on. Paul Volberding and I
did a couple of early trials.1

Hughes: What was the referral system? How did an AIDS patient actually
come to appear in one clinic or another here?

Ziegler: In the VA, it was hit or miss until we formed the AIDS clinic in
1985. If they had cancer, they came to the oncology clinic; if
they had infection, they would come to the infectious disease
clinic.

Hughes: Referred by a community physician?

Ziegler: Many patients were either in the system or got referred in by

community physicians when they turned out to be veterans, because
veterans have more or less free care here. So, of course, our
population was almost entirely male. It was generally the older
males. So the VA lagged behind the rest of the city a little bit
in its referral patterns for AIDS. We now have about 800 AIDS
patients registered, but in the early days, there were maybe
twenty, thirty, forty- -not too many. Not nearly the number they

1 J. L. Ziegler, P. A. Volberding, L. Itri. 13-cis retinoic acid for
Kaposi's sarcoma. Lancet 1984, 2:641; P. A. Volberding, D. I. Abrams, et
al. Vinblastine therapy of Kaposi's sarcoma in AIDS. Annals of Internal
Medicine 1985, 103:335-338.

259

were getting down at the General,
Conant's clinic.

for example, and in Marcus

Hughes: There were three clinics here, which I would think must have been
seeing AIDS patients—the dermatology clinic, the oncology
clinic, and the infectious disease clinic.

Ziegler: Primarily oncology. That's where I saw most of my patients,

because I was already part of the oncology clinic. So we saw the
Kaposi's, and the lymphadenopathy patients would come up there as
well. Not that they had malignancy, but they knew we were
interested in patients with enlarged lymph nodes.

Hughes: Who knew?

Ziegler: Well, the doctors around—it got around pretty quickly that we

were interested in this problem, so patients would filter in from
other clinics.

Laboratory Tests

Hughes: In those early days, what sorts of lab studies were you ordering?
Ziegler: You mean clinical lab studies?
Hughes: Yes.

Ziegler: Just the usual things. It was a little [while] before we could

understand why the CD4 lymphocyte count was the critical count in
HIV disease, so we would order just lymphocyte counts and blood
counts and sort of fly by the seat of our pants, do some skin
tests, see if they were positive, that sort of thing. But we
didn't have any sophisticated lab studies at all, not until the
CD4 count became available as a routine test.

Hughes: Did that hold you back?

Ziegler: Yes, I think so. It took a while to get set up. That was a very
complicated affair- -it involves flow cytometry and a big machine,
a technician; it was an expensive procedure. So we didn't get
set up for that until I guess '86, '87.

Hughes: You couldn't farm this work out to UCSF?

Ziegler: Yes, we did in the end, and sent blood over there. In fact, I

used to drive it over there myself and deliver it, to Dan Stites'

260

lab [in the Department of Laboratory Medicine]. They were the
first ones to run CD4 counts here. They were useful for getting
the baseline counts and so forth.

The AIDS Specimen Bank. UCSF

Hughes: Well, that leads rather nicely into the tissue bank. You are
given credit, and John Greenspan, for having the concept of
establishing a tissue bank.

Ziegler: Yes, I think these ideas all developed spontaneously in the

faculty dining room [at UCSF] . But we knew we were starting up
with an epidemic. We didn't know what was going to turn out to
be important, or not. We knew that we should start getting
baseline data to get patients registered as AIDS cases, and we
probably should store away some serum samples just in case it
turned out to be something we'd want to go back and look at.

I had already had a lot of experience with tissue banking
because of the work in Burkitt's lymphoma in Africa. We had a
huge serum and tissue bank there, that's still extant at the NCI.
So I had already learned how to bank serum.

We sought funds to do that from our very first grant from
the NIH [Spring 1983], and we were awarded funds to do that.
John Greenspan agreed to set up the bank.1 Then from there on,
all the credit goes to him. He did a fantastic job, and runs it
like the Chase Manhattan [Bank]. Every sample is accounted for,
there are rules for taking specimens out, and for collaborations,
and feedback for the results of the studies. It's a beautifully
run tissue bank.

Hughes: Are its contents available to any legitimate researcher anywhere?

Ziegler: Yes. He's written several articles about it,2 and it's

registered in the NIH repository of AIDS samples and so forth. I
must say, he probably has generated about 200 papers out of those
sera. For example, samples from one of the big epidemiology
cohorts is being kept there, the huge cohort of gay men that's

1 For more on the tissue bank, see the oral history in this series
with John S. Greenspan, Ph.D.

2 See, for example: J. S. Greenspan, M. Conant, et al. The UCSF AIDS
specimen bank. Laboratory Medicine 1991, 22( 11) :790-792.

261

being followed longitudinally [Warren Winkelstein's San Francisco
Men's Health Study].1 Well, if you wanted to go back and look at
all those sera and test a hypothesis, they're all sitting there.

Hughes: That is known nationally?

Ziegler: Oh, yes. I'm sure John can fill you in on all the details,
because he keeps the records, and publishes an account.2

Hughes: Was there any particular reason that he took the tissue bank on?

Ziegler: I think you'd have to ask him. That came about working on the
AIDS problem. He and Deb[orah Greenspan] had already, I think,
identified the oral hairy leukoplakia, for which he is now
credited as co-discoverer, and he was very keen to play a role in
the epidemic. John then got his oral AIDS center started up [in
the UCSF School of Dentistry] and became one of the great
champions of AIDS research. I think all of the credit for the
tissue bank, beyond the concept, goes to him. He really made it
work.

Association with the Gay Community
A New Experience

Hughes: Had you had previous contacts with the gay community?
Ziegler: No.

Hughes: What did that experience mean to you professionally and
personally?

Ziegler: Well, I had never really had very much to do with gay people in
my professional life—or my personal life, for that matter. So
it came as a big shock to me to find out this whole subculture.

1 For the history of the San Francisco Men's Health Study, see the
oral history in this series with Warren Winkelstein, M.D., M.P.H.

2 For an annual report, see, for example: J. S. Greenspan, P. A.
Volberding. AIDS Clinical Research Center [ACRC]. November, 1993.
[Available from ACRC, UCSF]

262

And of course, I didn't know anything about the gay community
before I arrived in San Francisco, until the early cases came to
my attention. I guess I learned everything by talking with
patients and hearing their stories.

They were very forthcoming, very friendly, and really
wonderful, intelligent, lovely people. I felt very badly for
them because they were just suffering from this terrible
epidemic. It never bothered me in any social way. I was never
embarrassed or discriminatory in any way. I just took it in
stride. I got very friendly with our patients.

My own secretary was a gay man, worked with me for five
years and developed AIDS and died, so I had one relationship with
a man whom I could see from health right straight through to the
end. It's very sad; he really was a lovely, lovely person, and
worked so hard.

Chairman, Sixth International Conference on AIDS, San
Francisco, June 20-24, 1990

Hughes: What about in terms of politics? I'm thinking particularly of
your role as an organizer of the Sixth International Conference
on AIDS, where--! don't have to tell you—there was quite a lot
of input from the gay activists.

Ziegler: Yes.
Hughes :
Ziegler:

Did that experience change your political views?

Yes, I would say it had a profound effect. The story is very
simple: When I took on this job as conference chairman in 1987,
we looked at the AIDS conferences as scientific gatherings for
traditionally advancing knowledge in the field, never thinking
really that patient involvement or people with the disease should
or could or would want to be involved in the more esoteric,
scientific aspects.

Well, the activists obviously changed the face of that
conference. Our colleague Bob Wachter, who was our program
director, should be totally credited with having his finger on
the pulse of that whole social change. He wrote a book about the

263

AIDS conference which is a very good read.1 He starts his book,
truthfully enough, by saying that when we were first approached
by the gay community, somebody said, "Look, cancel the
conference, because George Bush is requiring people coming into
the country to get HIV tested, and we can't have the conference
in the United States."

Being part bureaucrat, I said, "That's ridiculous. We've
made all these commitments. We've earmarked the finances.
There's no way I'm going to cancel this conference." And then
they said, "Well, if you can't cancel the conference, at least
move it to another place outside the country." We said, "No,
we've got these commitments."

And then the gay activists came to us with this great moral
dilemma: How can we condone putting on a conference in a country
that refuses to let the patients whom we are treating come to the
country without major discriminatory acts? Well, that kind of
hit me like a ton of bricks. I never really moralized about my
role as the conference director, but it became very quickly
apparent that we had to work hand in hand with the gay community
and work through this whole politico-social problem. Of course,
that whole story is told in Bob's book, and I don't have to tell
how we did it.

But I think it changed me. In the end, when we joined hands
with the AIDS activists and walked down Market Street, it was the
first time in my life I had ever taken to the streets for any
cause. And I must say, my heart was in it by that point. I
really did believe that the government had done badly by these
young men, that there was a homophobia and a stricture that was
predominantly very right-wing, Bush-Helms mediated in government,
and that it was holding up AIDS research, and had a negative,
adverse effect on these people. And I could really identify with
how strongly they felt about the issues.

The AIDS activists, I think, in turn, welcomed our
participation and our partnership, because we really reached out
to them and got them totally involved in the conference, put them
on all the committees. They made important program decisions,
and we negotiated everything with them right down to the last
detail. And in return, I have to say they kept their bargain.
They did not disrupt the conference until the very end. They did
promise a little "tweak". We weren't going to get away with a
huge conference like this in San Francisco without a word from

1 Robert M. Wachter, The Fragile Coalition; Scientists, Activists, and
AIDS. New York: St. Martin's Press, 1991.

264

the gay community. But they were very disciplined throughout the
conference. They went to all the sessions. It was a huge
success as far as nonprofit groups were concerned. There was a
real sense of community, I think, largely through Bob Wachter's
work with the activists and his ability to renegotiate with them
through this period.

And in the end, 1 must say that they won the day. I think
they made their statement, and they are now a part of the
landscape. So that's my story of the activists; a lot of
subplots of course.

Hughes: Yes. It's a story that can go on for hours.

NCI (National Cancer Institute)

Hypothesis: Separate Agents for AIDS and Kaposi's Sarcoma

Hughes: I read of an NCI [National Cancer Institute] program called SEER
[Surveillance, Epidemiology and End Results] which found that the
incidence of KS prior to 1980 in various participating cities,
San Francisco being one of them, was several times higher than in
cities such as Atlanta and Denver where AIDS is relatively rare.1
What does that mean?

Ziegler: There's a long story around KS and its epidemiology. But the

short version is that most people think that KS is caused by an
infectious agent, not HIV, but an agent that is passed along with
it, and that these were really two independent epidemics, both
following pretty much the pattern of advanced promiscuity in the
homosexual community in the seventies. And in point of fact, the
dermatologists, when they looked back and began to see that there
were a fair number of patients in their gay practices who had
Kaposi's sarcoma but who ended up not having HIV. And quite a
number, twenty, thirty, forty maybe. So for a very rare tumor,
that's a very high number of people in one risk group to develop
a tumor .

So the feeling was that there was another agent, that it was
being passed among gay men, that if you got it along with HIV,
you got bad Kaposi's sarcoma, or you had a much higher risk of

1 Robert S. Root-Bernstein, Rethinking AIDS; The Tragic Cost of
Premature Consensus. New York: The Free Press, 1993, p. 81.

265

getting Kaposi's sarcoma, than if you just got it by itself. But
if you got it by itself and you were a gay man, your risk was
higher than the general population. So my guess is that that
blip in the SEER data suggests that there was an agent in the
seventies transmitting Kaposi's sarcoma among gay men in those
endemic cities surveyed by SEER.

Hughes: An agent totally unconnected with HIV?

Ziegler: Totally unconnected, except when HIV accompanies it, it raises
the risk quite substantially.

Hughes: Do we then say now that HIV is a cause of Kaposi's?

Ziegler: I think we have to say that HIV is a cof actor that amplifies the
risk of getting KS. I guess the best analogy would be smoking
and asbestos exposure. If you get asbestos exposure, your risk
of lung cancer is not so high, except for certain kinds called
mesothelioma. If you smoke, your risk of lung cancer is
dramatically higher, depending on how long and how much you've
smoked. If you smoke and have asbestos exposure, the risk goes
up several hundred fold because of the interaction between the
two. So I think what we're talking about is sort of an
interaction phenomenon.

In other words, if you're a child in Africa and you're
unfortunate [enough] to get malaria and measles at the same time,
your likelihood of dying becomes very high, usually from
pneumonia. So these are disease interactions, and I think the
Kaposi-HIV is an example of that. I don't know for sure, because
nobody's found the Kaposi agent.1 I expect there's one out
there.

Hughes: It's amazing, with all the intense work, that an agent has not
been found.

Ziegler: Well, it's like Hodgkin's disease. People have thought for years
Hodgkin's disease was caused by an infection, and Epstein-Barr
virus got put up on the list, and maybe there are a few other
viruses as candidates. No one has been able to pin it down yet,
and we've had Hodgkin's around for a long time.

1 In 1995, a herpes virus, human hersvirus 8, was identified in KS
tumor cells. See, for example, J. Ambroziak, J. Blackburn, et al.
Herpesvirus-like sequences in HIV-infected and uninfected Karposi's Sarcoma
patients. Science 1995, 268:582-582.

266
Early Grants for AIDS Activities

Hughes: You spoke last time of the $1.4 million NCI grant, which you
believe was the first federal grant for AIDS. The American
Cancer Society grant, which you received in November, 1981, was
of course not a federal grant.

Ziegler: Yes. I suspect we got one of the very first AIDS grants from the
NCI; that I guess was in 1983.

Hughes: Yes, spring 1983. Please tell me as specifically as you can how
that money was spent.

Ziegler: It gave us the next leg up after the American Cancer Society

money ran out. That was only $50,000 for one year [January 1,
1982-December 31, 1982]. ' By the end of that year it was clear
we needed to continue the Kaposi clinic, we should start a serum
bank, we should start an epidemiologic study, and we should
provide some funds for various laboratories to go after the
immunology and the virology of the disease.

I can't remember the exact details of the grant, because I
think Paul Volberding was the principal investigator at the time,
but we divvied it up and basically kept the Kaposi clinic going,
started the serum bank, helped get Andrew Moss started with his
gay men's cohort, which was a very important epidemiologic
survey. Some money went to Jay [Levy], some went to Dan Stites's
immunology group, and one or two others.

Hughes: Well, how was it decided who was going to be PI [principal

investigator]? In this case, it was Volberding, and you were co-
Pi.

Ziegler: We never really worried about it. Paul and I just sort of traded
things back and forth over the years, and weren't concerned about
who got the credit for what . I think in those days , I had an
established career, and I had already written my papers and won
my prizes. Paul was on his ascendancy, and I thought it was
important for him to get some investigative experience. So
generally we worked it out as a kind of a trade-off. I think I
ended up with the directorship of the AIDS Clinical Research
Center and he ended up with the running of the grants. We just
went back and forth, just like the conference. We were good

1 Marcus A. Conant to Assemblyman Art Agnos, January 20, 1983.
(Marcus A. Conant Kaposi's Sarcoma Notebook, January-June, 1983. Conant ' s
dermatology practice office, San Francisco.)

267

friends and also just really very collegial about our academic
work. I can't remember a single time when we ever had a
disagreement.

Hughes: Amazing.

Ziegler: Yes, it is. He was just great to work with, easygoing, very
bright, very hardworking, very responsible.

Hughes: Where was Marcus Conant in all of this? He had an appointment at
UCSF as Associate Clinical Professor, but he wasn't a straight
down the line academic professor.

Ziegler: Yes.

Hughes: What difference, if any, did that make?

Ziegler: I think Marcus' career took a major shift when AIDS came along,
and I think he had to make a big decision which way to go. He
was obviously capable of managing and assimilating all of the
molecular biology and virology and immunology that went along
with AIDS, but I think his heart was in his private dermatology
practice. I think really when push came to shove, what he really
wanted to do was to take care of his patients and see them
through the best possible outcome of therapy.

Because of his silver tongue and his charisma and his
access, was able to become very politically important. He made
contact with Sacramento; he testified many times; he went on a
big crusade to get the state government to limit liability for
vaccine development, and he did a lot of this important work
behind the scenes. He just worked very hard for the politics of
AIDS at every level, including national. He started the AIDS
Clinical Research Center [1983], he ran it for a couple of years,
and we all kind of worked together.1 Then I saw his path veer
off toward his major interest in his patients, and toward a
political agenda that he felt strongly about. And he is very
effective at what he does. He is really good. He didn't abandon
the science; I'm sure he's still very current on what's going on,
but he just felt that with his talents and his interest, that was
the way to go.

1 See: Marcus A. Conant, Director. AIDS Clinical Research Center:
Progress Report, 1983-1984. January 1985. (J. S. Greenspan papers. UCSF
School of Dentistry, CN 92-0123, carton 3-92, folder: AIDS Specimen Bank
Report 83/84.)

268
B-Cell Immunodeficiency in AIDS and Immunostimulation

Hughes: Well, say something about the 1984 paper in JAMA on B-cell

deficiency, of which Art Ammann was prinicpal author.1 Tell me
how that ties in with T-cell deficiency, which was what most
people were thinking about, and with your theory of activation of
the immune system. [tape interruption while Dr. Ziegler reviews
paper]

Ziegler: The immunology of AIDS in the early eighties was almost as big a
mystery as it is now. There's still a long list of possible ways
that HIV can cause immunodeficiency, and nobody really knows
which is correct, or whether they all may be correct. But back
then, we were worried about the B cell arm of immunity,
particularly in children.

As a pediatrician, Art Ammann was worried about children's
antibody responses. He found that the B cells were all switched
on. They were as much activated as were the T cells. I think
what Art describes in that paper and what we subsequently came to
learn was that the whole immune system got stimulated, and as I
say, preempted. It was unable to do its job because it was in a
state of high alert. But all the cells were churning out useless
antibodies. The way the immune system normally works, as I
explained, is that it lies in wait, and when an alien comes in,
then it specifically responds to that antigen. So all this
nonspecific immunostimulation was doing no good. The system was
kind of "spinning its wheels."

But I think that was one of the earliest findings that
showed immunoactivation in AIDS. These patients had immune
complexes, and they had high gamma globulin levels. But when you
challenged them with an antigen, they couldn't make appropriate
antibody. That's reminiscent of other conditions where there's a
lot of immune stimulation, and you think the host is going to be
in great shape because it's got big lymph nodes and lots of gamma
globulin. It turns out they're not in great shape at all because
the lymphocytes are preempted.

Hughes: And was that a new idea?

Ziegler: I think it was a relatively new idea at the time. I don't think
we really appreciated how important it was with respect to HIV,

1 A. J. Ammann, G. Schiffman, et al. B-cell immunodeficiency in
acquired immune deficiency syndrome. Journal of the American Medical
Association 1984, 251, no. 11 : 1447-1449.

269

because it turned out subsequently that HIV becomes very
promiscuous, if you will, in lymphocytes that are already
activated and producing this positive feedback. So the more
activation, the more HIV replication you get. Now Anthony Fauci
is showing slides showing that when the immune system drops, the
activation goes up, and that these are reciprocal events which
actually worsen the AIDS.

In the early days, we thought, Well, here we have an immune
deficiency; maybe we should be stimulating the immune system.
Some people were actually thinking about giving BCG [Bacille
Calmette-Guerin] and some of these other old-fashioned immune
stimulants. Just the wrong thing. In fact, the next year, Dan
Stites and I wrote a paper suggesting that we should actually try
immunosuppressives to calm down the immune system, to put it at
rest.1 There was a group in France headed by a chap named Jean-
Marie Andrieu who actually did try cyclosporin treatment in
French patients, and got quite interesting results. But he was
very badly maligned at the time because, unfortunately, they made
an announcement in the press before they had published their
paper, and it got a big play in the newspapers, and AIDS
investigators thought they were kind of crazy.

Actually, as it turns out, it was not a bad idea at all, and
Anthony Fauci in his very latest paper in Nature last fall said,
"Cyclosporin might be working." [laughter] So the unfortunate
thing is that in the immunology of AIDS, you can find these very
trendy things happening, rediscoveries of old pieces of evidence
that make people take a fresh look at things. But I think from
my vantage, immunostimulation is bad news. It probably is also
good news for the virus, bad news for the host, and that's pretty
much what that paper showed.

AIDS; An Autoimmune Disease

Hughes: In 1986, you and Dan Stites published a paper suggesting that
AIDS is an autoimmune disease.2

1 J. L. Ziegler, D. P. Stites. Hypothesis: AIDS is an autoimmune
disease directed at the immune system and triggered by a lymphotropic
virus. Clinical Immunology and Immunopathology 1986, 41:305-313.

2 Ibid.

270

Ziegler: Yes. HIV gains access to the immune system through a sort of

lock-and-key arrangement. We were trying to figure out what the
CD4 molecule—this is the marker of one of the lymphocytes- -does
under normal circumstances. Why is it there in the first place?

It turns out that it is a recognition molecule for linking
lymphocytes with macrophages so they can read a new antigen. The
new antigen comes into the body, it gets into macrophages, gets
presented on the surface of the macrophage, and then each
individual lymphocyte has its own kind of code. If it codes in
to that new molecule, it latches on, with the help of the CD4
molecule, and it goes into an activation state, saying, "This is
an alien protein and I'm going to get myself duplicated to fight
it."

We postulated that the HIV must resemble the normal "ligand"
for CD4. This turns out to be a class II molecule found on the
surfaces of macrophages (and B cells). These "look-alikes" might
confuse the immune system. For example, if the body was making
antibodies to HIV, then those antibodies might cross-react with
the macrophages. Likewise, there is such a thing as anti-
antibodies, which might also cross-react with the CDA.

We reasoned in that paper that this so-called antigen
mimicry might disrupt the main recognition apparatus of the
immune system in such a way that the presence of alien invaders
couldn't be transmitted to the immune system because of this
blockade. Further, the MCH [major histo-compatibility complex]
class II mimicry might trigger a "host versus host" response, an
idea taken up by later workers.

Over the last six years, some supportive evidence suggests
that "autoimmunity" is at least one mechanism by which HIV does
its damage to the immune system. It gets a little more
complicated, because since then, there has been some information
about super-antigens that nonspecif ically stimulate the
lymphocytes, and then they just implode.

There are other theories that in fact HIV sort of becomes an
alien molecule and creates a kind of a graft-versus-host disease
within the body. We called it in our paper "host versus host."
but there is a condition called graft versus host, where if you
take immune cells from one person and put them into another,
there is an immune reaction that takes place where one set of
immune cells fights the other set. That seems to be what's
happening in AIDS. You get the same thing: You get
lymphadenopathy, you get immune stimulation, you get weakness,
weight loss, all the symptoms.

271

So anyway, that hypothesis still gets quoted in most
articles looking at the pathogenesis of AIDS, including Fauci's
recent one. And I think it's on the list of potential reasons
why the immune system fails.

Hughes: How was it received at the time?

Ziegler: I think the idea of autoimmunity was appealing, because a lot of
autoimmune conditions are caused by what we know as antigen
mimicry: Something gets into the body that is a look-alike. The
body makes an immune response to it, and then pari passu begins
to attack the other tissue antigens which resemble it. There are
plenty of diseases that are caused by that mechanism. Therefore,
it would seem logical that HIV, which is a virus carrying a
molecule that looks like a MHC class II antigen, could in fact
incite such a reaction. And I think there is some evidence that
it does. I don't think it's the main cause of immunodeficiency,
but I think it's probably one of the contributors.

AIDS Education

Hughes: What about AIDS education?

Ziegler: I was very interested in this aspect.1 We've obviously had lots
of audiences to educate—patients, doctors, nurses, general
population, and so forth. I worked a lot in that over the years.
We made a training video for house officers, which is often used.
We produced pamphlets about safety, prevention, and housestaff
training. We sat on committees [devising protocols for]
universal precautions, training medical students, AIDS
curriculum, et cetera. For two years [1988-1990], I was on the
board of trustees of the Marin Community Foundation. I was their
main AIDS man in Marin, and we held round-table forums and
conferences that had to do with AIDS education in the community.

Hughes: Was there any hesitation or censorship of sexually explicit
language?

1 Dr. Ziegler has been director since 1988 of the VA Center for AIDS
Research and Education. He was also co-principal investigator [1986-1989],
with Dr. L. Zegans, of the AIDS Professional Education Program, funded by
the National Institute of Mental Health. From 1988-1994 he was associate
investigator at the Center for AIDS Prevention Studies, UCSF, for the
International Training Program in AIDS Epidemiology, funded by NIH.

272

Ziegler: Well, Marin's a pretty liberal place. The county had a very
modest AIDS problem to start with. The epidemic has worsened
over the years. But no, there wasn't very much censorship.
There was a lot of community interest. So I did a lot of AIDS
education, here at the VA, at UCSF, in the community, making
videos and pamphlets and lecturing.

Alternative Therapy

Hughes: Do you care to comment on alternative therapies for AIDS?

Ziegler: Some are very interesting, although they are intuitive. Some of
them are awfully flaky. You never know when an alternative
therapy is going to turn up something positive. Rational therapy
is only rational on the surface. Then you get very empirical as
soon as you start looking a little deeper. But I've never
discouraged patients from alternate therapy, as long as it does
no harm, or doesn't interfere with a clinical trial or other
treatments known to be helpful.

In those days, gosh, there was everything under the sun--
huge, huge doses of vitamin C. There was a guy down on the
peninsula who gave grams and grams of the stuff, which one of my
patients took religiously. Vitamins, and nowadays I think
antioxidants--a whole bunch of alternative treatments are out
there.

The San Francisco Model of AIDS Care

Hughes: How do you define the San Francisco model of AIDS care?

Ziegler: I think that's basically Paul's bailiwick. The definition is the
creation of a multidisciplinary clinic with comprehensive care
for AIDS patients, and predominant management in the outpatient
setting. The idea is to try to get everything done on an
ambulatory basis so that people can stay out of hospitals as long
as possible and have a good quality of life. Part of this is the
involvement by the community NGOs [nongovernmental
organizations] --Meals on Wheels, hospice, and the support groups
that characterize the nonprofit organizations in San Francisco.
I think these are just immensely impressive, the way those groups
mobilized on a shoestring.

273
The Personal Impact of the Epidemic

Hughes: Do you think that the epidemic has changed the way you relate to
your patients?

Ziegler: Oh, yes. I'm much more humble, I think. [laughs] I'd never

been arrogant, but generally an academic comes to these problems
with a sense that modern science has the power to overcome
disease. Then you come face to face with a really intractable
illness. This disease is truly a major challenge. There are
small bits of progress here and there, and hopefully a vaccine or
something else will come in the future. But right now, we are
very limited in what we can do. So I think it's just a matter of
humility in the face of the adversity of nature that keeps you
honest in this business.

Hughes: Do you think of yourself as an AIDS physician?

Ziegler: Oh, not really. I think of myself as a physician first, and as
an AIDS physician second. My own career has been very eclectic.
I've done pediatrics, adult medicine, and general practice. I've
done oncology, I've done AIDS, research, education—a little bit
of everything. So I don't pigeonhole my professional life.

Hughes: Do you want to comment on how the epidemic has affected you
personally?

Ziegler: Sure. I've learned a great deal about activism and what it can
accomplish and what it can't. I've learned a lot about
homosexual culture and the homosexual community, and the IV drug
abusing culture and community, which I never knew and wouldn't
have really known much about otherwise. I think I've changed my
political views from conservative to a great deal more liberal
than they ever were, simply on the basis of personal contact with
people and watching the activists and what they can accomplish,
and empathizing [with] how they feel as a community, because it's
easy to identify with these young, well-educated people. This is
not a marginalized group by any means.

What else? I guess it's made me a little more humane, as
far as dealing with really dreadful illnesses are concerned. And
I think the collegiality that has developed among people who are
fighting the AIDS epidemic has been very rewarding for me
personally. I have the highest regard for my professional
colleagues, but we've also become in many ways personal friends,
just being thrown together in this arena. And that, I think, has
been a big plus. We all shared a lot of the same feelings and
same motivations, too.

274
The Epidemic's Impact on Health Care and Research

Hughes: What has been the impact of the epidemic on the way health care
delivery is structured in this country?

Ziegler: I suspect AIDS is one of the things that is propelling us towards
this so-called health care reform. Another major public health
catastrophe will really push us over the edge, but I think AIDS
gave a big shove in that direction. The cost of taking care of
otherwise healthy young people is becoming a major burden on the
health care system, along with business as usual. People are
still getting heart disease and cancer at the same rate. So it's
had a big impact there.

The activism issue has made everybody sit up and take
notice. I suspect we'll see more of that in other diseases.
We're certainly seeing it more now in breast cancer, and in
possibly other illnesses as well. Other impacts? Well, I think
it's helped to do what medicine needs to do anyway, and that is
to get more interdisciplinary networking. But it's also raised a
very interesting and important ethical issue about whom doctors
are obliged to treat, and I think reaffirms the Hippocratic Oath
of helping people and not discriminating against patients because
of whatever [disease] they might have. So I think there's been
an ethical benefit.

I think the epidemic has been a real shot in the arm for
research. Very often, research never ends up finding what it
started out to find. There are always little side arms that come
up and distract and attract, and many discoveries come
unexpectedly anyway. So being able to put this much effort into
a field in which there is now a huge body of knowledge of
virology and immunology is going to have major good spinoffs in
other directions. I'm sure a lot of people could make lists of
good things that have happened in other fields. Borrowing AZT
from cancer chemotherapy to use against the virus is a perfectly
good example of how these fields interact. And I'm sure there
will be plenty of discoveries in the AIDS field that will help
other diseases as well.

Hughes: Do you have anything that you want to add or set straight?

Ziegler: I don't think so. You've got a very good interview program here.
No, I don't think I could add anything.

Transcribed and Final Typed by Shannon Page
Editorial Assistance and Index by Celeste Newbrough

275

TAPE GUIDE--The AIDS Epidemic in San Francisco: The Medical Response, 1981.
1984: Volume IV

Interviews with Donald P. Francis. M.D.. D.Sc.

Interview 1: September 30, 1993

Tape 1, Side A 1

Tape 1, Side B 15

Tape 2, Side A 27

Tape 2, Side B not recorded

Interview 2: December 22, 1993

Tape 3, Side A 35

Tape 3, Side B 51

Tape 4, Side A 68

Tape 4, Side B 77

Interview 3: February 11, 1994

Tape 5, Side A 87

Tape 5, Side B 99

Tape 6, Side A 112

Tape 6, Side B not recorded

Interviews with Merle A. Sande, M.D.

Interview 1: September 21, 1993

Tape 1, Side A 117

Tape 1, Side B 128

Tape 2, Side A 141

Tape 2, Side B not recorded

Interview 2: September 23, 1993

Tape 3, Side A 150

Tape 3, Side B 168

Interview 3: January 3, 1994

Tape 4, Side A 171

Tape 4, Side B 182

Tape 5, Side A 191

Tape 5, Side B 200

276

Interviews with John L. Ziegler, M.D.

Interview 1: January 28, 1994

Tape 1, Side A 202

Tape 1, Side B 218

Tape 2, Side A 227

Tape 2, Side B not recorded

Interview 2: February 16, 1994

Tape 3, Side A 237

Tape 3, Side B 250

Tape 4, Side A 261

Tape 4, Side B 272

APPENDICES

A. AIDS Chronology, 1981-1985 277

B. Key Participants in San Francisco AIDS History, 1981-1984 290

C. Biographical Sketch and Curriculum Vitae, Donald P. Francis,

M.D., D.Sc. 293

D. Curriculum Vitae, Merle A. Sande, M.D. 307

E. Declaration of Merle Sande, M.D., dated October 10, 1984 329

F. Curriculum Vitae, John L. Ziegler, M.D. 338

277

APPENDIX A: AIDS CHRONOLOGY'--by Sally Smith Hughes

1968-1970

1974

1976

1978

1980

David Baltimore and Howard Temin independently discover reverse
transcriptase, a marker for retroviruses.

Charles Garfield founds Shanti Project to provide free volunteer
counseling to people with life-threatening illnesses.

Robert Gallo isolates T-cell growth factor ( inter leukin-2 ),
allowing T-cells to be cultured in vitro.

San Francisco Mayor George Moscone assassinated; Dianne Feinstein
becomes mayor.

Gallo demonstrates that retroviruses (HTLV-I and HTLV-II) can
infect humans.

1981:

February

March

April

May/ June
June 6

June 8

Michael Gottlieb, UCLA, diagnoses Pneumocystis carinii pneumonia
[PCP] in two homosexuals.

Gottlieb diagnoses another case of PCP in a homosexual.

Sandra Ford, drug technician for Centers for Disease Control
[CDC], officially notes increase in requests for pentamidine, for
treatment of PCP.

Constance Wofsy diagnoses CNS toxoplasmosis in gay patient at San
Francisco General Hospital [SFGH].

Gottlieb diagnoses two more cases of PCP in homosexuals.

Two Kaposi's sarcoma [KS] cases in San Francisco and Stanford
announced at UCSF dermatology grand rounds.

Donald Abrams and others see cases of PCP in gay men at SFGH.

CDC's Morbidity and Mortality Weekly Report [MMWR] publishes
Gottlieb and Wayne Sandera's report on PCP in 5 gay men.

First meeting of CDC Kaposi's Sarcoma /Opportunistic Infection
[KSOI] Task Force, headed by James Curran. Purpose to
characterize syndrome and determine frequency, risk, and etiology.
Surveillance and case file for KS and PCP initiated.

1 This chronology is an ongoing working draft created to assist the oral
history project; its focus is San Francisco and its accuracy contingent upon
the many sources from which it was derived.

278

June (late) First case of KS diagnosed in gay man at SFGH.

July City of San Francisco establishes reporting and case registry
system for KS01.

July 3 First press report of syndrome appears in New York Times.

MMWR reports Kaposi's sarcoma in 26 gay men.
July 13 First article on KS in New York Native.
August CDC requires health departments to notify CDC of all KSOI cases.

Aug. 28 MMWR reports first heterosexuals, including first female, with
KSOI.

September CDC begins case-control study with 50 gay KSOI patients and 120
"healthy" gay ccontrols to determine factors in homosexual
environment possibly causing KSOI.

Sept. 15 CDC and National Cancer Institute sponsor workshop on KS and
opportunistic infections. CMV leading candidate for cause.

Sept. 21 First KS Clinic and Study Group held at UCSF.

October Friedman-Kien et al. begin study of clinical course of KS in gay
men.

November Shanti begins to focus on psychosocial problems of people with
KSOI.

December First clinical descriptions of immunosuppression in IV drug users.

John Ziegler, Conant and Paul Volberding receive $50,000 from
American Cancer Society to support KS Clinic at UCSF; first grant
awarded for AIDS.

CDC investigators suspect that causal agent of AIDS is infectious
but cannot provide irrefutable evidence. Others support
"lifestyle" hypothesis.

Reagan proposes massive cuts in CDC budget.

Dec. 9 Marcus Conant passes out flyers on KS at American Academy of
Dermatology meeting in San Francisco.

Dec. 10 Durack at Duke suggests amyl nitrites ("poppers") might cause
immune dysfunction.

New England Journal of Medicine article links immune deficiency to
T4 helper cell/18 suppressor cell ratio.

279

1982:

Early 1982
January

March A

April

May

May 15

June 18
June 26
July
July 9
July 13

July 16
July 21

Syndrome is named gay-related immunodeficiency disease--GRID.

First case of immune deficiency linked to blood products is
reported in a hemophiliac.

Helen Schietinger becomes nurse-coordinator of KS Clinic at UCSF.

San Francisco health department makes first request for tax funds
to support AIDS prevention and community services; Board of
Supervisors appropriates $180,000 for AIDS programs.

MMWR lists four risk groups for AIDS--homosexuals , hemophiliacs,
Haitians, and IV drug users [IVDUs].

Congressional subcommittee hearing in Los Angeles on AIDS, Henry
Waxman (D-CA) , chairman.

(Mother's Day) Conant, Frank Jacobson, and Richard Keller write
articles of incorporation for Kaposi's Sarcoma Research and
Education Foundation, predecessor of San Francisco AIDS
Foundation.

Friedman-Kien et al. publish study showing promiscuity greatest
risk factor for KS. Authors support immune overload theory of
AIDS causation.

CDC reports cluster of PCP and KS cases in LA and Orange County,
suggesting infectious agent is cause of AIDS.

UCSF Nursing Services sponsors conference, Kaposi's Sarcoma and
Pneumocystis Pneumonia: New Phenomena among Gay Men.

CDC, FDA, and National Hemophilia Foundation representatives meet
to plan risk evaluation of blood products for hemophiliacs.

CDC publishes first report of 31 cases of opportunisitic
infections in Haitians.

First international symposium on AIDS, at Mt. Sinai Medical
Center, New York, sponsored by Mt. Sinai and New York University
schools of medicine.

MMWR reports first three cases of PCP in hemophiliacs,
representing first cases of KSOI caused by blood or blood
products .

KS Foundation operates hotline for advice and referrals regarding
AIDS, KS, and opportunistic infections [OIs] .

280

July 27 CDC adopts "acquired immune deficiency syndrome- -AIDS" as the
official name of the new disease.

August CDC asks blood banks not to accept high-risk donors; CDC
recommends hepatitis B core antigen testing.

Aug. 13 National Cancer Institute [NCI] issues RFA for research on AIDS.

Sept. 24 CDC publishes first official definition of AIDS: a disease due to
defect in cell-mediated immunity occurring in people with no known
cause for immune deficiency.

First? published use of term "AIDS", in MMWR. Rapid adoption of
term thereafter.

October KS Research and Education Foundation contracts with San Francisco
Department of Public Health [SFDPH] to provide AIDS education
services in San Francisco.

Oct. 29 UCSF Departments of Medicine and Dermatology and Cancer Research
Institute sponsor program in medical education, Acquired
Immunodeficiency Syndrome and Kaposi's Sarcoma. Almost 200
physicians and scientists attend.

November MMWR suggests that hospital staffs caring for AIDS patients use
hepatitis B precautionary measures.

December Shanti makes first in series of contracts with SFDPH to provide
counseling services and a housing program for people with AIDS
[PWAs].

Dec. 1 House of Representatives votes $2.6 million to CDC for AIDS
research.

Dec. A CDC presents Blood Products Advisory Committee with evidence of

AIDS transmission through blood supply; no official action taken.

Dec. 10 Aramann, Cowan, Wara et al. report first case of possible
transfusion AIDS, in MMWR.

Dec. 17 MMWR reports four cases of unexplained immune deficiency in
infants.

Late 1982 Most investigators convinced that AIDS is caused by an infectious
agent.

Nation's first AIDS specimen bank established in UCSF School of
Dentistry, coordinated by KS Clinic.

281

1983:

Early

January

Jan. 1

Jan. A

Jan. 7

Jan. 14

Jan. 19

February

Feb. 3

Feb. 7

New York City health department establishes formal AIDS
surveillance program.

Beginning of bathhouse crisis. Formal AIDS infection control
guidelines instituted at San Francisco General Hospital.

Montagnier, Barre-Sinoussi, and Chermann at Pasteur Institute,
seeking to isolate an AIDS virus, begin to grow cells from
lymphadenopathy patient.

President of New York Blood Center denies evidence of transfusion
AIDS.

Orphan Drug Act becomes law, giving exclusive marketing rights,
tax breaks, and other incentives to companies developing drugs for
rare diseases.

First outpatient clinic dedicated to AIDS (Ward 86) opens, at San
Francisco General Hospital.

CDC national conference to determine blood bank policy re blood
screening for AIDS; no consensus.

CDC adds heterosexual partners of AIDS patients as fifth risk
group for AIDS.

Montagnier et al. find traces of reverse transcriptase in
lymphadenopathy cell cultures.

San Francisco's Irwin Memorial Blood Bank [IMBB] adds medical
history questions designed to screen out donors from high-risk
groups.

National Hemophilia Foundation asks blood and plasma collectors to
screen out high-risk donors.

Irwin Memorial Blood Bank adds more questions about medical
history of potential donors.

At Cold Spring Harbor Workshop on AIDS, Robert Gallo suggests that
a retrovirus probably causes AIDS and presumes a variant of HTLV-I
or HTLV-II.

Physicians from UCSF KS Study Group urge IMBB to use hepatitis B
core antibody test to screen out blood donors with AIDS.

IMBB launches confidential questionnaire designed to detect
potential blood donors with AIDS. Bay Area Physicians for Human

282

Rights urges potential donors to refrain from donating if they
have AIDS symptoms .

March CDC establishes clinical definition of AIDS in attempt to
standardize epidemiological surveillance.

UCSF Task Force on AIDS created, mainly to establish infection
control policy.

California requires reporting of AIDS cases, but not AIDS -Related
Complex [ARC].

Public Health Service [PHS] recommends members of high risk groups
reduce number of sex partners.

Mervyn Silverman, SFDH director, forms Medical Advisory Committee
on AIDS .

Mar. A MMWR first refers to "high risk" groups: gays with multiple sex
partners, IVDUs, Haitians, and hemophiliacs.

CDC states that "available data suggests that AIDS is caused by a
transmissible agent."

Mar. 17-19 New York University sponsors AIDS symposium.
Mar. 24 FDA issues blood donor screening guidelines.

April Congressman Phillip Burton dies; Sala Burton eventually elected to
his seat.

City of San Francisco and Shanti open hospice-type care center for
neediest AIDS patients.

Conant, Volberding, John Greenspan, Frank Jacobson, and others
persuade Willie Brown to ask for $2.9 million in state funding for
AIDS research.

April 11 Date NCI officials later cite as when NCI became committed to
finding AIDS etiology.

April 14 Irwin Memorial Blood Bank [IMBB] adds donor sheet designed to
screen out donors at high risk for AIDS.

April 26 Recall of San Francisco Mayor Feinstein, supported by White
Panthers and some gay groups, fails.

May NIH announce $2.5 million for AIDS research. NCI and NIAID issue
RFA [Request For Applications] for research on an infectious
agent.

283

Heat treatment to reduce infectious agents in transfused blood
approved by FDA.

San Francisco health department issues first brochure on AIDS.
Feinstein declares first week in May AIDS Awareness Week.

May 2 "Fighting for our Lives" candlelight march in San Francisco to
bring attention to AIDS; similar march in NYC.

May 6 Journal of the American Medical Association [JAMA] press release:
"Evidence suggests household contact may transmit AIDS."

May 12 UCSF announces receipt of $1.2 million for AIDS research; Paul
Volberding, principal investigator

May 20 Montagnier publishes discovery of "T-cell lymphotrophic

retrovirus," later called lymphadenopathy-associated virus (LAV).

May 23 San Francisco Board of Supervisors votes $2.1 million for AIDS

programs, $1 million of which is for out- and inpatient wards at
SFGH.

May 24 Edward Brandt, Assistant Secretary of Health, declares AIDS
research //I priority.

May 31 Health department director Mervyn Silverman, backed by Feinstein
and San Francisco Board of Supervisors, requires city bathhouses
to post public health warnings about contracting AIDS.

June UC issues guidelines to protect AIDS patients and health workers.
San Francisco Men's Health Study begins to recruit participants.

Feinstein chairs first U.S. Conference of Mayors Task Force on
AIDS.

July California legislature approves $2.9 million for AIDS research.

Donald Abrams begins work at SFGH AIDS Clinic, bringing 200+
lymphadenopathy patients from UCSF.

July 26 12-bed inpatient Special Care Unit (Ward 5B) opens at SFGH--first
dedicated AIDS hospital unit in U.S.

July 28 Universitywide Task Force on AIDS created to advise UC president
on guidelines for and coordination of state-supported AIDS
research at UC.

284

August Willie Brown, Rudi Schmid, Conant and other AIDS researchers
criticize UC for delays in releasing state funds for AIDS
research.

September At Cold Spring Harbor NCI meeting on human T-cell leukemia

retroviruses, Montagnier et al. report LAV- like viruses in 5
lymphadenopathy patients and 3 AIDS patients, selective affinity
of LAV for CD4 helper lymphocytes, and evidence of similarities
between LAV and lentivirus causing equine infectious anemia.
Gallo presents findings of HTLV-I in 102 of AIDS patients; doubts
LAV is retrovirus.

UC states that there is no scientific reason for healthy medical
personnel to be excused from caring for AIDS patients.

Bureau of Infectious Disease Control, SFDPH, begins active
surveillance of AIDS cases in San Francisco.

Sept. 13 Montagnier sends Gallo sample of lymphadenopathy-associated virus
(LAV).

Sept. 21 UCSF Task Force on AIDS publishes infection control guidelines for
health care workers caring for AIDS patients.

November KS Research and Education Foundation contracts with State of

California Department of Health Services to provide information
and referral services on AIDS to other counties.

Mika Popovic in Gallo 's lab discovers method for growing AIDS
virus in T-cells.

San Francisco Department of Public Health asks for legal option to
make baths off-limits to PWAs. Lawyers decide that medical
uncertainties about AIDS prevent such action.

Jay Levy obtains six viral isolates from AIDS patients but decides
not to publish until further proof.

December Pasteur Institute applies for U.S. patent on diagnostic kit based
on ELISA test for LAV antibodies.

Feinstein votes against live-in lover legislation, angering gay
community.

AIDS Clinical Research Centers established with state funding at
UCSF and UCLA to collect clinical and laboratory data.

National Association of People with AIDS formed.
Entry "AIDS" added to Cumulated Index Medicus.

285

1984:

January

Jan. 6
Jan. 12

Council of State and Territorial Epidemiologists passes resolution
making AIDS a reportable condition.

Hospice of San Francisco contracts with SFDPH to include AIDS
patients in its care of terminally ill.

Annals of Internal Medicine reports case of heterosexual
transmission of AIDS before overt manifestation of disease
(hemophiliac to wife) .

American Red Cross, American Association of Blood Banks, and
Council of Community Blood Centers oppose proposal to screen out
high-risk groups from blood donor pool.

CDC updates its definition of AIDS.

NEJM publishes CDC documentation of first 18 transfusion-
associated AIDS cases.

February Chermann in talks in U.S. states that French have discovered AIDS
virus .

March President of New York Blood Center continues to deny HIV
transmission by blood.

Larry Littlejohn, gay activist, sponsors San Francisco ballot
initiative to close baths.

Mar. 2-4 19th Annual San Francisco Cancer Symposium, "Cancer and AIDS".
Conant, Abrams, Wofsy, Ziegler, Volberding speak.

March 6 Blood industry task force meets on surrogate testing; blood
bankers oppose it.

March 26 Government allots $1.1 million to develop AIDS antibody test to
seven institutions, including Irwin Memorial and Stanford blood
banks .

April Feinstein issues first formal statement that Silverman should

close baths. Silverman responds that he will formulate guidelines
banning sex activity in baths that spreads AIDS.

NIH applies for patents on Gallo's AIDS antibody test, a
diagnostic kit based on Western blot technique.

April 9 Silverman and state and San Francisco health officials outlaw sex
in bathhouses, rather than close them.

286

April 24 Margaret Heckler, Secretary of Health and Human Services,

announces discovery by Gallo et al. of AIDS virus, that an AIDS
test will be available soon, and that a vaccine will be available
in 18-24 months. Gallo had not yet published his results.

May Gallo publishes four reports and Montagnier one, in Science,

linking AIDS with a new retrovirus which Gallo calls HTLV-III and
Montagnier calls LAV.

Board of Supervisor's president Wendy Nelder chides Silverstein
for "shameful" delays in proposing sex guidelines for baths.
Silverman replies that he is waiting for board to transfer
authority to regulate baths from police to health department.

Rock Hudson diagnosed with AIDS.

May 1 IMBB and other Bay Area blood banks begin testing blood for
hepatitis B core antigen.

Summer Silverman orders bathhouse surveillance for unsafe sex.

June Board of Supervisors committee delays action on giving health
department authority to regulate baths until after Democratic
National Convention in San Francisco.

IMBB adopts directed blood donation program.
July Democratic National Convention in San Francisco.

August After gay lobbying, Board of Supervisors tables move to give
Silverman regulatory power over baths, killing his idea to
promulgate sex guidelines for baths.

Levy et al. isolate virus, ARV, which they claim to cause AIDS.
September Chiron Corp. announces cloning and sequencing of ARV genome.

Giovanni Battista Rossi in Italy isolates AIDS virus.
October Feinstein forms Mayors Advisory Committee on AIDS.

FDA approves Lyphomed's injectable pentamidine for PCP and gives
it orphan drug status.

Bureau of Communicable Disease Control, SFDPH, begins surveillance
of average monthly AIDS bed census.

Oct. 9 Silverman closes baths and private sex clubs as "menace" to public
health. Baths reopen hours later.

November Gallo et al. clone HTLV-III.

287

Nov. 28 San Franciso Superior Court Judge Roy Wonder rules baths can

remain open if monitored for safe sex practices every 10 minutes.

December Montagnier et al. report cloning of LAV; they also report CD4
molecule as LAV receptor.

Silverman resigns as director of SFDPH.

90 reported cases of transfusion AIDS; 49 reported cases of Factor
VIII hemophilia cases.

CDC recommends use of heat-treated blood products for
hemophiliacs; other specialists differ. Heat-treated blood
products become commercially available.

National Kaposi's Sarcoma Reasearch and Foundation renamed San
Francisco AIDS Foundation.

Dec. 26 Simon Wain-Hobson, Pierre Sonigo, Olivier Danos, Stewart Cole, and
Marc Alizon at Pasteur Institute publish LAV nucleic acid sequence

in Cell.

1985:

January Gallo et al. publish full nucleic acid sequence of HTLV-III.

Jan. 14 Irwin Memorial Blood Bank prohibits males having more than one sex
partner to donate blood.

February FDA approves Gallo 's AIDS diagnostic kit based on Western blot
technique.

Feb. 1 Paul Luciw, Jay Levy, Ray Sanchez-Pescador et al. at Chiron
publish ARV nucleic acid sequence.

Feb. 7 Dan Capon, M.A. Muesing et al. at Genentech publish ARV nucleic
acid sequence.

March San Francisco County Community Consortium founded for community-
based AIDS drug testing.

March 2 FDA approves Abbott Laboratory's commercial test for AIDS. Red

Cross contracts with Abbott, one of five companies supplying test,
and in days phases in test. Britain and France delay testing six
months to introduce their own antibody tests.

March 3 IMBB introduces genetically engineered hepatitis B antibody core
test.

March 4 First International Conference on AIDS, Atlanta

288

March 6 IMBB institutes anti-AIDS virus antibody test, the first blood
bank in U.S. to do so.

March 14 San Francisco Chronicle reports army study showing AIDS
transmission through heterosexual contact.

Spring California legislature and Gov. Deukmejian approve bill banning
HIV antibody testing without subject's written informed consent,
except at test sites where testing is anonymous. Bill also bars
employer and insurance company discrimination on basis of AIDS
status. $5 million appropriated to establish HIV community test
sites. Disclosure of test results to third party must be improved
in writing by test taker.

April CDC drops Haitians from high risk groups for AIDS.

May US Patent Office awards patent on Gallo's antibody test.

Summer AIDS diagnostic kits using ELISA become commercially available.

California law mandates every county to offer AIDS test at public
health centers; guidelines for preserving confidentiality.

June American Association of Blood Banks, American Red Cross, Council
of Community Blood Centers agree not to begin "look back" program
to identify people who have received AIDS-infected blood.

National Institute of Allergy and Infectious Diseases [NIAID]
creates first AIDS Treatment Evaluation Units, predecessor to AIDS
Clinical Trial Groups (ACTGs).

California public health clinics begin testing for AIDS.
June 24 IMBB adds bar codes for confidential exclusion of blood units.

September Mathilde Krim and Michael Gottlieb found American Foundation for

AIDS Research [AmFAR] , merging AIDS Medical Foundation of New York
and National AIDS Research Foundation of Los Angeles.

Martin Delaney and others found Project Inform.
October Public's awareness of AIDS rises with Rock Hudson's death.

Congress allots $70 million to AIDS research day after Hudson's
death.

December Pasteur Institute sues for share of royalties on AIDS antibody
test.

CDC first considers vertical transmission of AIDS virus; advises
infected women to "consider" delaying pregnancy until more known
about perinatal transmission.

289

CDC contracts with San Francisco AIDS Foundation to develop
materials for anonymous AIDS testing sites.

Late in year Department of Defense announces that new recruits
will be screened for AIDS and rejected if positive.

Third UC AIDS Clinical Research Center founded at UCSD. Goals of
three centers broaden to include rapid evaluation of new
therapeutic agents.

13-year-old Ryan White, a hemophiliac with AIDS, is barred from
school in Indiana.

CDC expands surveillance definition, in light of HIV antibody

test.

290

KEY PARTICIPANTS

in San Francisco AIDS History, 1981-1984
Appendix B

*'Donald A. Abrams, M.D. , AIDS clinician and member of original AIDS physician
team at San Francisco General Hospital (SFGH) ; early research on AIDS-
associated lymphadenopathy (swollen lymph glands); organizer of County
Community Consortium.

*Arthur J. Ammann, M.D. , pediatric immunologist at University of California,
San Francisco (UCSF) ; conducted early studies of AIDS-associated immune
deficiency in adults and children; reported first case of transfusion AIDS;
currently head of a pediatric AIDS foundation.

Francoise Barre-Sinoussi, retrovirologist at Pasteur Institute and member of
team which isolated AIDS virus.

Edward N. Brandt, Jr., M.D. , Ph.D., Assistant Secretary for Health, U.S.
Department of Health and Human Services, 1981-1984.

Conrad Casavant, immunologist in Department of Laboratory Medicine and
associate director of Clinical Immunology Laboratory at UCSF; died of AIDS in
1987.

Jean-Claude Chermann, retrovirologist at Pasteur Institute and member of team
which isolated AIDS virus.

*Marcus A. Conant , M.D., clinical professor at UCSF, and dermatologist with
private AIDS practice; diagnosed first case of Kaposi's sarcoma in San
Francisco; founder of first AIDS clinic (at UCSF); medical activist at local,
state, and federal levels.

James W. Curran, M.D., M.P.H., epidemiologist and director of AIDS research at
Centers for Disease Control (CDC), Atlanta, Georgia.

William Darrow, CDC sociologist.

Larry Drew, virologist at Mt. Zion Hospital, San Francisco.

*Selma K. Dritz, M.D. , M.P.H., epidemiologist at San Francisco Department of
Public Health (SFDPH); tracked early AIDS cases in San Francisco; addressed
medical and community groups on AIDS recognition and prevention.

Gaetan Dugas, French-Canadian airline steward who was among first to be
diagnosed with AIDS; sometimes mistakenly referred to as "Patient Zero" and
held responsible for early dissemination of AIDS.

1 The asterisk indicates that the individual has been interviewed for the
AIDS Medical Response oral history series.

291

Edgar Engleman, M.D. , medical director of Stanford University Hospital blood
bank.

Anthony S. Fauci, M.D., director of AIDS activities at National Institute of
Allergy and Infectious Diseases, later director of Office of AIDS Research,
currently director of NIAID, National Institutes of Health (NIH) .

*Donald P. Francis, M.D., D.Sc., epidemiologist and virologist at CDC in
Phoenix and Atlanta; conducted early epidemiological and virological studies
of AIDS; later became CDC advisor on AIDS to California Department of Health
Services; current director of research on AIDS vaccines at a biotechnology
company.

Robert Gallo, M.D. , retrovirologist at National Cancer Institute, NIH,
involved in controversy with Pasteur Institute over isolation of AIDS virus
and patent rights to HIV test.

*Deborah Greenspan, D.D.S., D.Sc., clinical professor of oral medicine at
UCSF; identified AIDS-associated hairy leukoplakia; instrumental in
establishing infection control procedures in dentistry.

*John S. Greenspan, D.D.S., Ph.D., professor of oral biology and oral
pathology at UCSF; organized and directs UCSF AIDS specimen bank; current
director of UCSF AIDS Clinical Research Center.

Margaret Heckler, Secretary of U.S. Department of Health and Human Services,
1983-1985.

Harold Jaffe, epidemiologist with the AIDS program at CDC.

*Jay A. Levy, M.D. , virologist and professor of medicine at UCSF; second to
isolate AIDS virus; devised early AIDS diagnostic test and heat treatment to
rid blood of HIV.

Luc Montagnier, virologist and member of Pasteur Institute team which isolated
AIDS virus.

*Andrew R. Moss, Ph.D., M.P.H., epidemiologist at SFGH; conducted early
epidemiological studies of AIDS in San Francisco showing high incidence in gay
community; later work focused on AIDS incidence in drug users and homeless.

*Herbert A. Perkins, M.D., scientific director (later president) of San
Francisco's Irwin Memorial Blood Bank; involved in formulating national blood
bank policy regarding blood screening for HIV; currently represents blood bank
in legal cases associated with transfusion AIDS.

*Merle A. Sande, M.D., professor of medicine and chief of medical services,
SFGH; chairman of AIDS advisory committees at university, health department,
and state levels.

292

Randy Shilts, journalist who covered AIDS for San Francisco Chronicle; author
of And the Band Played On; Politics. People, and the AIDS Epidemic; died of
AIDS in 1994.

*Mervyn F. Silvennan, M.D. , M.P.H., director, San Francisco Department of
Public Health; center of controversy over closure of San Francisco bathhouses;
current director of American Foundation for AIDS Research.

*Paul A. Volberding, M.D. , oncologist and chief of AIDS Services, SFGH; member
of original AIDS physician team at SFGH; prominent AIDS clinician.

Girish Vyas , Ph.D., professor of laboratory medicine, UCSF.

*Warren Winkelstein, M.D. , M.P.H., epidemiologist at University of California
School of Public Health; director of early on-going epidemiological study of
AIDS (San Francisco Men's Health Study); member of panel deciding in June 1994
to disprove expanded clinical trial of two AIDS vaccines.

*Constance B. Wofsy, M.D., infectious disease specialist at SFGH; member of
original AIDS physician team at SFGH; authority on Pneumocystis carinii
pneumonia and women with AIDS.

*John L. Ziegler, M.D. , oncologist at Veterans Administration Medical Center,
San Francisco; authority on AIDS-associated lymphoma and Kaposi's sarcoma.

293

Donald P. Francis. M.D.. D.Sc.

Dr. Donald Francis is currently President of VaxGen, Inc., a company
dedicated to developing a vaccine for HIV. In February of 1992 he
retired after 20 years in the U.S. Public Disease AIDS Advisor to the
State of California and Special Consultant to Mayor Art Agnos in San
Francisco. In the latter capacity he served as the Chair of the
Mayor's HIV Task Force. Dr. Francis is a third-generation California
physician having done his undergraduate studies at the University of
California at Berkeley. He received his M.D. from Northwestern
University and his Doctor of Science from Harvard. Before beginning
his work on AIDS, Dr. Francis was involved in epidemic control
around the world. He worked for the World Health Organization
eradicating smallpox from Sudan, India and Bangladesh. He was also
on the front line of the cholera epidemic in Nigeria in the early 1970s
and the developmental work on the hepatitis B vaccine, both in the
United States and the People's Republic of China. He began his work
on AIDS in 1981. He was one of the first scientists to suggest that
AIDS was caused by an infectious agent. As director of CDC's AIDS
Laboratory Activities, he worked closely with the Institut Pasteur to
prove that HIV was the cause of AIDS. He was also one of the
earliest scientists to realize the impact HIV would have on the United
States and has been an indefatigable advocate for a logical public
response. After retiring from CDC, Dr. Francis joined Genentech in
1993 to head up the clinical research of their candidate HIV vaccine.
In 1995, he became a founder and President of VaxGen, Inc., a spin-
off company which, in a developmental partnership with Genentech,
intends to develop a world-wide vaccine for HIV.

294

CURRICULUM VITAE

Personal

N a in e :

Home Address:

Bom:

Donald Pinkston Francis, M.D., D.Sc.

1565 Bellevue Ave.
Hillsborough, CA 94010

October 24, 1942, Los Angeles, CA

Education

1960-1961
1961-1964
1964-1968

1968

1969 - 1971

1971-1973

1975

1975-1977

1976
1976-1979

1979

Biological Sciences, College of Mariu,
Kentfield, CA

Biological Sciences, University of
California, Berkeley, CA

Medicine, Northwestern University,
School of Medicine, Chicago, IL

Doctor of Medicine

Pediatrics, Los Angeles

County/University of Southern

California Medical Center, Los Angeles, CA

Epidemiology, Epidemic Intelligence
Service, Centers for Disease Control,
Atlanta, GA

Virology, Postdoctoral Fellowship,

Harvard University, School of Public Health,

Boston, MA

Infectious Disease, Infectious Disease
Fellowship, Channing Laboratory,
Harvard Medical School, Boston, MA

Board Certified, Pediatrics

Doctoral Student, Harvard School of
Public Health, Boston, MA

Doctor of Science (Virology)

295

EXP&ttCE

July 1989-February 1992

August 1988- January 1992
July 1985-June 1989
September 1983-June 1985
May 1983-June 1985
July 1978-September1983
September 1976-November 1979
January-September 1976
July 1975-July 1977

May-June 1975

July 1974- June 1975

September 1973 - July 1974
January-September 1973
July 1971-December 1972

January-June 1971

January-December 1970

January-December 1969

Centers for Disease Control Regional AIDS Consultant, Region IX,
United States Public Hearth Service, San Francisco, California (Retired
2/1/92)

Special Consultant on AIDS, to Mayor Art Agnos, City and County of
San Francisco. San Francisco, California

Centers for Disease Control AIDS Advisor to the Department of Healin
Services, State of California, Berkeley, California

Assistant Director, Division of Viral Diseases, Centers for Disease
Control Atlanta, Georgia

Coordinator, AIDS Laboratory Activities, Division of Viral Diseases,
Centers for Disease Control, Atlanta, Georgia

Assistant Director for Medical Science, Hepatitis and Viral Entenns
Division, Centers for Disease Control, Phoenix, Arizona

Doctoral Student in Microbiology, Department of Microbiology, Harvarc
School of Public Health, Boston, Massachusetts

Postdoctoral Fellow in Microbiology, Department of Microbiology,
Harvard School of Public Health, Boston, Massachusetts

Research Fellow in Pediatrics, Channing Laboratory of Infectious
Disease, Harvard Medical School, Boston, Massachusetts

Consultant ; WHO : Smallpox Eradication, Bangladesh

State Program Coordinator, WHO : Smallpox Eradication. Lucknc.y,
U.P. , India

Consultant; WHO : Smallpox Eradication, Bareil/y, U.P ., ind.a
Consultant, WHO : Smallpox Eradication, Khartoum, Sudan

Epidemic Intelligence Service Officer, Centers for Disease Control,
assigned to Oregon State Hearth Division; Clinical Instructor of
Pediatrics, University of Oregon (Official entry into the Public Health
Service, CDC)

State Epidemiologist, U.S. Agency for International Development,
Centers for Disease Control, River's State, Nigeria

Resident in Pediatrics, University of Southern California Medical Center,
Los Angeles, California

Intern in Pediatrics, University of Southern California Medical Center,
Los Angeles, California

July-December 1968

Pediatric Fellow, Children's Bureau, Department of HEW, Punjab, India

296

and Awards

1968

1970

1975

1975-78
1977

1977

1983

1988

1989

1992

1994

U.S. Children's Bureau, Pediatric Fellowship Abroad
Pediatric Resident of the Year, LAC/USC Medical Center

Honorary Fellow, Indian Society for Malaria and

Other Communicable Diseases (for Smallpox Eradication)

U.S. Public Health Service, Career Development Award

Smallpox Eradication Certificate, World Health
Organization/Government of India (for smallpox
eradication)

U.S. Public Health Service, Commendation Medal (for
Smallpox Eradication)

U.S. Public Health Service, Group Award (for hepatitis B
vaccine efficacy studies)

Board of Directors Award/Cable Car Award (for
outstanding leadership in AIDS)

Thomas Parin ' Award, Americans for Sound AIDS Policy
(for outstanding work in AIDS)

U.S. Public Health Service, Meritorious Service Award
(for AIDS prevention efforts)

Legislative Resolution of Commendation, California State
Legislature

CenterOne Red Ribbon Award (for leadership in the fight
against AIDS)

297

Committee/Task Force Membership

1985-1988 California AIDS Task Force

1988-1988 California AIDS Leadership Committee (Co-chair, Education

and Prevention Subcommittee)

1988-1991 San Francisco Mayor's HIV Task Force (Chairman)

1988-1992 California AIDS Budget Task Force

1989-1992 California Medical Society, AIDS Task Force (Consultant)

1988-1991 Department of Defense, Retroviral Diseases Peer Review Panel

1991 California Ryan White CARE, Working Group

1993 Centers for Disease Control, Advisory Committee on Prevention

of HIV Infection (Consultant)

International AIDS Conference Committees

1985 1st International Conference, Program Committee

1986 2nd International Conference, International Advisory
Committee

1989 5th International Conference, Program Committee

1990 6th International Conference, Program Committee

293

T e s 1 i m o n y 1 1* a r t i c i p a n t

1985-1992 California Legislative Committees, multiple appearances

1987 National Academy of Science, Development of Vaccines for

AIDS (Participant)

1987 National Academy of Science, AIDS Oversight Committee

(Correspondent )

1987 World Health Organization, AIDS Short-term Consultant, Sudan

1989 President's Commission on AIDS

1990 U.S. House of Representatives, Budget Committee
1990 National Commission on AIDS

1992 Los Angeles Commission on AIDS

1992 U.S. House of Representatives, Oversight Committee

Clinical • Faculty A pppintmenty /Teaching

1971-1973 University of Oregon, School of Medicine

1987- Present University of California, San Francisco

1985-1992, Lecturer at:

Stanford University, Palo Alto, CA

UCSF School of Medicine, San Francisco, CA,

Hastings Law School, San Francisco, CA

University of California, Berkeley, CA

U.C. School of Public Health, Berkeley, CA

U.C. Santa Cruz, Santa Cruz, CA

299

Donald P. Francis, M.D., D.Sc.
Publications

Francis DP. Insulating public health from extremist politics. Do we need boards of
health? Am J Pubic Health 1994;84:720-1.

Francis DP and Singleton JA. Reporting HIV-1 infection through the provision of
essential services. JAIDS 1993:6:285-6.

Francis DP. Toward a comprehensive HIV prevention program for the CDC and the
nation. J Am Med Assn 1992^268:1444-47.

300

Donald P. Francis, M.D., D.Sc.
Publications

Francis DP. Anderson RE. Gorman ME. Fenstersheib M, Padian NS. Kizer, KW, Conant MA. Targeting AIDS
Prevention and Treatment Toward HIV-1 Infected Persons. JAMA 1989:262:2572-2576.

Francis DP. Margolis HS. Worldwide Elimination of Hepatitis B Transmission: We Have the Way, We need tne
Will. Letter to the Editor, JAMA 1989; 261:2400-2401.

The Epidemiology of AIDS: Expression, occurrence and control of human immunodeficiency Virus Type
infection Kaslow RA: Francis DP: (Editors), Oxford University Press , New York . 1989.

Kaslow RA. Francis DP. Epidemiology - General Considerations. Chapter 6, p87-116.
Francis DP. Kaslow RA Prevention - General Considerations. Chapter 15, p25 1-253.
Francis, DP. Immunization. Chapter 18, p3O9-312.

Ascher, MA, Gallo D. Francis DP. Human Retroviruses. Diagnostic Procedures for Viral. Rickettsial and
Chlamydial Infections. Chapter 31, p1 113-1 140. 6th Edition American Public Hearth Association 1989. Editors:
Nathalie J. Schmidt, Richard W. Emmons.

Francis, DP. Prospects for the Future. AIDS Principles, Practices and Politics. Part XI, p564-569. Reference
Edition, Hemisphere Publishing Corporation, 1989. Editors: Inge B. Corless, Mary Pitiman-LJndemann.

Padian N: Francis DP. Preventing the Heterosexual Spread of AIDS. (Letter to the Ed/tor) JAMA Vol 260, p
1869.

Kizer KW, Conant MA, Francis DP, Fraziear T. HIV Disease Prevention and Treatment: A Model for Local
Planning. Western Journal of Medicine. 1988. Oct; 149:481-485

Francis DP. Prospects for the Future. Death Studies (Hemisphere Publishing Corporation) 1988. I2p597-6l

Padian N; Marquis L Francis DP: Anderson RE: Rutherford GW; O'Malley PM; Winke/stein W Jr. Mais-:c--'sma/e
transmission of human immunodeficiency virus. JAMA Aug 14, 1987, 258(6 )p 788-90.

Del Tempelis C; Shell G; Hoffman M; Benjamin RA: Chandler A; Francis DP. Human immunodeficiency virus
infection in women in the San Francisco Bay area (letter). JAMA Agul 24-31, 1987, 258(4)p274-5.

Francis DP: Chin J. The prevention of acquired immunodeficiency syndrome in the United States. An objective
strategy for medicine, public health, business, and the community. JAMA Mar 13, 1987, 257(10)p 1357-65.

Halsey NA Reppert EJ; Margolis HS: Francis. DP: Fields HA Intradermal hepatitis B vaccination in an abbreviate
schedule. Vaccine (England) Dec 1986, 4(4)p228-32.

Futtz PN; McClure HM; Daugharty H; Brodie A; McGrath CR; Swenson B; Francis DP. Vaginal transmission of
human immunodeficiency virus (HIV) to a chimpanzee. J Infect Dis Nov 1986, 154(5)p896-900.

Francis DP: Feorino PM; McDougal S; Warfield D; GetchellJ; Cabradilla C; Jong M; Miller WJ; Schu/tz LD; Bailey
FJ; et al. The safety of the hepatitis B vaccine. Inactivation of the AIDS virus during routine vaccine manufactvrt
JAMA Aug 15, 1986. 256(7)p869-72.

• .

301

Donald P. Francis. M.D., D.Sc.

Publications

Page 2

Hadler SC; FrancisDP; Maynard JE; Thompson SE; Judson FN; Echenberg OF: Ostrow DG; O'Mal/ey PM; Penley
KA; Attman NL; et aJ. Long-term immunogenicity and efficacy of hepatitis B vaccine in homosexual men. N Engl J
MedJul24. 1986. 315(4)p209-14.

Xu ZY; FrancisDP: LJu CB; Purcell RH; Duan SC; Chen FU; Wen YM. Prevention of hepatitis B virus carriage of
infants using HBV vaccine in Shanghai. Prelimary report of a randomized double-blind placebo-controlled trial.
Chin Med J. Sep 1985, 98(9)p623-6.

Fultz PN; McClur HM; Swenson RB; McGrath CR; Brodie A; Getchell JP; Jensen FC; Anderson DC: Broderson
JR; Francis DP. Persistent infection of chimpanzees with human T-lymphotropic virus type
Ill/lymphadenopathy-associated virus: a potential model for acquired immunodeficiency syndrome. J Vircl Apr
1986, 58(1 )p1 16-24.

Stryker WS; Gunn RA Francis DP. Outbreak of hepatitis B associated with acupuncture. J Fam Pract Feb 1985.
22k: (2 )p 155-8.

Hicks DR: Martin LS; Getchell JP, Health JL Francis DP; McDougal JS; Curran JW; Voeller B. Inactivation of
HTLV-IH/LAV-infected cultures of normal human lymphocytes by nonoxynol-9 in virto (letter). Lancet Dec 21-28.
1985. 2(8469-70)p 1422-3.

Francis DP; Petricciani JC. The prospects for and pathways toward a vaccine for AIDS. N Engl J Med Dec 19,
1985. 3 13(25)p 1586-90.

Francis DP. Worldwide control of hepatitis B virus: an approaching reality? Pediatrics Nov 1985, 76(5)p85l-2.

Xu ZY; Liu CB; Francis DP; Purcell RH; Gun ZL; Duan SC; Chen FU; Margolis HS; Huang CH; Maynara JE
Prevention of perinatal acquisition of hepatitis B virus carriage using vaccine: preliminary report of a rsr.zcmzez.
double-blind placebo-controlled and comparative trial. Pediatrics Nov 1985, 76(5)p713-8.

Francis DP; Jafffe HW; Fultz PN; Getchell JP; McDougal JS; Feorino PM. The natural history of mfec::or. v.::n ire
lymphadenopathy-associated virus/human T-lymphotropic virus type III. Ann Intern Med Nov 1985,
103(5)p719-22.

After MJ; Hadler SC: Francis DP, Maynard JE. The edpidemiology of non-A. non-B hepatitis in the United States.
Prog Clin Biol Res 1985. 182p71-9.

Francis DP: Kalyanaraman VS; Feorino PM. The cause of acquired immunodeficiency syndrome - is it known?
Prog Clin Biol Res 1985. 182p277-83.

Heyward WL; Bender TR; McMahon BJ; Hall DB; Francis DP. LanierAP; Alward WL; Ahtone JL Murphy BL;
Maynard JE. The control of hepatitis B virus infection with vaccine in Yupik Eskimos. Demonstration of safety.
immunogenicity, and efficacy under field conditions. Am J Epidemiol Jun 1985, 121 (6)p9 14-23.

Feorino PM; Jaffe HW; Palmer E; Peterman TA: Francis DP, Kalyanaraman VS; Weinstein RA; Stoneburner RL:
Alexander WJ; Ravesky C; et al. Transfusion-associated acquired immunodeficiency syndrome. Evidence for
persistent infection in blood donors. N Engl J Med May 16, 1985, 2 12(20)p 1293-6.

Jaffe HW; Feorino PM; Darrow WW; O'Malley PM; Getchell JP; Warfield DT; Jones BM; Echenberg DF; Francis
DP, Curran JW. Persistent infection with human T-lymphotropic virus type lll/lymphadenopathy-associa'.ea virus
in apparently healthy homosexual men. Ann Intern Med May 1985, 102(5)p627-8.

Alward WL; McMahon BJ; Hall DB; Heyward WL; Francis DP: Bender TR. The long-term serological course of
asymptomatic hepatitis B virus carriers and the development of primary hepatocellular carcinoma. J Infect Dis Apr
1985, 151(4)p604-9.

Donald P. Francis, M.D.. D.Sc.

Publications

Page 3

McMahon BJ; A/ward WL; Hall DB; Heyward WL; Bender TR: Francis DP; Maynard JE. Acme hepatitis B virus
infection: relation of age to the clinical expression of disease and subsequent development of the earner staid
J Infect Dis Apr 1985, 151(4)p599-603.

Palmer EL; Harrison AK; Ramsey BB; Feornio PM; Francis DP; Evatt BL; Kalyanaraman VS; Martin ML
of two human T cell leukemia/lymphotropic viruses in cuttured lymphocytes of a hemophiliac with acquired
immunodeficiency syndrome. J Infect Dis Mar 1985. 151(3)p559-63.

McDougal JS; Cort SP; Kennedy MS; Cabridilla CD; Feorino PM; Francis DP; Hicks D; Kalyanaraman VS: Martin
LS. Immunoassay for the detection and quantitation of infectious human retrovirus,
lymphadenopathy-associated virus (LAV). J Immunol Methods Jan 21. 1985, 76(1)p717-83.

Francis DP: Feorino PM; Broderson JR; McClure HM; Getchell JP; McGrath CR; Swenson B; McDougal JS;
Palmer EL; Harrison AK; et al. Infection of chimpanzees with lymphadenopathy-associated virus (letter 1. Lancl
Dec 1, 1984. 2(84 1 4 )p 1276-7.

Palmer EL; Ramsey RB; Feorino PF; Harrison AK; Cabradilla C; Francis DP, Poon MC; Evatt BL Human T-cell
leukemia virus in lymphocytes of two hemophiliacs with the acquired immunodeficiency syndrome. An Intern
Med Sep 1984. 101(3)p293-7.

Feorino PM; Kalyanaraman VS; Haverkos HW, Cabradilla CD; Warfield DT; Jaffe HW; Gottlieb MS, Gc/dfmger D.
Chermann JC; Barr-Sinoussi F; Spira TT; McDougal JS; Curran JW, Montagnier L' Murphy FA; Francis DP
Lymphadenopathy-Associated Virus Infection of a Blood Donor - Recipient Pair with Acquired
Immunodeficiency Syndrome. Science July 6, 1984, Vol 25 p69-72.

Kalyanaraman, VS;Cabradi!la,CD;Getchell,CD;Narayanan,R.;Braff,EH;Chermann,JC;Barre-Sinoussi.FL.;
Montagnier.L; Spira. TJ;Kaplan.J;Fishbein.D;Jaffe.HW;Curran.JW;Francis, D. P. Antibodies to the core protein1
lymphadenopathy-associated virus (LAV) in patients with AIDS . Science July 1984:225(4659): 32 1-3.

Hadler SC; Murphy BL' Schable CA; Heyward WUE. "c/s DP; Kane MA Epidemiological analysis of me
significance of low-positive test results for antibody L nepatitis B surface and core antigent. J Clin M/crobiol Ap
1984, 19(4)p521-5.

Jaffe HW; Francis DP. McLane MR; Cabradilla C; Curran JW; Kilbourne BW; Lawrence DN; Haverkos HW; Spirx
TJ; Dodd RY; et al. Transfusion-associated AIDS: serologic evidence of human T-cell leukemia virus infection <
donors. Science Mar 23. 1984. 223(4642)p 1309- 12.

Hadler SC; De Monzon M; Ponzetto A; Anzola E; Rivero D; Mondotfi A; Bracho A; Francis DP; Gerber MA; Thur
S; et al. Delta virus infection and severe hepatitis. An epidemic in the Yucpa Indians of Venezuela. Ann Intern
Med Mar 1984, 100(3)p339-44.

Francis DP: Hadler SC; Prendergast TJ; Peterson E; Ginsberg MM; Lookabaugh C; Holmes JR; Maynard JE.
Occurrence of hepatitis A. B, non-A/non-B in the United States. CDC sentinel county hepatitis study I. Am J
Med Jan 1984. 76(1)p69-74.

Miller KD; Gibbs RD; Mulligan MM; Nutman TB; Francis DP. Intradermal hepatitis B virus vaccine: immunogemc
and side-effects in adults. Lancet Dec 24-31. 1983. 2{8365-66)p 1454-6.

Carl M; Francis DP; Maynard JE. Food-borne hepatitis A; recommendations for control. J Infect Dis Dec 1983,
148(6)p 1 133-5.

Evatt BL; Stein SF; Francis DP; Lawrence DN; McLane MF; McDougal JS; Lee TH; Spira TJ; Cabradilla C; Mullt
Jl; Essex M. Antibodies to human T cell leukaemia virus-associated membrane antigens in haemophiliacs:
evidence for infection before 1980. Lancet See 24. 1983. 2(8352)0698-700.

303

Donald P. Francis, M.D., D.Sc.

Publications

Page 4

After MJ; Favero MS: Francis DP. Cost benefit for vaccination for hepatitis B in hemodialysis centers (letter). J
Infect Dis Oct 1983, 148(4)p770-1.

Francis DP. Hepatitis B virus vaccine. An opportunity for control (editorial). JAMA Oct 14, 1983,
250(14)p1891-2.

Evatt BL; Stein SF; Francis DP: Lawrence DN; McLane MF; McDougal JS; Lee TH; Spira TJ; Cabradilla C; Mullens
Jl; Essex M. Antibodies to human T cell leukaemia virus-associated membrane antigens in haemophiliacs:
evidence for infection before 1980. Lancet Sep 24, 1983, 2(3252)p698-700.

Rogers MF; Morens DM; Stewart JA; Kaminski RM; Spira TJ; Feorino PM; Larsen SA; Francis DP: Wilson M;
Kaufman L National case-control study of Kaposi's sarcoma and Pneumocystis carinii pneumonia in homosexual
men:L Part 2. Laboratory results. Ann Intern Med Aug 1983, 99(2)p151-8.

Essex M; McLane MF; Lee TH; Tachibana N; Mullens Jl; Kreiss J; Kasper CK; Poon MC; Landay A; Stem SF;
Francis DP: Cabradilla C; Lawrence DN; Evatt BL Antibodies to human T-cell leukemia virus membrane antigen
(HTLV-MA) in hemophiliacs. Science Sep 9, 1983, 221(4615)p1061-4.

Francis DP: Curran JW; Essex M. Epidemic acquired immune deficiency syndrome: epidemiologic evidence for
a transmissible agent JNCI Jul 1983, 71(1)p1~4.

Essex M; McLane MF; Lee TH; Falk L; Howe CW; Mullins Jl; Cabradilla C; Francis DP. Antibodies to cell
membrane antigens associated with human T-cell leukemia virus in patients with AIDS. Science May 20, 1983,
220(4599)p859-62.

Francis DP. Selective primary health care: strategies for control of disease in the developing world. III. Hepatitis B
virus and its related diseases. Rev Infect Dis Mar-Apr 1983, 5(2)p322-9.

Hadler SC; Erben JJ; Matthews D; Starko K: Francis DP: MaynardJE. Effect of immunoglobulin on hepatitis A in
day-care centers. JAMA Jan 7. 1983. 249(1 )p48-53.

Mann JM; Francis DP; Hoffman RE; Montes J. Assessment of immunoglobulin use for hepatitis A control in New
Mexico. Public Health Rep. Nov-Dec 1982, 97(6)p516-20.

Heyward WL; Bender TR; Lanier AP; Francis DP; McMahon BJ; Maynard JE. Serological markers of hepatitis B
virus and alpha-fetoprotein levels preceding primary hepatocellular carcinoma in Alaskan Eskimos. Lancet Ocr
23. 1982, 2(9304)p889-91.

Francis DP: Hadler SC; Thompson SE; Maynard JE; Ostrow DG; Attman N; Braff EH; O'Malley P; Hawkins D;
Judson FN; Penley K; Nylund T; Christie G; Meyers F; Moore JN Jr; Gardner A; Doto IL; Miller JH; Reynolds GH;
Murphy BL; Schable CA; Clark BT; Curran JW; Redeker AG. The prevention of hepatitis B with vaccine. Report of
the Centers for Disease Control mufti-center efficacy trial among homosexual men. Ann Intern Med Sep 1982,
97(3)p362-6.

Francis DP: Favero MS: Mavnard JE. Transmission of hepatitis B virus. Semin Liver Dis Feb 1981, 1(1)p27-32.

Carl M; Blakey PL Francis DP: Maynard JE. Interruption of hepatitis B transmission by modification of a
gynaecologist's surgical technique. Lancet Mar 27, 1982, 1 (8274 )p73 1-3.

Reiner NE; Judson FN; Bond WW; Francis DP; Peterson NJ. Asymptomatic rectal mucosal lesions and hepatitis
B surface antigen at sites of sexual contact in homosexual men with persistent hepatitis B virus infection. Ann
Intern Med Feb 1982. 96(2)p 170-3.

Reingold AL,' Kane MA; Murphy BL; Checko P; Francis DP: MaynardJE. Transmission of hepatitis B by an oral
surgeon. J Infect Dis Feb 1982. 145(2)p262-8.

Donald P. Francis, M.D.. D.Sc.

Publications

PageS

Hadler SC; Erben JJ: Francis DP: Webster HM; Maynard JE. Risk factors for hepatitis A in day-care centers, j
Infect Dis Fob 1982. 145(2)p255-61.

Heyward WL; LanierAP, Bender TR; Hardison HH;I Dohan PH; McMahon BJ: Francis DP. Primary hepatocellular
carcinoma in Alaskan natives, 1969-1979. Int J Cancer Jul 15, 1981. 28(1 )p47-50.

Francis DP: Essex M; Cotter SM; Gutensohn N; Jakowski R; Hardy WD Jr. Epidemiologic association between
virus-negative feline leukemia and the horizontally transmitted feline leukemia virus. Cancer Lett Mar 1981,
12(1-2)p37-42.

Hadler SC; Sorley DL; Acree KH; Webster HM; Schable CA: Francis DP. Maynard JE. An outbreak of hepatitis B
in a dental practice. Ann Intern MedAug 1981. 95(2)p 133-8.

Orenstein WA; Wu E; Wllkins J; Robinson /C Francis DP: Timko N; Wayne R. Hospital-acquired hepatitis A:
report of an outbreak. Pediatrics Apr 1981. 67(4)p494-7.

Orenstein WA; Wu E; Wilkins J; Robinson K: Francis DP: Timko N; Wayne R. Simultaneous amebic liver abscess
and hepatitis A Am J Gastroenterol Jan 1981. 75(1)p52~4.

Francis DP: Essex M; Maynard JE. Feline leukemia virus and hepa titis B virus: a comparison of late
manifestations. Prog Med Virol 1981, 27p 127-32. Am J Epidemiol Mar 1980, 1 1 1(3)p337-46

Osterholm MT; Kantor RJ; Bradley DW; Hall WN: Francis DP: Aaron HC; Washburn JW; Velde D. Immunoglobu/in
M-specific serologic testing in an outbreak of foodborne viral hepatitis, type A Am J Epidemiol Jul 7960,
112(1 )p8-16.

Francis DP, Essex M; Jakowski RM; Cotter SM; Lerer TJ; Hardy ED Jr. Increased risk for lymphoma and
g/omerulonephritis in a closed population of cats exposed to feline leukemia virus. Am. J. Epidemiol March 1980,
1 11 (3)p337-46.

Francis DP: MavnardJE. Immunoglobulin to prevent hepatitis B (letter). Lancet May 17, 1980, 1(8177)p1086.

Francis DP: Essex M; Cotter S; Jakowski RM; Hardy WD Jr. Feline leukemia virus infections: the significance of
chronic viremia. Leuk Res 1979, 3(6)p435-4 1.

Francis DP: Maynard JE. The transmission and outcome of hepatitis A, B, and non-A, non-B: a review. Epioemiol
Rev 1979, 1p17-31.

Francis DP; Cotter SM; Hardy WD Jr, Essex M. Comparison of virus-positive and virus-negative cases of feline
leukemia and lymphoma. Cancer Res. Oct 1979, 39(10)p3866-70.

Francis DP. Essex M; Cotter SM; Gayzagian D; Hamm D. A simple method for quantitating salivary levels of virus
using calcium alginate swabs. J Clin Pathol May 1979, 32(5)p4 14-5.

John TJ; Ninan GT; Rajagopalan MS; John F; Flewett TH; Francis DP: Zuckerman AJ. Epidemic hepatitic B
caused by commercial human immunoglobulin. Lancet May 19, 1979, 1(8125)p1074.

Francis DP: Essex M; Gayzagian D. Feline leukemia virus: survival under home and loboratory conditions. J. Clin
MicrobiolJan 1979,9(1 )p154-6.

Francis DP. Smith DH; Highton RB; Simpson Dl; et a/. Ebola fever in the Sudan, 1976: Epidemiologic aspects of
the disease. Ebola Virus Haemorrhagic Fever, ed. Pattyn, Elsevier/North-Holland Press, Amsterdam, New York
1978.

305

Donald P. Francis, M.D., D.Sc.

Publications

Page 6

WHO InternationalStudy Team: Ebola haemorrhagic fever In Sudan, 1976. Bull WHO 1978, 56p24 7-270.

Francis DP: Essex M. Leukemia andtymphoma: infrequent manifestations of common viral infections? A review.
J Infect Dls Dec 1978. 138(5)p9 16-23.

Francis DP; Pope RS; Pasternak EJ. Measles control In Oregon. Public Health Rep May-Jun 1978.
93(3)p2 16-20.

Ellis DS; Simpson IH: Francis DP: Knobloch J; Bowen ET; Lolik P. Deng IM. infrastructure of Ebola virus particles
in human liver. J Clin Pathol Mar 1978. 31 (3)p201-8.

Francis DP: Essex M; Hardy WD Jr. Excretion of feline leukaemia virus by naturally Infected pet cats. Nature Sep
15, 1977. 269 (5625) p252-4.

Francis DP: Herrmann KL; McMahon JR; Chavigny KH; Sanderlin KC. Nosocomial and maternally acquired
herpesvirus hominis Infections. A report of four fatal cases of neonates. Am J Dis Child Aug 1975,
129(8)p889-93.

Francis DP: Holmes MA; Brandon G. Pasteurella multocida. Infections after domestic animal bites and scratches.
JAMA Jul 7, 1975, 233(1 )p42-5.

Fraser DW; Glosser JW; Francis DP: Phillips CJ; Feeley JC; Sulzer CR. Leptospriosis caused by serotype
Fort-Bragg. A suburban outbreak. Ann Intern Med (United States) Dec 1973, 79(6)p786-9.

Cheldelin LV: Francis DP: Tilson H. Postpartum rubella vaccination. A survey of private physicians in Oregon.
JAMA Jul 9, 1973. 225(2)p158-9.

306

Donald P. Francis. M.D., D.Sc.

Major Accomplishments
(Since joining the Public Health Service)

August 1988 - January 1992

July 1985 - June 1989

May 1983 - June 1985

July 1978 - May 1983

SpeciaJ Consultant on AIDS to Mayor Art Agnos, City and County of
San Francisco, San Francisco. California. Chair the Mayor's HIV
Task Force, a broadly-based group consisting of business , religious
and health care professionals.

AIDS Advisor - State of California, Department of Health Services,
Berkeley, California. Consultant - WHO, Sudan (August 1987)
Member of the California AIDS Leadership Commttee (July 1988 to
present). Assisted the State of California in instituting one of the
most advanced HIV-prevention programs.

Assistant Director, Division of Viral Diseases and Coordinator. AIDS
Laboratory Activities, Atlanta, Georgia. Established the CDC AIDS
Laboratory which performed much of the early work et/ologically
Unking the AIDS virus (HIV) with AIDS.

Assistant Director, Hepatitis Laboratories Division, CDC.
Phoenix, Arizona. Designed and completed a trial of the newly
developed hepatitis B vaccine. Designed and coordinated the first
placebo-controlled trial of HBV vaccine in newborn babies
(collaboratively. with the People's Republic of China).

July 1985 - July 1979

October 1976 - December 1976
May 1975 - June 1975
July 1974 - March 1975
October 1973 - June 1974
January 1973 - October 1973

July 1973
April 1971

Infectious Disease Fellow, Harvard Medical School, Virology Doctoral
Student, Harvard School of Public Health. Completed fellowhip in
infectious disease. Completed doctoral degree in virology (awarded
in November of 1979), studying the transmission and outcome of
feline leukemia virus.

WHO Consultant, Sudan. Member of a four-man team investigating
and controlling the first outbreak of African Hemorragic Fever
(Ebola Virus)

WHO Consultant. Smallpox Eradication Programme, Bangladesh.
Helped design and implement the program for elimination of smallpc*
from Bangladesh.

State Program Coordinator. WHO Smallpox Eradication Programme.
Lucknow. India. Helped design and supervise the eradication of
smallpox from the state of Uttar Pradesh, India.

WHO Medical Officer, Smallpox Eradication Programme. Lucknow.
India. Helped design and supervise the eradication of smallpox from
Bareilly Division, Uttar Pradesh , India.

WHO Medical Officer, Smallpox Eradication Programme, Knanoum.
Sudan. Designed and directed a national surveillance/control
program for smallpox in Sudan. Assured the absence of smallpox
from Sudan.

Completion of Epidemic Intelligence Service training program.

Member of the CDC team, Yugoslavia. Termination of smallpox
transmission in Kosovo Province, Yugoslavia.

APPENDIX D
307

MERLE A. SANDE

Curriculum vitae
BORN: September 2, 1939

CHILDREN: Suzanne 1962 Eric 1970

Cathleen 1964 Sarah 1973

EDUCATION:

B.S. Washington State University, Pullman, Washington 1957-1961

M.D. University of Washington School of Medicine, Seattle, Washington,

1961-1965

PROFESSIONAL CAREER:

1 965 - 1 966 Intern in Medicine, The New York Hospital, New York, New York

1 966 - 1 968 Assistant Resident in Medicine, The New York Hospital, New York,

New York.

1968 - 1969 Assistant Resident in Medicine (Infectious Diseases), The New York

Hospital, New York, New York

1969 - 1971 Clinical Instructor in Medicine, University of Texas Health Science

Center at San Antonio, San Antonio, Texas

1971 - 1974 Assistant Professor of Medicine, University of Virginia School of

Medicine, Division of Infectious Diseases, Charlottesville, Virginia

1974 - 1978 Associate Professor of Medicine, University of Virginia School of

Medicine, Division of Infectious Diseases, Charlottesville, Virginia

1976 - 1978 Vice-Chairman of Medicine, University of Virginia School of Medicine,

Charlottesville, Virginia

1978 - 1980 Professor of Internal Medicine, University of Virginia School of

Medicine, Division of Infectious Diseases, Charlottesville, Virginia

1979 Acting Chairman of Medicine, University of Virginia School of
Medicine, Charlottesville, Virginia

1980 - 1996 Professor of Medicine, University of California, San Francisco School of

Medicine, San Francisco, California

M. Sande, MD
March 1997

308

PROFESSIONAL CAREER: (continued)

1980 - 1996 Vice-Chairman of Medicine, University of California, San Francisco

School of Medicine, San Francisco, California

1980 - 1996 Chief of Medical Services, San Francisco General Hospital, San

Francisco, California

1 996 - present Professor and Chairman, Department of Medicine, and the Clarence M.

and Ruth N. Birrer Presidential Endowed Chair in Internal Medicine,
University of Utah School of Medicine, Salt Lake City, Utah.

MILITARY SERVICE:

1969 - 1971 Captain, U.S. Air Force, Wilford Hall Lackland Air Force Base, San

Antonio, Texas

BOARD CERTIFICATION:

1971 American Board of Internal Medicine

1974 Subspecialty of Infectious Diseases

EDITORIAL APPOINTMENTS:

1981 - 1983 Infection and Immunity, Editorial Board

1 980 - present Antimicrobial Agents and Chemotherapy, Editorial Board
1988 - present AIDS, Editorial Board,

1 988 - present Journal of Acquired Immune Deficiency Syndromes, Editorial Board

1 989 - present Journal of Infectious Diseases, Editorial Board

1991 - present Infectious Diseases in Clinical Practice, Editorial Board

1994 - present Bulletin of the New York Academy of Medicine: A Journal of Urban
Health, Editorial Board

1 997 - present Drug Resistance Updates, Editorial Board

M. Sande, MD
March 1997

309

PROFESSIONAL SOCIETY MEMBERSHIPS AND HONORS:

Albemarle County Medical Society

Alpha Omega Alpha

American Association for the Advancement of Science

American Clinical & Climatological Association

American College of Physicians, Fellow, Virginia Chapter, ACP, Secretary/Treasurer, 1975-
1979

American Federation for Clinical Research

American Medical Writers award, 1995

American Society for Clinical Investigation (ASCI)

American Society of Internal Medicine

American Society for Microbiology

American Thoracic Society

Association of American Physicians (AAP)

Association of Professors of Medicine (APM)

California Academy of Medicine

California Society of Internal Medicine

Infectious Diseases Society of America ; Council member, October 1986 - October 1989;
Chairman, AIDS Subcommittee; Vice President, October 1990 - 1991; President-
Elect, October 1991 - 1992; President, October 1992 - 1993.

International AIDS Society

Medical Examiner, City of Charlottesville, County of Albemarle, Virginia

National Advisory Allergy & Infectious Diseases Council, Council member,
1 November 1987-31 October 1991

Pacific Inter-Urban Clinical Club

Phi Beta Kappa

Phi Kappa Phi

San Francisco Chapter of International Association of Business Communicators' 1987
Communications Leader Award

Society of Experimental Biology and Medicine

Southern Society for Clinical Investigation

The National Foundation for Infectious Diseases, Board of Directors, 1981 - 1982, 1996 -

Virginia Thoracic Society

Western Society for Clinical Research

Western Association of Physicians

COMMITTEES:

ADDS Advisory Board to Director of Public Health, City and County of San Francisco, Member,

1981 - 1995
AIDS Advisory Committee, Department of Health Services, State of California, Ex Officio

member, December 1985-1995

M. Sande, MD
March 1997

310

COMMITTEES (continued)

AIDS Drug Advisory Committee, Department of Health Services, State of California, Member,

1991-1992
AIDS Leadership Committee of the Department of Health Services, State of California, Member,

May 1988-October 1989; member, Education & Prevention Subcommittee
AIDS Task Force, National Foundation for Infectious Diseases, member, 1986 - 1990
American Board of Internal Medicine, Subspecialty Board on Infectious Diseases, Member, July

1992- 1997
American Heart Association Council on Cardiovascular Disease in the Young, Committee on

Rheumatic Fever, Endocarditis, and Kawasaki Disease, Member
Bay Area Infectious Diseases Society, President, September 1 984-December 1986
Bowman Foundation, University of Virginia, Charlottesville, Virginia, Chairman, 1978 - present
Data and Safety Monitoring Board of the National Institute of Allergy and Infectious Diseases,

National Institutes of Health, Member, 01 July 1992 - 1996

IDS A/FDA Contract, Subcommittee on Guidelines for Meningitis, member, 1988 - 1990
Infection-control Advisory Committee to Director of California Department of Health Services,

Member, 1988
Interscience Confence on Antimicrobial Agents and Chemotherapy, Program Committee, 1981-

1985; Associate Member, December 1985 - December 1988; Liaison representative to ISC,

1985 - 1988; Hoechst-Roussel Award Committee, 1986 - 1990
Infectious Diseases Society of America, Council member, October 1986 - October 1989;

Chairman, AIDS Subcommittee; Vice President, October 1990 - 1991; President-Elect,

October 1991-1992; President, October 1992 - 1993
Infectious Diseases Subcommittee for the Medical Knowledge Self- Assessment Program VI,

American College of Physicians, 1982 - 1983.
Inter- American Society for Chemotherapy, Member, 1986

International Society of Chemotherapy, Executive Committee, co-opted member, 1985 - 1989
Maxwell Finland 1993 Award, Member, Chairman's Committee, National Foundation for

Infectious Diseases

Mayor Dianne Feinstein's AIDS Task Force, Chairman, 1984-1987
National Institute for Allergy and Infectious Disease, Data Monitoring and Safety Board,

1990-1996

San Francisco Medical Society AIDS Task Force, Consultant, 1985 - 1990
The National Foundation for Infectious Diseases, Board of Directors, 1981 - 1982
The United States Pharmacopeia on Infectious Disease Therapy, Drug Information Advisory

Panel, 1980-1987
University of California, San Francisco AIDS Coordinating Council, Chairman, June 1988 -

1996
University of California, San Francisco Task Force on AIDS, Founding Chairman, 1982 - May

1988

University of California Systemwide Task Force on AIDS, Chairman, 1983 - June 1988
Veterans Administration Central Office, Career Development Committee, 1984 - 1986

M. Sande, MD
March 1997

311

COMMITTEES (continued)

Virginia Partners of the Americas, Executive Committee, 1976 - 1979
University of Utah Graduate Medical Education Committee, 1996 to present
University of Utah Health Sciences System Management Committee, 1996 to present
University of Utah Clinical Sciences Council, 1996 to present
University of Utah Medical Board, 1996 to present

ORIGINAL WORK

1 . Kilbourn E, Christenson W, Sande MA: Antibody response in man to influenza virus
neuramidase following influenza. J Rirol 2:761-62, 1968

2. Barondess J, Sande MA: Some changing aspects of aortic regurgitation: an autopsy study.
Trans Am Clin Climatol Assoc 80:23-36, 1968; Arch Intern Med 124:600-05, 1969.

3. Sande MA, Levison M, Lucas D, Kay d: Bacteremia associated with cardiac
catheterization. N Engl J Med 281 : 1 104-06, 1969.

4. Sande MA, Alonso D, Smith J, Hook E: Left atrial tumor presenting with hemoptysis and
pulmonary infiltrates. Am RevRespirDis 102: 258-63,1970.

5. Sande MA, Kaye D: Evaluation of methods for determining antibacterial activity of serum
and urine after colistimethate injection. Clin Pharmacol Ther 1 1 :873-82, 1970.

6. Sande MA, Johnson WD Jr, Hook EW, Kay D: Sustained bacteremia in patients with
prosthetic cardiac valves. N Engl J Med 286:1067-70, 1972

7. Shafig S. Sande MA, Curruthers R, Killip T, Milhorat A: Skeletal muscle in idiopathic
cardiomyopathy. J Neurol Sci 15:303-20, 1972.

8. Merrill C, Gwaltney J, Hendley J, Sande MA: Rapid identification of pneumococci: Gram
stain versus the Quellung reaction. N Engl J Med 288:510-12, 1973.

9. Sande MA, Overton JW: In vivo antagonism between gentamicin and chloramphenicol in
neutropenic mice. J Infect Dis 128:247-50, 1973.

10. Rein MF, Westervelt FB, Sande MA: Pharmacodynamics of cefazolin in the presence of
normal and impaired renal function. Antimicrob Agents Chemother 4:366-71, 1973.

1 1 . Wenzel RP, Hendley JO, Sande MA, Gwaltney JM Jr: Revised ( 1 972-73) bivalent
influenza vaccine. Serum and nasal antibody responses to parenteral vaccination. J Am
Med Assoc 226:435-38, 1973.

M. Sande, MD
March 1997

312

12. Ries KM, Cobbs GC, Gillenwater JY, Levison ME, Mandell GL, Sande MA, Kay D:
Double-blind comparison of carbenicillin indanyl sodium ampicillin and cephalexin in
treatment of urinary tract infection. Antimicrob Agents Chemother 4:593-96, 1973.

13. Rein MF, Sande MA: Osteomyelitis caused by concurrent infection with Mycobacterium
tuberculosisand Blastomyces dermatitidis. Am Rev Respir Dis 109:286-89, 1974.

14. Macllvwaine WA IV, Sande MA, Mandell GL: Penetration of antistaphylo/coccal
antibiotics into the human eye. Am J Ophthalmol 77:589-92, 1974.

15. Graybill JR, Sande MA, Reinarz JA, Shapiro SR: Controlled penicillin anaphylaxis
leading to desensitization. South MedJ 67:62-64,1974.

16. Sande MA, Irvin RG: Penicillin-aminoglycoside synergy in experimental Streptococcus

endocarditis. J Infect Dis 129:572-76,1974.

1 7. Dacey RG, Sande MA: Effect of probenecid on cerebrospinal fluid concentrations of
penicillin and cephalosporin derivatives. Antimicrob Agents Chemother 6:437-41, 1974.

1 8. Hook EW III, Sande MA: Role of the vegetation in experimental Streptococcus viridans
endocarditis. Infect Immun 10:1433-38, 1974.

19. Sande MA, Johnson ML: Antimicrobial therapy of experimental endocarditis caused by
Staphvlococcus aureus. J Infect Dis 131:367-75, 1975.

20. Greenlee JE, Johnson WD, Campa JF, Adelman LS, Sande MA: Adult toxoplasmosis
presenting as polymyositis and cerebellar ataxia. Ann Intern Med 82:367-71, 1975.

21 . Sande MA, Mandell GL: Effect of rifampin on nasal carriage of Staphvlococcus aureus.
Antimicrob Agents Chemother 7:294-97, 1975.

22. Bolton WK, Sande MA, Normansell DE, Sturgill BC, Westervelt FB Jr.: Vevtriculojugular
shunt nephritis with Corynebacterium bovis. Successful therapy with antibiotics. Am J
Med 59:41 7-23, 1975.

23. Hendley JO, Sande MA, Stewart PM, Gwaltney JM Jr.: Speard of Streptococcus
Pneumoniae in families. I. Carriage rates and distribution of types. J Infect Dis 132:55-61,
1975.

24. Gwaltney JM Jr., Sande MA, Austrian R., Hendley JO: Spread of Streptococcus
pneumoniae in families. II. Relation of transfer of S. pneumoniae to incidence of colds
and serum antibody. J Infect Dis 132:62-68, 1975.

M. Sande, MD
March 1997

313

25. Sande MA, Gadot F, Wenzel RP: Point source epidemic of Mycoplasma pneumoniae
infection in a prosthodontics laboratory. Am Rv Respir Dis 1 12:213-1 7, 1975.

26. Guerrant RL, Moore RA, Sande MA: Toxigenic E. coli in infantile diarrhea in Brazil. N
Engl J Med 293:567-73, 1975.

27. Utz JP, Sande MA, Garriques IL, Mandell GL, Warner JF, McGehee RF, Shadomy S:
Combined amphotericin B flucytosine chemotherapy in human cryptococcosis. J Infect Dis
132:368-73, 1975.

28. Evans FO Jr, Sydnor JB, Moore WEC, Moore GR, Manwaring JL, Brill AH, Jackson RT,
Hanna S, Skaar JS, Holdeman LV, Fitz-Hugh GS, Sande MA, Swaltney JM Jr: Sinusitis of
the maxillary antrum. N Engl J Med 293:735-39, 1975.

29. Dilworth JA, Stewart P, Swaltney JM Jr, Hendley JO, Sande MA: Methods to improve
detection of pneumococci in respiratory secretions. J Clin Microbiol 2:453-55, 1975.

30. Hood EW III, Roberts RB, Sande MA: Antimicrobial theraphy of experimental
enterococcal endocarditis. Antimicrob Agents Chemother 8:564-70, 1975.

31 . Joyce RA, Sande MA: Mechanisms of anaemia in experimental bacterial endocarditis:
anaemia in experimental endocarditis. Scand J Haematol 15:306-1 1, 1975.

32. Strausbaugh LJ, Dilworth FA, Swaltney JM Jr., Sande MA: In vitro susceptibility studies
with josamycin and erythromycin. Antimicob Agents Chemother 9:546-48, 1976.

33. Sande MA, Courtney KB: Nafcillin-gentamicin synergism in experimental staphylococcal
endocarditis. J Lab Clin Med 88:1 18-24, 1976.

34. Wenzel RP, Hunting KJ, Osterman CA, Sande MA: Providencia stuartii hospital pathogen:
potential factors for its emergence and transmission. Am J Epidemiol 104:170-80, 1976.

35. Minoro MR, Sande MA, Dilworth JA, Mandell GL: Cefamandole treatment of pulmonary
infection caused by Gram-negative rods. J Antimicrob Chemother 2:49-53, 1976.

36. Sherertz RJ, Dacey R, Sande MA: Cefamandole in the therapy of experimental
pneumococcal meningitis. J Antimicrob Chemother 2:159-65, 1976.

37. Strausbaugh LJ, Bolton WK, Dilworth JA, Guerrant RL, Sande MA: Comparative
pharmacology of josamycin and erythomycin stearate. Antimicrob Agents Chemo 10:450-
56, 1976.

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38. Thompson RL, Sande MA, Wenzel RP, Hoke CH, Swaltney JM Jr.: Swine influenzae
infection in civilians. Report of two cases. N Engl J Med 295:714-15, 1976.

39. Bodine JA, Strausbaugh LJ, Sande MA: Ampicillin and an ester in experimental
Hemophilius influenzae meningitis. Clin Pharmacol Ther 20:727-32, 1976.

40. Hamory B, Ignatiadis P, Sande MA: Intrathecal ammikacin administration. Use in the
treatment of gentamicin-resi slant Klebsiella pneumoniae meningitis. J Am Med Assoc
236: 197374, 1976.

41 . Suratt PM, Swaltney JM Jr, Sande MA: A rapid method of disinfecting the
bronchofiberscope. Am Rev Respir Dis 1 14:1 198-2000, 1976.

42. Strausbaugh LJ, Mandaleris CD, Sande MA: Cefamandole and ampicillin therapy in
experimental /haemophilus influenzae meningitis. J Infect Dis 135:210-16, 1977.

43. Strausbaugh LJ, Mandaleris CD, Sande MA: Comparison of four aminoglycoside
antibiotics in the therapy of experimental E. coli meningitis. J Lab Clin Med 89:692-701 ,
1977.

44. Guerrant RL, Strausbaugh LJ, Wenzel RP, Hamory BH, Sande MA: Nosocomial
bloodstream infections caused by gentamicin-resistant Gram-negative bacilli. Am J Med
62:894-901, 1977.

45. Barros F, Korzeniowski OM, Sande MA, Martins K, Santos LC, Rocha H: In vitro
antibiotic susceptibility of salmonellae. Antimicrob Agents Chemother 1 1:1071-73, 1977.

46. Sande MA, Bowman CR, Calderone RA: Experimental Candida albicans endocarditis:
characterization of the disease and response to therapy. Infect Immun 17:140-47, 1977.

47. Scheld WM, Korzeniowski OM, Sande MA: In vitro susceptibility studies with cefaclor
and cephalexin. Antimicrob Agents Chemother 12:290-92, 1977.

48. Korzeniowski OM, Scheid WM, Sande MA: Comparative pharmacology of cefaclor and
cephalexin. Antimicrob Agents Chemother 12:157-62, 1977.

49. Strausbaugh LJ, Sande MA: Factors influencing the therapy of experimental Proteus
mjrabjlis meningitis. J Infect Dis 137:251-60, 1978.

50. Korzeniowski OM, Wennersten C, Mollering RC Jr., Sande MA: Penicillin-netilmicin
synergism against Streptococcus faecalis. Antimicrob Agents Chemother 13:430-34, 1978.

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5 1 . Scheld WM, Valone JA, Sande MA: Bacterial adherance in the pathogenesis of
endocarditis: interaction of bacterial dextran, platelets and fibrin. J Clin Invest 61:1394-
1404, 1978.

52. Calderone RA, Rotondo RJ, Sande MA: Candida albicans endocarditis: ultrastructural
studies of vegetation formation. Infect Immun 20:279-289, 1978.

53. Sande MA, Sherertz RJ, Zak O, Strausbaugh LJ: Cephalosporin therapy of experimental
meningitis. J Infect Dis 137 (Suppl): S161-68, 1978.

54. Gwaltney JM Jr, Sydnor T, Hamory B, Seale D, Sande MA: controlled trial of
trimethoprim-sulfa in the treatment of acute maxillary sinusitis. Current Chemother 1 :120-
21,1978.

55. Korzeniowski OM, Carvalho EM Jr., Rocha H, Sande MA: Evaluation of cefamandole
therapy of patients with bacterial meningitis. J Infect Dis 137 (Suppl): S160-63, 1978.

56. Sande MA, Sherertz RJ, Zak O, Dacey RG, Bodine JA, Strausbaugh LJ: Factors
influencing the penetration of antimicrobial agents into the cerebrospinal fluid of
experimental animals. Scand J Infect Dis 14: (Suppl):S 160-63, 1978.

57. De Carvalho EM, Filho, Costra E, Silva 1C, Silva CP, Costa YA, Korzeniowski OM, Sande
MA, Rocha H: Tratamento da meningite bacteriana com cefamandole. Published in
Revista do Instituts de Medicina Tropical de Sao Paulo, 1978.

58. Scheld WM, Brown RS Jr, Sande MA: Comparison of netilmicin with gentamicin in the
therapy of experimental E. coli meningitis. Antimicrob Agents Chemother 13:899-904,
1978.

59. Miller J, Sande MA, Gwaltney JM Jr, Hendley JO: Diagnosis of pneumococcal pneumonia
by antigen detection of sputum. J Clin Microbiol 7:459-62, 1978.

60. Spyker DA, Thomas BL, Sande MA, Bolton WK: Pharmacokinetics of cefa/clor and
cephalexin: dosage nomograms for impaired renal function. Antimicrob Agents Chemother
14:172-77, 1978.

61 . Scheld WM, Royston D, Harding SA, Hess CE, Sande MA: Simultaneous disseminated
aspergillosis and zygomycosis in a leukemic patient. South Med J 72:1325-28, 1979.

62. Harding SA, Scheld WM, Feldman PS, Sande MA: Pulmonary infection with capsule-
deficient Cryptococcus neoformans. Virchows Arch [Pathol Anat] 382:1 13-18, 1979.

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63. Scheld WM, Fletcher DD, Fink FN, Sande MA: Response to therapy in an experimental
rabbit model of meningitis due to Listeria monocytogenes. J Infect Dis 140:287-94, 1979.

64. Scheld WM, Fink FN, Fletcher DD, Sande MA: Mecillinam-ampicillin synergism in
experimental Enterobacteriaceae meningitis. Antimicrob Agents Chemother 16:271-76,
1979.

65. Harding SA, Scheld WM, McGowan MD, Kelley WJ, Sande MA: Enzyme-linked
immunosorbent assay for detection of Streptococcus pneumoniae antigen in experimental
meningitis. Trans Am Neurol Assoc 103:142-46, 1979.

66. Dacey RG, Welch JE, Scheld WM, Winn HR, Jane MA, Sande MA: Alterations of
cerebrospinal fluid outflow resistance in experimental bacterial meningitis. Trans Am
neurol Assoc 103:142-46, 1979.

67. Scheld WM, Thomas JH, Sande MA: Influence of preformed antibody on experimental
Streptococcus sanguis endocarditis. Infect Immun 25:781-85, 1979.

68. Scheld WM, Park TS, Dacey RG, Jane JA, Winn HR, Sande MA: Clearance of bacteria
from cerebrospinal fluid to blood in experimental meningitis. Infect Immum 24:102-05,
1979.

69. Hamory BH, Sande MA, Sydnor A Jr, Scale DL, Gwaltney JM Jr: Etiology and
antimicrobial therapy of acute maxillary sinusitis. J Infect Dis 139:197-202, 1979.

70. Roberts TL III, Futrell JW, Sande MA: Antibiotic penetration into normal and inflamed
tissues as reflected by peripheral lymph. Ann Surg 189:395-403, 1979.

71 . Moellering RC, Korzeniowski OM, Sande MA, Wennersten CB: Species-specific
resistance to antimicrobial synergism in Streptococcus faecium and Streptococcus faecalis.
J Infect Dis 140:203-08, 1979.

72. Bennett JE, Dismukes WE, Dumas RJ, Medoff G, Sande MA, Gallis H, Leonard J, Fields
BT, Bradshaw M, Haywood H, McGee ZA, Gate TR, Cobbs Cb, Warner JF, Ailing DW: A
comparison of amphotericin B alone and combined with flucytosine in the treatment of
cryptococcal meningitis. N Engl J Med 302:126-31, 1979.

73. Rogers BH, Donowitz GR, Walker GK, Harding SA, Sande MA: Opportunistic pneumonia.
A clinicopathologic study of five cases caused by an unidentified acid- fast bacterium. N
Engl J Med 301:959-61, 1979.

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74. Strausbaugh LJ, Murray TW, Sande MA: Comparative penetrations of six antibiotics into
the cerebrospinal fluid of rabbits with experimental staphylococcal meningitis. J
Antimicrob Chemother 6:363-71, 1980.

75. Scheld WM, Dacey RG, Winn HR, Welsh JE, Jane JA, Sande MA: Cerebrospinal fluid
outflow resistance in rabbits with experimental meningitis. Alterations with penicillin and
methylprednisolone. J Clin Invest 66:243-53, 1980.

76. Bolton WK, Scheld WM, Spyker DA, Overly TL, Sande MA: Pharmacokinetics of
moxalactam in subjects with varying degrees of renal dysfunction. Moxalactam in subjects
with renal dysfunction. Antimicrob Agents Chemother 18:933-38, 1980.

77. Grogan EL, Sande MA, Clark RE, Nolan SP: Experimental endocarditis in calf after
tricuspid valve replacement. Ann Thorac Surg 30, 1980.

78. Hodge RH Jr, Krongaard L, Sande MA, Kaiser DL: Multiple use of disposable insulin
syringe-needle units. J Am Med Assoc 244:266-67, 1980.

79. Scheld WM, Brown RS Jr., Harding SA, Sande MA: Detection of circulating antigen in
experimental Candida albicans endocarditis by an enzyme-linked immunosorbent assay. J
Clin Microbiol 12:679-83, 1980.

80. Sande MA, Scheld WM: Bacterial adherence in endocarditis: interaction of bacterial
dextran, platelets, fibrin and antibody. Scand J Infect Dis 24 (Suppl): 100-05, 1980.

81. Sande MA, Scheld WM: Combination antibiotic therapy of bacterial endocarditis. Ann
Intern Med 92:390-395, 1980.

82. Giampaolo C, Scheld WM, Boyd J, Savory J, Sande MA, Wills M: Leukocyte and bacterial
interrelationships in experimental meningitis. Ann Neurol 9:328-33, 1981 .

83. Sande MA, Korzeniowski OM, Allegro GM, Brennan RO, Zak O, Scheld WM: Intermittent
or continuous therapy of experimental memingitis due to Streptococcus pneumoniae in
rabbits: preliminary observations on the postantibiotic effect in vivo. Rev Infect Dis 3:98-
109,1981.

84. Wenzel RP, Osterman CA, Donowitz LG, Hoyt JW, Sande MA, Martone WJ, Peacock JE,
Levine Jl, Miller GB Jr.: Identification of procedure-related nosocomial infections in high-
risk patients. Rev Infect Dis 3:701-07, 1981.

85. Scheld WM, Spyker DA, Donowitz GR, Golton WK, Sande MA: Moxalactam and
cefazolin: comparative pharmacokinetics in normal subjects. Antimicrob Agents
Chemother 19:613-19, 1981.

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86. Giampaolo C, Scheld WM, Savory J, Sande MA, Wills WR, Boyd JC: A multivariate
approach to prognostication in experimental bacterial meningitis. Am J Clin Pathol
76:442-49,1981.

87. Gwaltney JM Jr., Sydnor A Jr., Sande MA: Etiology and antimicrobial treatment of acute
sinusitis. Ann Otol Rhinol Laryngol 90 (Suppl): 68-71, 1981.

88. Bolton WK, Scheld WM, Spyker DA, Sande MA: Pharmacokinetics of cefoperazone in
normal volunteers and subjects with renal insufficiency. Antimicrob Agents Chemother
19:821-25,1981.

89. Scheld WM, Zak O, Vosbeck K, Sande MA: Bacterial adhesion in the pathogenesis of
infective endocarditis: effect of subinhibitory antibiotic concentrations of streptococcal
adhesion in vitro and the development of endocarditis in rabbits. J Clin Invest 68:1381-84,
1981.

90. Scheld WM, Calderone RA, Alliegro GM, Sande MA: Yeast adherence in the pathogenesis
of Candida endocarditis. Proc Exp Biol Med 168:208-13, 1981.

91 . Oblinger MJ, Bowers JT, Sande MA, Mandell GL: Moxalactam therapy versus standard
antimicrobial therapy for selected serious infections. Rev Infect Dis 4 (Nov-Dec Suppl):
S639-49, 1982.

92. Korzeniowski O, Sande MA, and the National Collaborataive Endocarditis Study Group:
Combination antimicrobial therapy for Staphylococcus aureus endocarditis in patients
addicted to parenteral drugs and in nonaddicts: a prospective study. Ann Intern Med
97:496-503, 1982.

93. Scheld WM, Giampaolo C. Boyd J, Savory J, Wills MR, Sande MA: Cerebrospinal fluid
prognostic indices in experimental pneumococcal meningitis. J Lab Clin Med 100:218-29,
1982.

94. Sande MA: Antimicrobial therapy of two serious bacterial infections: enterococcal
endocarditis and nosocomial pneumonia. Arch Intern Med 142:2033, 1982.

95. Scheld WM, Johnson ML, Gerhardt EB, Sande MA: Clindamycin therapy of experimental
Staphlococcus aureus endocarditis. Antimicrob Agents Chemother 21:646-49, 1982.

96. Scheld WM, Brodeur JP, Sande MA, Alliegro GM: Comparison of cefopera/zone with
penicillin, ampicillin, gentamicin, and chloramphenicol in the therapy of experimental
meningitis. Antimicrob Agents Chemother 22:652-56, 1982.

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97. Sande MA, Korzeniowski OM, Scheld WM: Factors influencing the pathogenesis and
prevention of infective endocarditis. Scand J Infect Dis 31(Suppl): 48-54, 1982.

98. Ernst JD, Sande MA: Antibiotic combinations in experimental infections in animals. Rev
Infect Dis 4:302- 10, 1982.

99. Spyker DA, Gober LL, Scheld WM, Sande MA, Bolton WK: Pharmacokinetics of cefaclor
in renal failure: effects of multiple doses and hemodialysis. Antimicrob Agents Chemother
21:278-281, 1982.

100. Siegel D, Sande MA: Patterns of antibiotic use in a busy metropolitan emergency room:
analysis of efficacy and cost-appropriateness. West J Med 138:737-41, 1983.

101 . Gualtieri RJ, Donowitz GR, Kaiser DL, Hess CE, Sande MA: Double-blind randomized
study of prophylactic trimethoprim-sulfamethoxazole in granulocytopenic patients with
hematologic malignancies. Am J Med, 1983.

102. Chambers HF, Korzeniowski OM, Sande MA, and the National Collaborative Endocarditis
Study Group: Staphylococcus aureus endocarditis: clinical manifestations in addicts and
nonaddicts. Medicine 62:170-177, 1983.

103. Scheld WM, Sande MA: Bactericidal versus bacteriostatic antibiotic therapy of
experimental pneumococcal meningitis in rabbits. J Clin Invest 71 :41 1-419, 1983.

104. Simon GL, Smith RH, Sande MA: Emergence of rifampin-resistant strains of
Staphylococcus aureus during combination therapy with vancomycin and rifampin: a report
of two cases. Rev Infect Dis 5 (Suppl 3): S507-S508, 1983.

105. Hackbarth CJ, Ernst JD, Sande MA: Inhibition of isolation of Escherichia coli in blood
cultures by trimethoprim-sulfamethoxazole. J Infect Dis 147-964-965, 1983.

106. Drake TA, Sande MA: Studies of the chemotheapy of endocarditis: correlation of in vitro,
animal model, and clinical studies. Rev Infect Dis 5 (Suppl 2): S345-S354, 1983.

107. Ernst JD, Decazes JM, Sande MA: Experimental pneumococcal meningitis: the role of
leukocytes in pathogenesis. Infect Immun 41:275-279, 1983.

108. Ernst JD, Rusnak M, Sande MA: Combination antifungal chemotherapy for experimental
disseminated candidiasis: lack of correlation between in vitro and in vivo observations with
amphotericin B and rifampin. Rev Infect Dis 5 (Suppl 3)S626-S630, 1983.

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109. Freedman JM, Hoffinan SH, Scheld WM, Lynch MA, da Silva HR, Rocha H, Sande MA:
Moxalactam for the treatment of bacterial meningitis in children. J Infect Dis 148:886-891,
1983.

110. Scheld WM, Calderone RA, Brodeur JP, Sande MA: Influence of preformed antibody on
the pathogenesis of experimental Candida albicans endocarditis. Infect Immun 40:950-055,
1983.

111. Drake TA, Hackbarth CF, Sande MA: Value of serum tests in combined drug therapy of
endocarditis. Antimicrob Agents Chemother 24:653-657, 1983.

1 12. Zak O, Scheld WM, Sande MA: Rifampin in experimental endocarditis due to
Staphvlococcus aureus in rabbits. Rev Infect Dis 5 (Suppl 3): S481-S490, 1983.

113. Decazes JM, Ernst JD, Sande MA: Correlation of in vitro time-kill curves and kinetics of
bacterial killing in cerebrospinal fluid during ceftriaxone therapy of experimental
Escherichia coli meningitis. Antimicrob Agents Chemother 24:463-467, 1983.

1 14. Conte JE, Hadley WK, Sande MA, and the University of California at San Francisco Task
Force on AIDS: Infection control guidelines for patients with the acquired immune
deficiency syndrome (AIDS). N Engl J Med 309:740-744, 1983.

115. Cooke M, Sande MA: The diagnosis and outcome of bowel enfarction on an acute medical
service. Am J Med 75:984-992, 1983.

116. Rusnak MG, Drake TA, Hackbarth CJ, Sande MA: Single versus combination antibiotic
therapy for pneumonia due to Pseudomonas aeruginosa in neutropenic guinea pigs. J Infect
Dis 149:980-985, 1984.

117. Wilson WR, Wilkowske CJ, Wright AJ, Sande MA, Geraci JE: Treatment of streptomycin-
susceptible and streptomycin-resistant enterococcal endocarditis. Ann Intern Med 100:816-
823, 1984.

118. Tauber MG, Zak O, Scheld WM, Hengster B, Sande MA: The postantibiotic effect in the
treatment of experimental meningitis caused by Streptococcus pneumoniae in rabbits. J
Infect Dis 149:575-583, 1984.

119. Tauber MG, Doroshow CA, Hackbarth CJ, Rusnak MG, Drake TA, Sande MA:
Antibacterial activity of beta-lactam antibiotics in experimental meningitis due to
Streptococcus pneumoniae. J Infect Dis 149:568-574, 1984.

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120. Chambers HF, Mills J, Drake TA, Sande MA: Failure of a once-daily regimen of cefonicid
for treatment of endocarditis due to Staphylococcus pneumoniae. Rev Infect Dis 6 (Suppl
4):S870-74, 1984.

121 . Drake TA, Rodgers GM, Sande MA: Tissue factor is a major stimulus for vegetation
formation in enterococcal endocarditis in rabbits. J Clin Invest 73:1750-53, 1984.

122. Chambers HF, Hackbarth CJ, Drake TA, Rusnak MG, Sande MA: Endocarditis due to
methicillin-resistant Staphylococcus aureus in rabbits: expression of resistance to beta-
lactam antibiotics in vivo and in vitro. J Infect Dis 149:894-903, 1984.

123. da Silva HR, Costa YA, Santos LCS, Costa E, Freedman J, Hoffman S, Scheld M, Sande
M, Rocha H: Eficcia do moxolactam no tratamento de meningites purulentas causadas por
Haemophilus influenzae e Neisseria meningitidis. Mem Inst Oswaldo Cruz 79:29-35,
1984.

124. Scheld WM, Rocha H, Sande MA, Bryan JP: Rationale for clinical trials evaluating
ceftriaxone in the therapy of bacterial meningitis. Am J Med 77 (4C):42-49, 1984.

125. Kapusnik J, Parenti F, Sande MA: The use of rifampicin in staphylococcal infections - a
review. J Antimicrob Chemother 13 (SupplC):61-66, 1984.

126. Chambers HF, Sande MA: Teicoplanin versus nafcillin and vancomycin in the treatment of
experimental endocarditis caused by methicillin-susceptible or -resistant Staphylococcus
aureus. Antimicrob Agents Chemother 26:61-64, 1984.

127. Ernst JD, Hartiala KT, Goldstein IM, Sande MA: Complement (C-5)-derived chemotactic
activity accounts for accumulation of polymorphonuclear leukocytes in cerebrospinal fluid
of rabbits with pneumococcal meningitis. Infect Immun 46:81-86, 1984.

128. Bryan JP, Rocha H, da Silva HR, Taveres A, Sande MA, Scheld WM: Comparison of
ceftriaxone and ampicilllin plus chloramphenicol for the therapy of acute bacterial
meningitis. Antimicrob Agents Chemother 28:361-68, 1985.

129. Toy PTCY, Lai L-W, Drake TA, Sande MA: Effect of fibronectin on the adherence of
Staphylococcus aureus to fibrin thrombi in vitro. Infect Immun 48:83-86, 1985.

130. Sullam PM, Tauber MG, Hackbarth CJ, Chambers HF, Scott KG, Sande MA: Pefloxacin
therapy for experimental endocarditis caused by methicillin-susceptible or methicillin-
resistant strains of Staphylococcus aureus. Antimicrob Agents Chemother 27:685-87,
1985.

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131. Gordin FM, Hackbarth CJ, Scott KG, Sande MA: Activities of peflosacin and ciprofloxacin
in experimentally induced Pseudomonas pneumonia in neutropenic guinea pigs.
Antimicrob Agents Chemother 27:452-54, 1985.

132. Gerberding JL, Hopewell PC, Kaminsky LS, Sande MA: Letter to the editor. Transmission
of hepatitis B without transmission of AIDS by accidental needlestick. (Letter) N Engl J
Med 312:56-57, 1985.

133. Sullam PM, Tauber MG, Hackbarth CJ, Sande MA: Therapeutic efficacy of teicoplanin in
experimental enterococcal endocarditis. Antimicrob Agents Chemother 27:135-136, 1985.

134. Sullam PM, Tauber MG, Hackbarth CJ, Sande MA: Antimicrobial activity of gentamicin in
experimental enterococcal endocarditis. Antimicrob Agents Chemother 27:224-26, 1985.

135. Sullam PM, Drake TA, Tauber MG, Hackbarth CJ, Sande MA: Influence of the
developmental state of valvular lesions on the antimicrobial activity of cefotaxime in
experimental enterococcal infections. Antimicrob Agents Chemother 27:320-23, 1985.

136. Tauber MG, Khayam-Bashi H, Sande MA: Effects of ampicillin and corticosteroids on
brain water content, cerebrospinal fluid pressure, and cerebrospinal fluid lactate levels in
experimental neumococcal meningitis. J Infect Dis 151:528-34, 1985.

137. Wilson WR, Zak O, Sande MA: Penicillin therapy for treatment of experimental
endocarditis caused by viridan streptococci in animals. J Infect Dis 151:1028-1033, 1985.

138. Morris DL, Chambers HF, Morris MG, Sande MA: Hemodynmic characteristics of patients
with hypothermia due to occult infection and other causes. Ann Intern Med 102:153-57,
1985.

139. Tauber MG, Sande MA: Pathogenesis of bacterial meningitis: contributions by
experimental models in rabbits. Infection 12(S1):S3, 1985.

140. Tauber MG, Hackbarth CJ, Scott KG, Rusnak MG, Sande MA. New cephalosporins
cefotaxime, cefpimizole, BMY 28142, and HR 810 in experimental pneumococcal
meningitis in rabbits. Antimicrob Agents Chemo 27:340-42, 1985.

141. Sullam PM, Drake TA, Sande MA: Pathogenesis of endocarditis. AM J Med 78 (Suppl
6B):1 10-15, 1985.

142. Hackbarth CJ, Chambers HF, Sande MA: Serum bactericidal activity of rifampin in
combination with other antimicrobial agents against Staphylococcus aureus. Antimicrob
Agents Chemother 29:61 1-13, 1986.

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143. Hackbarth CJ, Chambers HF, Sande MA: Serum bactericidal liter as a predictor of outcome
in endocarditis. Eur J Clin Microbiol 5:93-97, 1986.

144. Shibl AM, Hackbarth CJ, Sande MA: Evaluation of pefloxacin in experimental Escherichia
coli meningitis. Antimicrob Agents Chemother 20:409-41 1, 1986.

145. Small PM, Tauber MG, Hackbarth CJ, Sande MA: Influence of body temperature on
bacterial growth rates in experimental pneumococcal meningitis in rabbits. Infect Immun
52:484-87, 1986.

146. Chaisson RE, Ross J, Gerberding JL, Sande MA: Clinical aspects of adult epiglottitis.
West J Med 144:700-703, 1986.

147. Kapusnik JE, Sande MA: Novel approaches for the use of aminoglycosides: the value of
experimental models. J Antimicrob Chemother 17 (Suppl. A)7-10, 1986.

148. Kapusnik JE, Sande MA: Challenging conventional aminoglycoside dosing regimens. The
value of experimental models. Am J Med 80 (Suppl. 6B): 179-1 81, 1986.

149. Rinaldi, MG, Drutz DJ, Howell A, Sande MA, Wolfsy CB, Hadley WK: Serotypes of
Cryptococcus neoformans in patients with AIDS. Correspondence. J Infect Dis 153:642,
1986.

150. Carpenter TC, Hackbarth CJ, Chambers HF, Sande MA: Efficacy of ciprofloxacin for
experimental endocarditis caused by methicillin-susceptible or -resistant strains of
Staphylococcus aureus. Antimicrob Agents Chemother 30:382-84, 1986.

151. Gerberding JL, UCSF Task Force on AIDS: Recommended infection control policies for
patients with human immunodeficiency virus infection: an update. N Engl J Med
315:1562-1564, 1986.

152. Hackbarth CJ, Chambers HF, Stella F, Shibl AM, Sande MA: Ciprofloxacin in
experimental Pseudomonas aeruginosa meningitis in rabbits. J Antimicrob Chemother 1 8
(Suppl D):65-69, 1986.

153. Havlin DV, Witt MD, Sande MA: A 32-year-old man with the acquired immunodeficiency
synrome and pneumococcal meningitis. West J Med 146:618-19, 1987.

1 54. Gerberding JL, Bryant-LeBlanc CE, Nelson K. Moss AR, Osmond D, Chambers HF,
Carlson, JR, Drew WL, Levy JA, Sande MA: Risk of transmitting the human
immunodeficiency virus, cytomegalovirus, and hepatitis B virus to health care workers
exposed to patients with AIDS and AIDS-related conditions (ARC). J Infect Dis 156:1-8,
1987.

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155. Tauber MG, Shibl AM, Hackbarth CJ, Larrick JW, Sande MA: Antibiotic therapy,
endotoxin release into cerebrospinal fluid and brain edema in experimental E. coli
meningitis in rabbits. J Infect Dis 156:456-462, 1987.

156. Gordin FM, Rusnak MG, Sande MA: Evaluation of combination chemotherapy in a lightly
anesthetized animal model of psuedomonas pneumonia. Antimicrob Agents Chemother
31:398-403,1987.

157. Sande MA, Brooks-Fournier RA, Gerberding JL: Efficacy of ciprofloxacin in animal
models of infection: endocarditis, meningitis, and pneumonia. Am J Med 82 (Suppl 4A):
63-66, 1987.

158. Sande MA, Sande ER, Woolwine JD, Hackbarth CJ, Small PM: The influence of fever on
the development of experimental Streptococcus pneumoniae meningitis. J Infect Dis
156:849-850, 1987.

159. Tureen JH, Stella FB, Clyman RI, Mauray FE, Sande MA: The role of prostaglandins in
experimental meningitis in rabbits. J Pediatr Infect Dis 6:1 151, 1987.

160. Sande MA, Brooks-Fournier RA, Gerberding JL: Use of animal models in evaluation of the
quinolones. Rev Infect Dis lOO(Suppl): S113-S116, 1988.

161. Tauber MG, Borschberg U, Sande MA: Influence of granulocytes on brain edema,
intracranial pressure, and cerebrospinal fluid concentrations of lactate and protein in
experimental meningitis. J Infect Dis 157: 456-64, 1988.

162. Jacobson JE, Cello JP, Sande MA: Cholestasis and disseminated cytomegalovirus disease
in patients with the acquired immunodeficiency syndrome. Am J Med 84:218-224, 1988.

163. Kapusnik JE, Hackbarth CJ, Chambers HF, Carpenter T, Sande MA: Single, large, daily
dosing versus intermittent dosing of tobramycin for treating experimental pseudomonas
pneumonia. J Infect Dis 158:7-12, 1988.

164. Tauber MG, Kunz S, Zak O, Sande MA: Influence of antibiotic dose, dosing interval, and
duration of therapy on outcome in experimental pneumococcal meningitis in rabbits.
Antimicrob Agents Chemother 33:418-423, 1989.

165. Dworkin RJ, Tureen JG, Kennedy SL, Sachdeva M, Sande MA: Evaluation of FCE 22101
in experimental meningitis caused by Escherichia coli and Streptococcus pneumoniae. J
Antimicrob Chemother 23 (Suppl C):143-148, 1989.

M. Sande, MD
March 1997

325

166. Jacobson MA, Hahn SM, Gerberding JL, Lee BL, Sande MA: Ciprofloxacin for Salmonella
bacteremia in the acquired immunodeficiency syndrome (AIDS). Ann Intern Med
110:1028-1029,1989.

167. Wharton JM, Sande MA: Infective endocarditis: management and prophylaxis. Diagnosis
11:31-35, 1989.

168. Sande MA: A guide to empiric therapy for acute bacterial meningitis. Modem Medicine
57:100-111, 1989.

1 69. Bisno AL, Dismukes WE, Durack DT, Kapaan EL, Karchmer AW, Kaye D, Rahimtoola
SH, Sande MA, Sanford JP, Watanakunakom C, Wilson WR: Antimicrobial treatment of
infective endocarditis due to viridans streptococci, enterococci, and staphylococci. J Am
Med Assoc 261: 1471-1477, 1989.

170. Krumholz HM, Sande MA, Lo B: Community-acquired bacteremia in patients with
acquired immunodeficiency syndrome: clinical presentation, bacteriology, and outcome.
Am J Med 86:776-779, 1989.

171. Chuck SL, Sande MA: Infections with Cryptococcus neoformans in the acquired
immunodeficiency syndrome. N Engl J Med 321 : 794-799, 1989.

1 72. Dworkin RJ, Lee BL, Sande MA, Chambers HF: Treatment of right-sided Staphylococcus
aureus endocarditis in intravelous drug users with ciprofloxacin and rifampicin. Lancet
ii:1071-1073, 1989.

173. Lam YW, Kapusnik-Uner JE, Sachdeva M, Hackbarth C, Gambertoglio JG, Sande MA:
The pharmacokinetics of teicoplanin in varying degrees of renal function. Clin Pharmacol
Ther47(5):655-661,1990.

174. Cooke M, Sande MA: HFV epidemic and training in internal medicine - challenges and
recommendations. N Engl J Med 321 :1334-1338, 1990.

1 75. Tureen JH, Tauber MG, Sande MA: Loss of autoregulation of cerebral blood flow in brain.
J Clin Invest 85:577-581, 1990.

176. Dworkin R, Modin G, Kunz S, Rich R, Zak O, Sande M: Comparative efficacies of
ciprofloxacin, pefloxacin, and vancomycin in combination with rifampin in a rat model of
methicillin-resistant Staphylococcus aureus chronic osteomyelitis. Antimicrob Agents
Chemother 34:1014-1016, 1990.

M. Sande, MD
March 1997

326

177. Lam YWF, Kapusnik-Uner JE, Sachdeva M, Hackbarth C, Gambertolglio JG, Sande MA:
The pharmacokinetics of teicoplanin in varying degrees of renal function. Clin Pharmacol
Ther47(5):655-661, 1990.

178. Redd SC, Rutherford GW III, Sande MA, Lifson AR, Hadley WK, Facklam RR, Spika JA:
The role of human immunodeficiency virus infection in pneumococcal bacteremia in San
Francisco residents. J Infect Dis 162:1012-1017, 1990.

179. Jacobson MA, Hopewell PC, Yajko DM, Hadley WK, Lazarus E, Mohanty PK, Modin
GW, Feigel DW, Cusick PS, Sande MA: Natural history of disseminated Mycobacterium
avium-complex infection in AIDS. J Infect Dis 164:994-998, 1991.

180. Tureen JH, Tauber MG, Sande MA: Effect of indomethacin on pathophysiologic changes in
experimental meningitis in rabbits. J Infect Dis 163:647-649, 1991.

181. Lee BL, Padula AM, Kimbrough RC, Jones SR, Chaisson RE, Mills J, Sande MA:
Infections complications by respiratory pathogens associated with ciprofloxacin therapy.
(Letter) N Engl J Med 325:520-521, 1991.

182. Small PM, Schecter GF, Goodman PC, Sande MA, Chaisson RE, Hopewell PC: Treatment
of tuberculosis in patients with advanced human immunodeficiency virus infection. N Engl
J Med 324:289-294, 1991.

183: Tauber MG, Sande MA: Pharmacodynamics of antibiotics in experimental bacterial
meningitis - rapid bacterial killing in the cerebrospinal fluid. Scand J Infect Dis
74(Suppl): 173-1 78, 1991.

184. Sande MA and the AIDS Subcommittee of the IDSA: IDSA statement on healthcare
workers with HIV infection 1991. Clin Infect Dis 14:14, 1992.

185. Lee BL, Padula AM, Tauber MG, Chambers HF, Sande MA: Oral SCH39304 as primary,
salvage, and maintenance therapy for cryptococcal meningitis in the acquired
immunodeficiency syndrome. J AIDS 5:600-604, 1992.

186. Tureen JH, Tauber MG, Sande MA: Effect of hydration status on cerebral blood flow and
cerebrospinal fluid lactic acidosis in rabbits with experimental meningitis. J Clin Invest
89:947-953, 1992.

187. Wenzel RP, Andriole VT, Bartlett JG, Batt MD, Bullock WE, Cobbs CG, Light B, Martin
MA, Sanford J, Sande MA: Antiendotoxin monoclonal antibodies for gram-negative
sepsis: Guidelines from the IDSA. Clin Infect Dis 14:973-976, 1992; Reply. Clin Infect
Dis 15:371-372, 1992.

M. Sande, MD
March 1997

327

188. Sande MA, Whitley RJ, McCrancken GH Jr, Lentnek A, Scheld WM: Evaluation of new
anti-infective agents for the treatment of toxoplasma encephalitis. Clin Infect Dis 15(Suppl
l):S182-8, 1992.

189. Porter SB, Sande MA: Toxoplasmosis of the central nervous system in the acquired
immunodeficiency syndrome. N Engl J Med 327:1643-1648, 1992.

190. O'Reilly T, Kunz S, Sande ER, Zak O, Sande MA, Tauber MG: Relationship between
antibiotic concentrations in bone and therapeutic efficacy in staphylococcal osteomyelitis in
rats - azithromycin in comparison with rifampicin and clindamycin. Antimicrob Agents
Chemother 36:2693-2697, 1992.

191. Sullam PM, Sande MA: Role of platelets in endocarditis: Clues from von Willebrand
disease. (Editorial) J Lab Clin Med 120:507-509, 1992.

192. Drew R, Waskin H, Hyslop N, Lee BL, Sande MA, Saag M, Albrecht J, Gailis H: SCH
39304 versus ketoconazole for the treatment of oropharyngeal candidiasis in HIV-infected
patients. J Acquir Immune Defic Syndr 5(6): 600-4, 1992

193. Tauber MG, Sande E, Fournier MA, Tureen J, Sande MA: Fluid administration, brain
edema, and cerebrospinal fluid lactate and glucose concentrations in experimental
Escherichia coli meningitis. J Infect Dis 1 168:473-476, 1993.

194. Komaromy M, Bindman AB, Haber RJ, Sande MA: Sexual harassment in medical training.
N Engl J Med 328:322-326, 1993.

195. Sande MA, Carpenter Ccj, Cobbs, CG, Holmes KK, and Sanford JP for the NIAID State-
of-the-Art Panel on Anti-Retroviral Therapy for Adult HIV-infected Patients: Antiretroviral
therapy for adult HIV-infected patients: recommendations from a state-of-the-art
conference. J Am Med Assoc 270 (21):2583-2589, 1993.

196. Safrin S, Lee BL, Sande MA: Adjunctive folinic acid with trimethoprimsulfamethoxazole
for Pneumocystis carinii pneumonic in AIDS patients is associated with an increased risk of
therapeutic failure and death. J Infect Dis 170:912-7, 1994.

197. Peiperl L, Sande MA: Tuberculosis and human immunodeficiency virus disease. West J
Med 160:252-253, 1994.

198. Gilbert DN, Lawton SE, Loeb L, Goldstein EJC, Sanford JP, Mandell GL, Sande MA:
Report to the IDSA from the Task Force on Health Care Reform. Clin Infect Dis, 19(2):
372-5, 1994.

M. Sande, MD
March 1997

328

199. Hambleton J, Aragon T, Modin G, Northfelt D, Sande MA: Outcome of febrile neutropenia
in hospitalized patients infected with the human immunodeficiency virus. Clinical Inf Dis
20:363-71, 1995.

200. Chambers HF III, Kartalija M, Sande MA: Ampicillin, sulbactam and rifampin combination
therapy of experimental methicillin-resistant Staphylococcus aureus endocarditis in rabbits.
J Inf Dis 171:897-902, 1995.

201. Hellmann NS, Nsubuga PS, Baingana-Baingi DJ, Desmond-Hellermlann SD, Mbidde EW,
Granowitz CB, Sande MA: Single-dose Ampicillin/Sulbactam versus Ceftriaxone as
Treatment for Uncomplicated Gonorrhea in a Ugandan STD Clinic Population with a High
Prevalence of PPNG Infection. Journal of Tropical Medicine 98:95- 100, 1995.

202. Gurley J, Lum N, Sande MA, Lo B, Katz M: Patients Found Down in Their Homes. N
Engl J Med 334:1710-1716, 1996.

203. Kartalija M, Kaye K, Tureen J, Qingxiang L, Tauber MG, Elliott BR, Sande MA:
Treatment of experimental cryptococcal meningitis with fluconazole-impact of dose and
addition of flucytosine on mycologic and pathophysiologic outcome. J Infect Dis, 173(5):
1216-21, 1996.

204. Scheuner J, Mladenovic J, Gardner L, Clayton C, Sande M: Developing Strategies for the
Future of Academic Public Hospitals. AJM, 101(5): 449-454, 1996.

205. Neighbor ML, Cohen PT, Siegel D, Newman M, Larkin H, Hadley WK, Yajko DM, Feigal
DW Jr, Sande MA: Ciprofloxacin in the treatment of acute infectious diarrhea. (Submitted
1997)

206. Nathan C, Kabins SA, Sande MA, Costerton JW, Weinstein RA: Induction of serum
resistance in Pseudomonas aeroginosa by "Ts and Blues" (pentazocine and tripelennamine).
(Submitted 1997)

207. Lee BL, Flaherty D, Strauss L, Schachter J, Mills J, Hadley D, Sande MA: Etiology of
pharyngitis in adults. (Submitted 1997)

208. Grant RM, Baingana G, LeBlond RF, Katongole-Mbidde E, Baingana B, Lee B, Gannnoum
MA, Sande MA: Comparison of oral fluconazole 400mg/d versus 800mg/d for intital
therapy of cryptococcal meningitis in HFV-infected patients. (Submitted 1997)

M. Sande, MD
March 1997

329 ^v APPENDIX E

October 10, 1984

DECLARATION OF MERLE SANDE, M.D.

I, Merle Sande, M.D., do hereby make the following
declaration in support of the Application for a Temporary
Restraining Order and Order to Show Cause Re: Preliminary
Injunction.

1. I attended the University of Washington School of
Medicine, and received my M.D. from that institution in 1965.
From 1965 to 1969, I did my internship and residency at New York
Hospital in New York, New York. From 1969 to 1971, I was a
Clinical Instructor in Medicine at the University of Texas
Medical School in San Antonio and was a Captain in the United
States Air Force, based at Lackland Air Force Base. I spent the
next eight years teaching courses at the University of Virginia
in the field of infectious diseases. I am board certified in the
fields of Infectious Diseases and Internal Medicine, and have
worked in these fields for fifteen years. I have published
approximately 200 professional papers, edited three textbooks,
and served on numerous national boards and as a national
consultant in infectious diseases. A copy of my curriculum yitae
is attached hereto as Exhibit 1 and is incorporated herein by
reference as though fully set forth.

2. At present, I am a Professor of Medicine and Vice
Chairman of the Department of Medicine at the University of
California at San Francisco ("UCSF"). I am also Chief of Medical
Services at San Francisco General Hospital ("SFGH"). I have helc

26ij those positions since 1980.

330

1 3. As Chief of Medical Services at SFGH, I am

2 responsible for the care of all patients who come to that

3 facility and have under my direct supervision approximately fift]

4 full-time faculty members, one hundred house staff/ and thirty

5 post graduate fellows in various medical specialties. In

6 addition to doing research on numerous bacterial infections, I

7 have also been directly involved in the care of patients with

8 viral and bacterial infections. I have also been involved with

9 epidemics of menigicocccal meningitus, microplasma pnuemonia, an*

10 influenza.

11 4.1 have been extensively involved with AIDS, defined

12 herein to refer to patients meeting the criteria of the Center

13 for Disease Control ("CDC") in Atlanta (which includes the

14 presence of diseases considered diagnostic of an underlying

15 immunity deficiency such as Kaposi's Sarcoma, central nervous

16 system lymphoma, or infections such as pneumocystis pneumonia)
I saw my first case of AIDS in the spring of 1982. Since that

18 time, I have been directly involved in strategies for caring for

19 AIDS patients, developing infectious control measures, and

20 administering research and patient care funds.

21 The AIDS ward at SFGH is under my direction, along with

22 Drs. Volberding and Wolfsey. I direct the house staff in the

23 care of AIDS patients, and am currently involved in numerous

24 studies on the various expressions of the disease and its

25 diagnostic and therapeutic oddities. I personally have seen an

22
23
24
25

331

participated in the care of approximately 100 AIDS patients at

SFGH.

As Chairman of UCSF's AIDS task force, I have been
intensively involved in infection control measures dealing with
this patient population. Our decisions regarding infectious
control were published in September, 1983 in the New England
Journal of Medicine and have been adapted worldwide. I am
currently aiding in studies at SFGH dealing with the risk of AIDS
to health care workers. An additional assignment has been my
appointment as Chairman of a UCSF task force whose responsibility
is to dispense approximately 3 and a half million dollars of
state-directed funds for AIDS research to schools related to the
Univerity of California. I have also lectured widely in the
United States and Europe on the field of AIDS and next week am
running a symposium in Washington, D.C. with the four most
prominent experts in the field.

5. AIDS is a disease that is characterized by the
elimination and destruction of T-cells, which are responsible for
the cellular immune response through which the body responds to
malignancies and various pathogens. Destruction of these cells
leads to severe immunological impairment, which results in the
development of various malignancies and incredibly severe
opportunistic infections. An antibody directed against a
retrovirus known as HTLVIII, or LAV, has been identified and is
present in the majority of patients with AIDS. This virus is
labile and easily killed by physical means, such as soap and heat

332

To ray mind, the most amazing aspect of this disease has
been the fact that it has remained within certain high-risk
groups, namely: homosexual males, intravenous drug abusers,
individuals who have received blood or blood products, persons
who have had direct contact with equatorial Africa or Haiti,
sexual partners of any of the other high-risk groups and,
finally, offspring of patients with AIDS. All evidence suggests
that it is very difficult to transmit this virus from person to
person unless there is direct sexual contact or an exchange of
blood products. This view is supported by the fact that, to
date, not a single health care worker or person directly involve
in the care of AIDS patients and who is not a member of one of
the high-risk groups noted above has developed the disease.
Early studies also indicate that these health care workers do no
have antibody to the virus.

We have evidence that the virus may have sprung out of
equatorial Africa and has been there for a period of time. In mj
opinion, the reason that the disease did not spread rapidly at
that time and place is because there was no "multiplier." It no
appears clear that promiscuous homosexual sex in the United
States has been the key multiplier, in addition to the exchangin
of needles in the intravenous drug-abusing population.

6. Data showing that the AIDS disease has spread widely
in the gay community have come from a number of different
cities. The most impressive data comes from San Francisco, wher
the CDC and San Francisco Public Health Department co-sponsored

333

•

program beginning in 1978 and aimed at determining the natural
history and protectiveness of the hepatitis B vaccine. They
originally enlisted approximately 6,800 predominantly gay males,
from which they recently selected 770 for further study. Blood
sera obtained from these individuals in 1978 and retrospectively
tested for antibody to the AIDS virus shows that between 1978 and
1980, less than 6 percent were positive for the AIDS virus. By
1984, using a test that does not pick up all the positives, the
percentage had increased to 65 percent. The actual percentage is
more likely in the 70-80 percent range. Whether the data from
this representative patient population can be extrapolated into
the rest of San Francisco's gay population is unknown, but the
data certainly indicates that a large number of the gay
population in fact has come into contact with the AIDS virus.

Testing of control groups of females and heterosexual males
has shown that the incidence of positive antibody tests is less
than 1 percent. This includes studies performed both at the CDC
and on blood donors. Recent studies done at UCSF by Dr. Jay Levy
supports the initial observation that antibodies to this
retrovirus are essentially absent from the straight population
and non high-risk groups. It is also of interest that studies in
New York City show that the antibody prevalence to this AIDS
agent in intravenous drug abusers approaches 60 to 80 percent.

7. As I have previously indicated, transmission of the
virus appears to be quite difficult, if not impossible, by casual
contact and to the best of our knowledge is transmitted through

334

the exchange of infected body secretions. The best bet at the
present time is that the virus is found in high concentrations i
semen and that the exchange of semen between individuals
represents the most likely and most important mode of
transmission. There is also strong data suggesting that the
exchange of infected blood from one individual to another is alsc
an important mode of transmission. But of equal interest is the
fact that, to date, patients who have received accidental needle
sticks from patients with AIDS have not developed the antibody

10 and therefore have not been infected by that mode. All this dat;

11 suggests that it takes a fairly intensive exposure that may be

12 related to dose of either semen or blood products. The virus ha

13 also been shown to have been transmitted in utero from infected
mothers to their offspring. However, other children in the

15 family have not become infected, so it appears that close contac

16 between mother and child is not now associated with transmission

17 8 . In San Francisco, the disease has been found almost

18 exclusively in the gay community. The most common mode of

19 transmission is most likely due to rectal intercourse. We canno

20 say that it is not transmitted through oral intercourse, but

21 believe that the likelihood of the disease being spread by

22 kissing is unlikely. The data strongly suggests that the number

23 of different sexual contacts is a dominant risk factor in the
spread of this disease and undoubtedly represents the

25| "multiplier" that was required to initiate the epidemic.

26i However, there is also data suggesting that vaginal intercourse

335

may also transmit the disease in that there have been female
sexual partners of bisexual males who have acquired the disease.
Also, in equatorial Africa, female prostitution is apparently one
of the leading risk factors. Still unclear is whether the
transmission of the virus requires a break in the mucosal
barriers of the mouth or the rectum in order to transmit the
disease. However, it is likely that the spread would be
facilitated by traumatic sexual practices that lead to bleeding,
such as "fisting" or other traumatic anal intercourse.

9. The aspect of the AIDS epidemic that has most
affected me personally has been the impact of the disease on San
Francisco General Hospital. At present, the disease is doubling
every eight months, and all evidence suggests that it will
continue along these lines indefinitely. About a year ago, our
AIDS ward opened at SFGH with twelve beds, which was ample to
handle the patient load at the time. Yesterday we had
twenty-eight patients in the hospital. At this rate, if measures
are not taken to distribute this patient population, a year from
now we will have nearly 100 patients in the hospital and would
have reached the point where our current services and facilities
would be overloaded. Within the next three years, San Francisco
will be facing an incredibly severe problem *.hat will become
increasingly obvious in terms of caring for this patient
population. The City will also incur an enormous financial loss
because, at current rates, each patient's care will cost
approximately $100,000 from initial diagnosis to death. If, as

8
9

10
11

201

22!

23!

336

we suspect, a high percentage of the gay community is already
infected with the AIDS virus and if this equates itself with
significant disease, we can expect to have as many as 20,000 or
30,000 patients in the City before the epidemic reaches its
peak. The impact on the San Francisco General Hospital is such
that we can predict that within several months to a year, we wil
be unable to fulfill our mission and commitment to the City's
non-AIDS population.

10. i have been asked, as an expert in the field, what
would recommend as a strategy for the prevention of AIDS. My
response is that since it is unlikely the disease would be sprea
in a community that was not heavily involved in multiple sexual
encounters, the best strategy would be to find some way to stop
the sexual practices that transmit the disease. Thus, to the
extent education would be effective in reducing this behavior,
the expected end result would be a reduction in the spread of t
disease. Another approach would be to eliminate places or
establishments where these sexual practices are facilitated --
where the ease of having anonymous sex and finding multiple
sexual partners is increased. Therefore, it has been my feeling
for the past year and a half that a positive move by the San
Francisco Department of Public Health Department along these

lines would have a significant impact and effect on the spread
AIDS.
25! / / /

26] / / /

•i

337

In my judgment, the data currently available allows us to
state categorically that the anonymous and multiple sexual
encounters encouraged, fostered, facilitated and promoted by
bathhouses, sex clubs, and similar facilities in San Francisco
has a strong and dramatic effect on the spread of AIDS. I
therefore believe it is the obligation of the San Francisco
Department of Public Health to make a strong and definite
statement regarding the control of this behavior and to close any
facilities under its jurisdiction where such activities are being
carried out. Physicians and public health officials have a
special responsibility to examine the data and make a strong
statement regarding this serious epidemic.

I declare under penalty of perjury under the laws of the
State of California that the foregoing is true and correct.

Executed on October (& , 1984, at San Francisco,
California .

MERLE SANDE, M.D.

3384D

338 APPENDIX F

CURRICULUM VITAE
Revised - 9/1/96

NAME: John L. Ziegler, M.D.

DATE & PLACE OF BIRTH: October 28, 1 938, New York, New York

MARITAL STATUS: Married

EDUCATION:

1 956-60 Amherst College, Amherst, MA, BA (English)

1960-64 Cornell University Medical College, New York, NY, MD

EMPLOYMENT AND APPOINTMENTS:

1 964-66 Intern and Assistant Resident, Second (Cornell) Medical Division, Bellevue

Hospital, New York, NY (Fellow, Department of Medicine, Cornell University

Medical College)

1 966-67 Clinical Associate, Medicine Branch, National Cancer Institute, and Admitting

Officer, National Cancer Institute

1967-72 Director, Uganda Cancer Institute, Makerere University Medical School, Kampala,

Uganda; Senior Investigator, Medicine Branch, National Cancer Institute

1 972-75 Chief, Pediatric Oncology Branch, Division of Cancer Treatment, National Cancer

Institute

1 975-80 Deputy Clinical Director, National Cancer Institute and Associate Director, Clinical

Oncology Program, Division of Cancer Treatment, National Cancer Institute

1 980-81 Editor-in-Chief, Journal of the National Cancer Institute, National Cancer Institute

1981-96 Associate Chief of Staff for Education and Staff Physician, Veterans Affairs

Medical Center, San Francisco, California; Professor of Medicine in Residence,
School of Medicine, University of California, San Francisco

1994-96 Senior Scientist (on detail from Department of Veterans Affairs), International

Agency for Research on Cancer, World Health Organization, Lyon, France. On
special assignment to Makerere University, Kampala, Uganda.

CERTIFICATION:

Diplomate, American Board of Medical Examiners (June 1964)

Qualified, American Board of Internal Medicine (October 1970)

Diplomate in Internal Medicine (October 1973)

Diplomate in the Subspecialty of Oncology, American Board of Internal Medicine (October 1 973)

License to practice medicine (New York State, Washington, D.C.)

Certificate, Intensive Course on Epidemiology and Statistics, London School of Hygiene and

Tropical Medicine (June 1993)

Candidate, M.Sc. Epidemiology, London School of Hygiene and Tropical Medicine (Sept. 1997)

PROFESSIONAL SOCIETIES:
American Association for Cancer Research 1968-81
American Federation of Clinical Research 1972-92
American Society of Clinical Investigation 1973-
American Society of Clinical Oncology 1968-
American Society of Hematology 1968-81
Association of Physicians of East Africa 1967-72
Association of Surgeons of East Africa (Honorary) 1967-72

339

Uganda Medical Association 1967-72
Council of Biology Editors 1980-81
Western Association of Physicians 1 983-
Westem Society for Clinical Investigation 1983-

MEMBERSHIP (selected activities):

American Cancer Society's Scientific Advisory Committee for Clinical Investigations (Immunology

and Immunotherapy) 1974-77; (Chemotherapy) 1982-85, Chairman
Immunotherapy Committee, Tumor Immunology, National Cancer Institute 1973-75
Medical Board, Clinical Center. National Institutes of Health 1975-80
Clinical Research Committee, National Cancer Institute (Chairman) 1975-80
American Joint Committee for Cancer Staging and End Results Reporting 1976-80
Consultant, SEER Program, Division of Cancer Cause and Prevention, NC1 1977-79
Editorial Board, Cancer Chemotherapy Reports, 1975-78
Consultant, National Bladder Cancer Task Force 1 978-80
Scientific Advisor, NCI Bladder Cancer Project, Cairo, Egypt 1973-79
Consultant, Institute of Medicine, National Academy of Sciences (Workshop on Research in

Developing Countries) 1979
Admissions Committee, Uniformed Services University for the Health Sciences, Appointment by

Surgeon General, USPHS 1980-81

Executive Committee, Northern California Oncology Group 1982-84
Corresponding Editor, West African Journal of Medicine 1986-
Member, Chief Medical Director's Steering Committee on AIDS, Veterans Administration Central

Office 1987-89

Consultant, World Health Organization 1986, 1987, 1988
Trustee (appointed by the President, University of California), Marin Community Foundation

1988-90

Member, National Task Force for the NIH Strategic Plan (Population-based Studies) July, 1992
Chairman, Steering Committee, Pilot Evaluation of AIDS Retrovir Treatment in Africa (WHO,

Family Health International, Burroughs Wellcome Co.) 1992-93

ACADEMIC APPOINTMENTS:

1967-72 Honorary Lecturer in Medicine, Makerere University Medical School, and

Honorary Senior Registrar, Mulago Hospital, Kampala, Uganda; Lecturer in

Surgery, Harvard College; Clinical Associate Professor, Cornell University

Medical College
1 976-78 Associate Clinical Professor of Medicine, George Washington University Medical

School
1979-81 Associate Clinical Professor of Medicine, Georgetown University School of

Medicine

1980-81 Professor of Medicine, Uniformed Services University of the Health Sciences

1 990-91 Visiting Fulbright Professor of Medicine, Makerere University Medical School,

Kampala, Uganda (on Sabbatical leave from UCSF)

1992-93 Visiting Professor, University of Cambridge and Associate, Darwin College

1992-96 Visiting Professor, London School of Hygiene and Tropical Medicine

1994-96 Visiting Fulbright Professor of Medicine, Makerere University Medical School,

Kampala, Uganda
1995-96 Visitor Oxford University

MILITARY SERVICE:

1966-81 Medical Director, U.S. Public Health Service

340

AWARDS:

United States Public Health Service Commendation Medal, July 1 969

Albert and Mary Lasker Award, November 1972

Heath Award, M.D. Anderson Hospital, November 1983

Fulbright Research Scholar, Makerere University, Kampala, Uganda, 1990-91

Howard Gilman Foundation Honors Program Lecturer, New York University, 1991

Fulbright Research Scholar, Makerere University, Kampala, Uganda, 1994-95

RESEARCH ACTIVITY AT UCSF AND VA:

1 981 -82 Principal Investigator for a $50,000 grant awarded from American Cancer Society

to establish Kaposi's sarcoma clinic at UCSF (with Drs. Conant and Volberding)

1983-86 Co-Principal Investigator (with Dr. P. Volberding): Cooperative Agreement on

Laboratory and Clinical Studies of AIDS (NCI, $1.4 million)

1983-85 Co-Principal Investigator (with Dr. H. Lichtenstein): National Institute of Aging

Academic Award ($78,000, terminal year) to establish geriatric teaching program
at VA Medical Center

1985-92 Director, AIDS Clinical Research Center, University of California San Francisco

(State funded, $1.1 million annually)

1986-89 Co-Principal Investigator (with Prof. L. Zegans): AIDS Professional Education

Program (NIMH contract, $400,000)

1987-92 Co-Principal Investigator (with Dr. Volberding): Program Project Grant on

Laboratory and Clinical Studies in AIDS (NIAID, $3.66 million for 5 years)

1987-92 Associate Investigator (Dr. Susan Allen, PI): African AIDS: Risk Factors, Virology

and Pathology (NIAID, $1.5 million for 5 years)

1987-92 Co-Principal Investigator (with Dr. P. Jensen): VA Cooperative Study (298) on

Zidovudine in Patients with ARC (Veterans Administration $510,993 for 3 years)

1988-93 Associate Investigator (Dr. Elizabeth Holly, PI): Epidemiology of Non-Hodgkin's

Lymphoma and Retroviruses (NCI, $4.3 million for 5 years)

1 988-94 Associate Investigator, Center for AIDS Prevention Studies, (Dr. Stephen Hulley,

PI): International Training Program in AIDS Epidemiology (NIMH/NIDA, $10
million for 5 years)

1988-93 Director, VA Center for AIDS Research and Education and Director, AIDS Clinical

Unit (Veterans Administration, $1.5 million for 5 years)

1988-90 Chairman, 6th International Conference on AIDS, San Francisco, June 20-24,

1 988-93 Co-Principal Investigator with Dr. P. Volberding, UCSF Center for AIDS Research

(NIAID, $4.1 million for 5 years)

1988-93 Associate Investigator Case-Control Partner Study on HIV Transmission in

Uganda (Rockefeller Foundation, $330,000)

1 989-90 Chairman, Scientific Advisory Committee, Substance Abuse Treatment Research

Unit (NIDA, $8.7 million for 5 years)

341

1990-91 Visiting Fulbright Professor, Makerere University Medical School, Ministry of

Health, Kampala, Uganda

1992-93 Consultant, Family Health International. AIDS Treatment Initiative in Developing

Countries.

1994-95
1994-96

TEACHING:

Visiting Fulbright Professor, Makerere University Medical School, Ministry of
Health, Kampala, Uganda

Senior Scientist, International Agency for Research on Cancer, WHO. Principal
Investigator, "Case-Control Study of Kaposi's Sarcoma in Uganda." CDC-VAMC
Interagency Research Agreement ($530,000).

Oncology Attending, VA Medical Center, 3 months/year

Oncology Attending, Moffitt Hospital, 1 month/year

Medicine Attending, VAMC, 1 month/year

Introduction to Clinical Medicine Preceptor, VAMC, 2 months/year

Problem Solving Course for First Year Students, 2 months/year

Director, Postgraduate Program in Medicine (M. Med. Degree), Dept. of

Medicine, Makerere University Medical School, Kampala, Uganda, 1990-91

Visiting Professor, London School of Hygiene and Tropical Medicine (Taught in

DTM&H Course, and advised M.Sc. students) 1992-94
Visiting Professor, University of Cambridge, School of medicine, Addenbrooks

Hospital, Cambridge, U.K. (Taught introduction to Clinical Medicine)

1992-93
Faculty Advisor, M.Med Program, Makerere University Medical School,

Kampala, Uganda, 1994-96

COMMITTEES:

UCSF University Governance (summary, 1981-91): Committee on Education, (Academic Senate),
Curriculum Committee, Subcommittee on Evaluation, Residency Review Committee, Research
Evaluation and Allocation Committee, Advisory Committee on Postdoctoral Affairs, Education
Policy Committee, Universitywide Committee in Geriatrics, Editorial Board of UCSF Magazine,
Dean's AIDS Advisory Committee (ex officio), Chancellor's Advisory Council on AIDS, member,
UCSF Comprehensive Cancer Center, member, Cancer Research Institute

Veterans Administration Medical Center: Clinical Education Committee (Chair), Learning
Resources Advisory Committee (Chair), Medical Executive Board, AIDS Coordinating Committee,
Dean's Committee, Clinical Advisory Committee

BIBLIOGRAPHY:

BURKITTS LYMPHOMA/Original Work

1. Ziegler, JL and Miller, DG: Lymphosarcoma resembling the Burkitt tumor in a Connecticut
girl. JAMA 198:1071-1073, 1966.

2. Ziegler, JL, Cohen, MH, Vogel, CL, Sheagren, JN and Carbone, PP: Immunologic studies
in American patients with Burkitt-like lymphoma. Cancer Res 26:2527-2531. 1967.

342

3. Ziegler, JL, Carbone, PP, Berard, CW and Thomas, LB: Burkitt's tumor in the United
States: Diagnosis, treatment and prognosis. In Clifford, Linsell and Timms (eds.): Cancer in
Africa, East Africa Publishing House, Nairobi, 1968, pp. 239-251.

4. Carbone, PP, Berard, CW, Bennett, JM, Ziegler, JL, Cohen, MH and Gerber, P: Burkitt's
tumor: Combined clinical staff conference at the National Institutes of Health. Ann Int Med 70:817-
832, 1969.

5. Cohen, JMH, Bennet, JM. Berard, CW, Ziegler, JL, Vogel, CL, Sheagren, JN and
Carbone, PP: Burkitt's tumor in the United States. Cancer 23:1 259-1 272, 1969.

6. Cohen, MH, Ziegler, JL and Carbone, PP: Burkitt's tumor in the United States. The
Cancer Bulletin 20:68-74, 1969

7. Henle, G, Henle, W, Clifford, P, Diehl, V, Kafuko, GW. Kirya, BG, Klien, G, Morrow, RH,
Manube, GMR, Pike, P, Tukei, P and Ziegler, JL: Antibodies to EB virus in Burkitt's lymphoma and
control groups. J Nat Cancer Inst 43:1147-1157, 1969.

8. Brown, CH, Ziegler, JL, Templeton, C and Carbone, PP: Cyclophosphamide toxicity in
Ugandan and American patients with lymphoma. Cancer 26:462-467, 1970.

9. Pass, L, Ziegler, JL, Herberman, RB, and Morrow, RH: Evaluation of the effect of
remission plasma on untreated patients with Burkitt's lymphoma. J Nat Cancer Inst 44:145-149,
1970.

10. Pass, L, Herberman, RB, Ziegler, JL: Delayed cutaneous hypersensitivity to autologous
extracts of Burkitt's lymphoma cells. New Eng J Med 282:776-780, 1970.

1 1 . Ziegler, JL, Cohen, MH, Morrow, RH, Kyalwazi, SK and Carbone, .PP: Immunologic
studies in Burkitt's lymphoma. Cancer 25:734-739, 1970.

12. Ziegler, JL, Morrow, RH, Bluming, AZ, Pass, L, Templeton, AC, Templeton, C and
Kyalwazi, SK: Clinical features and treatment of childhood lymphoma in Uganda. Int J Cancer
5:415-425, 1970.

13. Ziegler, JL, Morrow, RH, Pass, L, Kyalwazi, SK, Carbone, PP: Treatment of Burkitt's
lymphoma with Cyclophosphamide. Cancer 26:474-484, 1970.

14. Ziegler, JL, Bluming, AZ, Morrow, RH, Pass, L and Carbone, PP: Central nervous system
involvement in Burkitt's lymphoma. Blood 36:718-728, 1970.

15. Ziegler, JL, Morrow, RH, Kyalwazi, SK and Carbone, PP: Treatment of Burkitt's lymphoma
with Cyclophosphamide, In Dutcher (ed.): Comparative Leukemia Research, S Karger, Basel, pp.
701-705, 1970.

16. Morrow, RH, Pike, MC, Smith, PG, Ziegler, JL and Kisuule, A: Burkitt's lymphoma: A time-
space cluster of cases in Bwanba County of Uganda. Brit Med J 2:491, 1971.

17. Bluming, AZ. Ziegler, JL, Pass, L and Herberman, RB: Delayed cutaneous sensitivity
reactions of autologous Burkitt's lymphoma protein extracts. Clin Exp Immunol 9:713-719. 1971.

18. Ziegler, JL and Bluming, AZ: Intrathecal chemotherapy in Burkitt's lymphoma. Brit Med J
3:508-512,1971.

19. Ziegler, JL, Wright, DH and Kyalwazi, SK: The differential diagnosis of Burkitt's lymphoma
of the face and jaws. Cancer 27:503-51 4, 1971.

343

20. Henle, G, Henle, W. Klein, G, Gunven, P, Clifford, P. Morrow, RH and Ziegler, JL:
Antibodies to early EBV-induced antigens in Burkitt's lymphoma. J Nat Cancer Inst 46:861-871 ,
1971.

21. Henle, G, Henle, W, Clifford, P, Diehl. V, Kafuko, GW, Kirya, BG, Klein, G, Morrow, RH,
Manube, GMR, Pike, P, Tukei, PM and Ziegler, JL: Antibodies to Epstein-Barr virus in Burkitt's
lymphoma and control groups. J Nat Cancer Inst 43:1147-57, 1969.

22. Carbone, PP, Ziegler, JL, Morrow, RH, Kyalwazi, SK, Brown. CH, DeVrta, VT and Berard,
CW: Burkitt's tumor. A comparative study in Africa and the United States. In Ultmann, et al. (eds.):
Current Concepts in the Management of leukemia and Lymphoma, Springer-Verlag, New York,
pp. 126-136, 1971.

23. Ziegler, JL, Bluming, AZ, Pass, L and Morrow RH: Relapse patterns in Burkitt's
lymphoma. Cancer Res 32:1267-1272, 1972.

24. Ziegler, JL, Bluming, AZ, Morrow, RH, Cohen, MH, Fife, EH, Finerty, JR and Woods, R:
Burkitt's lymphoma and malaria. Trans Roy SocTrop Med Hyg 66:286-291, 1972.

25. Iverson, U, Iverson, OH, Bluming, AZ, Ziegler, JL and Kyalwazi, SK: Cell kinetics of
African cases of Burkitt's lymphoma: A preliminary report. Europ J Cancer 8:305-308, 1972.

26. Bluming, AZ, Ziegler, JL and Carbone, PP: Bone marrow involvement in Burkitt's
lymphoma: Results of a prospective study. Brit J Hemat 22:369-376, 1972.

27. Ziegler, JL, Bluming, AZ, Magrath, IT and Carbone, PP: Intensive chemotherapy in
patients with generalized Burkitt's lymphoma. Int J Cancer 10:254-263, 1972.

28. Ziegler, JL: Chemotherapy of Burkitt's lymphoma. Cancer 30:1534-1540, 1972.

29. Ziegler, JL and Magrath, IT: BCG immunotherapy in Burkitt's lymphoma: Preliminary
results of a randomized clinical trial. J Nat Cancer Inst Monogr 39:199-202, 1974.

30. Kufe, D, Magrath, IT, Ziegler, JL and Speigelman, S: Burkitt's tumors contain particles
encapsulating RNA-instructed DNA polymerase and high molecular weight virus-related RNA.
Proc Nat Acad Sci 70:734-741 , 1973.

31. Iversen, O, Iverson, U, Ziegler, JL and Bluming, AZ: Cell kinetics in Burkitt's lymphoma.
Europ J Cancer 10:155-163, 1974.

32. Magrath, IT, Ziegler, JL and Templeton, AC: A comparison of clinical and histological
features of childhood malignant lymphoma in Uganda. Cancer 33:285-294, 1974.

33. Bodmer, JG, Bodmer, WF, Ziegler, JL and Magrath, IT: HL-A and Burkitt's tumor. A study
in Uganda. Tissue Antigens 5:59-62, 1 975.

34. Richman, SD, Appelbaum, F, Levenson, SM, Johnston, GS and Ziegler, JL: Ga
scintigraphy in Burkitt's lymphoma. Radiology 117:639-645, 1975.

35. Magrath, IT and Ziegler, JL: Failure of BCG immunotherapy in Burkitt's lymphoma. Brit
Med J 1:615-618, 1976.

36. Andersson, M, Klein, G, Ziegler, JL and Henle, W: Association of Epstein-Barr viral
genomes with American Burkitt's lymphoma. Nature 260:357-359, 1976.

344

37. Ziegler, JL, Magrath, IT, Mkrumah, F, Perkins, IV and Simon, RS: Evaluation of CCNU
used for the prevention of CNS involvement in Burkitt's lymphoma. Cancer Chemother Rep
59:115-156, 1975.

38. Ziegler, JL, Magrath, IT and Bluming, AZ: Management of Burkitt's lymphoma involving
the central nervous system. Afr J Med Sci 5:121-124, 1976.

39. Ziegler, JL: Spontaneous remission in Burkitt's lymphoma. J Nat Cancer Inst Monograph
44:61-65, 1976.

40. Ziegler, JL, DeVita, VT, Graw, RG, Herzig, G, Leventhal, BG, Levine, AS and Pomeroy, T:
Combined modality therapy of American Burkitt's lymphoma. Cancer 38:2225-2231, 1976.

41 . Ziegler, JL, Andersson, M, Klein, G, and Henle, W: Detection of Epstein-Barr virus DMA in
American Burkitt's lymphoma. Int J Cancer 38:2225-2231 , 1976.

42. Bender, RA, Bleyer, WA, Drake, JC, and Ziegler, JL: In vitro correlates of clinical
response to methotrexate in acute leukemia and Burkitt's lymphoma. Brit J Cancer 34:484-492,
1976.

43. Mann, RG, Jaffe, ES, Brayland, RC, Nanba, K, Frank, MM, Ziegler, JL and Berard, C:
Non-endemic Burkitt's lymphoma is a B-cell tumor related to germinal centers. New Eng J Med
295:685-691, 1976.

44. Ziegler, JL: Treatment results in 54 American patients with Burkitt's lymphoma are similar
to the African experience. New Eng J Med 297:75-80, 1977.

45. Gunven, P, Klein, G, Ziegler, JL, Magrath, IT, Olweny, CL, Henle, W, Henle, G, Svedmyr,
A and Demisse, A: Epstein-Barr virus (EBV) associated and other anti-viral antibodies during
intense BCG administration to Burkitt's lymphoma patients in remission. J Nat Cancer Inst 60:31-
37, 1978.

46. Appelbaum, FR, Deisseroth, AB, Graw, RG, Jr, Herzig, GP, Levine, AS, Magrath, IT,
Pizzo, PA, Poplack, DG and Ziegler, JL: Prolonged complete remission following high dose
chemotherapy of Burkitt's lymphoma in relapse. Cancer 41:1059-1063, 1978.

47. Appelbaum, FR, Herzig, GP, Ziegler, JL, Levine, AS, Graw, RG and Deisseroth, AB:
Successful engraftment of cryopreserved autologous bone marrow in patients with malignant
lymphoma. Blood 52:85-95, 1978.

48. Ziegler, JL, Magrath, IT, Deisseroth, AB, Glaubiger, DD, Kent, HC, Pizzo, PA, Poplack,
DG, and Levine, AS: Combined modality treatment of Burkitt's lymphoma. Cancer Treatment Rept
62:2031-2034,1978.

49. Dunnick, NR, Reaman, GH, Head, GL, Shawker, TH and Ziegler, JL: Radiographic
manifestations of Burkitt's lymphoma in American Patients. Am J Radiol 132:1-6, 1979.

50. Ziegler, JL, Magrath, IT and Olweny, CLM: Cure of Burkitt's lymphoma. Lancet 2:936-938,
1979.

51. Magrath, I, Lee, YJ, Anderson, T, Henle, W, Ziegler, JL, Simon, R and Schein, P:
Prognostic factors in Burkitt's lymphoma: Importance of total tumor burden. Cancer 45:1507-
1515, 1980.

52. Cohen, LF, Balow, JE, Magrath, I, Poplack, D and Ziegler, JL: Acute tumor lysis
syndrome: A review of 37 patients with Burkitt's lymphoma. Amer J Med 68:486-491 , 1980.

345

53. Ziegler, JL, Drew, WL, Miner, RC, Mintz, L, Rosenbaum, E, Gershow, J, Lennette, ET,
Greenspan, J, Shellitoe, E, Beckstead, J, Casavant, L and Yamamoto, K: Outbreak of Burkitt's-
like lymphoma in homosexual men. Lancet 2:631-633, 1982.

54. Olweny, CLM, Katongole-Mbidde, E, Otion, D, Lwanga, SK, Magrath, IT and Ziegler, JL:
Long-term experience with Burkitt's lymphoma in Uganda. Int J Cancer 26:261-266, 1980.

BURKITTS LYMPHOMA/lnvited Reviews

55. Ziegler, JL and Kyalwazi, SK: Recent research in Burkitt's lymphoma. East Afr Med
49:670-675, 1971.

56. Ziegler, JL: Das Burkitt-Lymphoma. Munchner Medizinische Wochenschrift 1 14:13-18,
1972.

57. Ziegler, JL: Management of Burkitt's lymphoma. Pediatric Annals 4:60-70, 1975.

58. Ziegler, JL, Deisseroth, AB, Appelbaum, FR and Graw, RG: Burkitt's lymphoma. A model
for intensive chemotherapy. Sem Oncol 4:317-323, 1977.

59. Ziegler, JL: Management of Burkitt's lymphoma - an update. Cancer Treatment Rev
6:95-105, 1979.

60. Magrath, IT and Ziegler, JL: Bone marrow involvement in Burkitt's lymphoma and its
relationship to acute B-cell leukemia. Leukemia Reviews 4:33-59, 1979.

61 . Ziegler, JL: Burkitt's lymphoma: Lessons for the oncologist, In Recent Advances in
Management of Children with Cancer, Tokyo, pp. 158-163, 1980.

62. Ziegler, JL: Medical progress. Burkitt's lymphoma. N Eng J Med 305:735-745, 1981.
BURKITT'S LYMPHOMA/Chapters in Books

63. Ziegler, JL: Burkitt's lymphoma. In Shaper, Kibukamusoke and Hutt (eds.): Medicine in a
Tropical Environment, St. Alban's, Knight & Co., Ltd., 1971, pp. 360-371.

64. Ziegler, JL and Burchenal, JH: Treatment of Burkitt's tumor. In Molander and Pack (eds.):
Lymphosarcoma and Related Diseases, Charles C. Thomas, New York, 1974, Chap. 12, pp. 332-
342.

65. Ziegler, JL: Burkitt's lymphoma. In Holland and Frei (eds.): Cancer Medicine, Lea and
Febiger, Philadelphia, 1973, pp. 1321-1330.

66. Ziegler, JL, Bluming, AZ, Fass, L, Morrow, RH and Iverson, OH: Burkitt's lymphoma. Cell
kinetics treatment and immunology. In Dutcher and Chieco-Bianchi (eds.): Comparative Leukemia
Research, S. Karger, Basel, 1973, pp. 1046-1052.

67. Ziegler, JL and Magrath, I: Burkitt's lymphoma. In loachim (ed.): Pathobiology Annual
1974. Appleton Century Crofts, New York, 1974, pp. 129-142.

68. Ziegler, JL and Magrath, I: Treatment of Burkitt's lymphoma. In Deeley (ed.): Malignant
Diseases in Children, Buttersworth, London, 1974, pp. 360-371.

69. Ziegler, JL and Magrath, IT: Burkitt's lymphoma. In Bucalosi, et al. (eds.): II Linfomi
Maligni, Casa Editrice Ambrosiana, Milan, 1974, pp. 281-290.

346

70. Ziegler, JL: Management of Burkitt's lymphoma. In Pochedly, C (ed.): Management of
Cancer in Children, Publishing Sciences Group, Inc., Acton, MA, 1975, pp. 187-202.

71 . Magrath, IT and Ziegler, JL: BCG immunotherapy in Burkitt's lymphoma. In Mathe and
Werner (eds.): Recent Results in Cancer Research, Springer- Vertag, New York, 1974, Vol. 47,
pp. 461-465.

72. Ziegler, JL: Burkitt's lymphoma. Symposium on advances in treatment of cancer. Med
Clin of North America, 61:1073-1083, 1977.

73. Iverson, OH, Bjerkness, R, Iverson, U, Ziegler, JL and Bluming, AZ: Cell kinetics in
Burkitt's lymphoma. In Drewinko and Humphrey (eds.): Growth Kinetics and Biochemical
Regulation in Normal and Malignant Cells, Williams & Wilkins Co., Baltimore, MD, 1977, pp. 675-
686.

74. Ziegler, JL: Management of Burkitt's lymphoma. In Carter, SK, Glatstein, E and
Livingston, RB (eds.): Principles of Cancer Treatment, McGraw-Hill, New York, 1982, pp. 902-
907.

75. Ziegler, JL: Burkitt's lymphoma. In Graham-Pole, J (ed.): Non-Hodgkin's Lymphoma in
Children, PSG Publishing Co., 1979.

76. Ziegler, JL: Burkitt's lymphoma. In Gellis, SS and Kagan, BM (eds.): Current Pediatric
Therapy, Philadelphia, W.B.S., 1980, pp. 295-297.

77. Ziegler, JL: Burkitt's lymphoma: lessons for the oncologist. In Ford, RJ, Fuller, CM,
Hagemieister, FB (eds.): New Perspectives in Human Lymphoma, 1984, pp. 439-452.

KAPOSI'S SARCOMA/AIDS/Original Work

78. Master, SP, Taylor, JL, Kyalwazi, SK and Ziegler, JL: Immunologic studies in Kaposi's
sarcoma in Uganda. Brit Med J 1:600-602, 1970.

79. Taylor, JL, Templeton, AC, Vogel, CL, Ziegler, JL and Kyalwazi, SK: Kaposi's sarcoma in
Uganda: A clinicopathological study. Int J Cancer 8:122-135, 1971.

80. Taylor, JF and Ziegler, JL: Delayed cutaneous hypersensitivity reactions in patients with
Kaposi's sarcoma. Brit J Cancer 30:312-313, 1975.

81. Olweny, CLM, Kaddamukasa, A, Atine, I, Owor, R, Magrath, IT and Ziegler, JL: Childhood
Kaposi's sarcoma: Clinical features and therapy. Brit J Cancer 33:555, 1976.

82. Drew, WL, Conant, MA, Miner, RC, Huang, ES, Ziegler, JL, Groundwater, JR, Gullet, JH,
Volberding, PA, Abrams, Dl and Mintz, L: Cytomegalovirus and Kaposi's sarcoma in young
homosexual men. Lancet 2:125-127, 1982.

83. Levy, JA and Ziegler, JL: Hypothesis. Acquired immunodeficiency syndrome is an
opportunistic infection and Kaposi's sarcoma results from secondary immune stimulation. Lancet
2:78-81,1983.

84. Moss, AR, Baccetti, P, Gorman, M, Dritz, S, Conant, M, Abrams, Dl, Volberding, P and
Ziegler, JL: AIDS in the "gay" areas of San Francisco. Lancet 1:923-924, 1983.

85. Ammann, AJ, Schiffman, G, Abrams, D, Volberding, P, Ziegler, J, Conant, M: Acquired B-
cell immunodeficiency in acquired immunodeficiency disease. JAMA 251:1447-1449, 1984.

347

86. Ziegler, JL, Beckstead, JH, Volberding, P, et al.: Non-Hodgkin's lymphoma in 90
homosexual men. Relationship to generalized lymphadenopathy and acquired immunodeficiency
syndrome. N Eng J Med 311:565-570, 1984.

87. Ziegler, JL, Bragg, L, Abrams, Dl, et al.: High grade Non-Hodgkin's lymphoma in patients
with AIDS. Ann NY Acad Sci 437:412-419, 1984.

88. Ziegler, JL, Volberding, PA and Itri, L: 13-cis retinoic acid for Kaposi's sarcoma. Lancet
2:641,1984.

89. Moss, AR, Bacchetti, P, Osmond, D, Dritz, S, Abrams, D, Conant, M, Volberding, P and
Ziegler, JL: Incidence of acquired immunodeficiency syndrome in San Francisco. J Inf Dis
152:152-161, 1985.

90. Stites, DP, Casavant, CH, McHugh, JM, Moss, AR, Beal, SL, Ziegler, JL, Saunders, AM
and Warner, NL: Flow cytometric analysis of lymphocyte phenotypes in AIDS using monoclonal
antibodies and simultaneous dual immunofluorescence. J Immunol Immunopath 38:161-177,
1986.

91. Volberding, PA, Abrams, Dl, Conant, M, Kaslow, K, Vranizen, K and Ziegler, JL:
Vinblastine therapy of Kaposi's sarcoma in AIDS. Ann Int Med 103:335-338, 1985.

92. Kaplan, LD, Abrams, Dl, Feigal, Jr., DW, McGrath, MS, Ziegler, JL, Volberding, PA:
AIDS-associated Non-Hodgkin's lymphoma in San Francisco. JAMA 261:719-724, 1989.

93. Kahn, JO, Kaplan, LD, Ziegler, JL, Volberding, PA, Crowe, S, Saks, S, Abrams, Dl:
Intralesional recombinant tumor necrosis factor-alpha for AIDS associated Kaposi's sarcoma. J
AIDS 2:217-223, 1989.

94. Hellmann, SD, Mbidde, EK, Kizito, A, Hellmann, NS, Ziegler, JL. The value of a clinical
definition for epidemic Kaposi's sarcoma (KS) in predicting HIV seropositivity in Africa. J AIDS
4:647-51, 1991.

95. Allen, S, Vandeperre, P, Serufilira, A, Lapage, P, Caroel, M, DeClerq, A, Tice, J, Black, D,
Nsengumuremyi, F, Ziegler, J, Levy, J, Hulley, S. Human immunodeficiency virus and malaria in a
representative sample of childbearing women in Kigali, Rwanda. J Infect Dis 164:67-71 , 1991 .

96. Ziegler, JL. Endemic Kaposi's sarcoma and local volcanic soils. Lancet 342:1 348-51 ,
1994.

KAPOSI'S SARCOMA/AIDS/lnvited Reviews

97. Ziegler, JL, Vogel, CL and Templeton, AC: Kaposi's sarcoma: A comparison of classical,
endemic and epidemic forms. Sem Oncol 11:47-52. 1984.

98. Ziegler, JL: Kaposi's sarcoma in homosexual men. JNCI 68:337-338, 1982.

99. Ziegler, JL, Stites, DP: Hypothesis: AIDS is an autoimmune disease triggered by a
lymphotropic retrovirus. Clin Immunol Immunopathol 41:305-313, 1986.

100. Ziegler, JL: AIDS and cancer. Ann Inst Pasteur/lmmunol 138:253-260, 1987.

101. Ziegler, JL: Pathogenesis of AIDS-associated Kaposi's sarcoma. Lymphology 21:15-18.

348

102. Ziegler, JL (rapporteur). Interrelations of tropical diseases and HIV infection. Report of an
informal consultation held at the Kenya Medical Research Institute, Dec. 1-4, 1987. World Health
Organization (TDR/GPA).

103. Editorial. "Biologic" differences in acquired immune deficiency syndrome-associated non-
Hodgkin's lymphomas? J Clin Oncol 9:1329-31, 1991.

104. Greenspan, JS, Conant, MA, Ziegler, JL, Volberding, PA, Desouza, YG. The UCSF AIDS
Specimen Bank. Lab Med, 22:99-101, 1991.

105. Ziegler, JL: Clinical trials in Africa: An opportunity for whom? Jasmin, C (ed): Cancer,
AIDS, and Society. ESF Editeur, Paris, 1992, pp189-196

KAPOSI'S SARCOMA/AIDS/Chapters in Books

106. Lutzner, M and Ziegler, JL: Kaposi's sarcoma. In Fitzpatrick, T, Eisen, A, Wolff, K,
Freedberg, I and Auten, K (eds.): Dermatology in General Medicine. New York, McGraw-Hill,
1979, pp. 742-749.

107. Ziegler, JL: AIDS and oncogenesis. In Vaeth, JM (ed.): Frontiers in Radiation Therapy
and Oncology. Karger, Basel, 1985, pp. 99-104.

108. Conant, MA and Ziegler, JL: Pathophysiology of acquired immunodeficiency syndrome. In
Thiers, B and Dobson, RL (eds.): Pathophysiology of Skin Disease. Churchill Livingstone, New
York, 1986, pp. 387-399.

109. Ziegler, JL and Abrams, Dl: The lymphadenopathy syndrome and AIDS. In DeVita, VT,
Hellman, S and Rosenberg, S: Acquired Immune Deficiency Syndrome. McGraw-Hill, New York,
1985, pp. 223-234.

110. Ziegler, JL and Levy, JA: The acquired immunodeficiency syndrome and cancer. In Klein,
G: Advances in Virology. Raven Press, New York, 1984, pp. 239-255.

111. Ziegler, JL: Non-Hodgkin's lymphoma and other cancers associated with AIDS. In Levy,
JA (ed.): AIDS: Pathogenesis and Treatment. Marcel Dekker, New York, 1988, pp. 359-370.

112. So, YT, Choucair, A, Davis, RL, Wara, WT, Ziegler, JL and Sheline, GE: Neoplasms. In
Rosenblum, ML, Levy, RM, Bredesen, DE, (eds.): AIDS and the Nervous System. Raven Press,
New York, 1988, pp. 285-300.

113. Ziegler, JL: The natural history of AIDS. In Petricciani, JD, Gust, ID, Hoppe, PA and
Krijnen, HW (eds.): AIDS: The Safety of Blood and Blood Products. John Wiley and Sons,
Chichester, JK, 1987, pp. 21-32.

114. Ziegler, JL: AIDS and cancer. In Carbone, PP and Brain, M. (eds.): Current Therapy in
Hematology-Oncology. BC Decker, 1988, pp. 350-353.

115. Ziegler, JL: Kaposi's sarcoma and angiogenesis. In Ziegler, JL and Dorfman, R. (eds.):
Kaposi's Sarcoma: Pathophysiology and Clinical Management. Marcel Dekker, New York, 1988,
pp. 151-168.

116. Ziegler, JL and Dorfman, R: Overview of Kaposi's sarcoma: History, epidemiology and
biomedical features. In Ziegler, JL and Dorfman, R (eds.): Kaposi's Sarcoma: Pathophysiology
and Clinical Management. Marcel Dekker, New York, 1988, pp. 1-22.

349

117. Ziegler, JL and Stites, DP: AIDS: An autoimmune disease triggered by a retrovirus? In
Andrieu J-M and Even, P (eds.): AIDS: A Viral-Induced Immune Disorder. Royal Society of
Medicine, London, 1988, pp. 69-73.

118. Ziegler, JL and Mcgrath, M: Lymphomas in HIV positive individuals. In Magrath, IT (ed.):
The Non-Hodgkin's Lymphomas. Edward Arnold Publisher, 1990, pp. 155-159.

1 1 9. Ziegler, JL: Kaposi's sarcoma: An overview. J AIDS 3:51 -53, 1 990.

120. Ziegler, JL: Neoplasms in patients with immunocompromise. In Stites, DP and Terr, Al
(eds.): Clinical and Basic Immunology. Appleton-Lange Publications, East Norwalk, CT, 1991, pp.
588-98, (and 1994. 1997 editions).

121. Ziegler, JL. HIV and malignancy. In Lever, A (ed): The molecular biology of HIV and
AIDS, in press, 1994.

122. Ziegler, JL. AIDS and Malignancy. Medicine. The Medicine Group (Journals) Inc.,
September, 1996 issue.

KAPOSI'S SARCOMA/AIDS/Book

123. Ziegler, JL and Dorfman, R (eds.): Kaposi's Sarcoma: Pathophysiology and Clinical
Management. Marcel Dekker, New York, 1987.

MALIGNANCIES/CHEMOTHERAPY/OriginalWork

124. Kiryabwire, JWM, Lewis, MG, Ziegler, JL and Loefler, I: Malignant melanoma in Uganda.
East Afr Med J 45:498-507, 1968.

125. Ziegler, JL, Lewis, MG, Luyombya, JMS, and Kiryabwire, JMW: Immunologic studies in
patients with malignant melanoma in Uganda. Brit J Cancer 23:729-735, 1969.

126. Pass, L, Herberman, RB, Ziegler, JL and Kiryabwire, JWM: Cutaneous hypersensitivity
reactions to autologous extracts of malignant cells. Lancet 1 :1 16-1 18, 1970.

127. Vogel, CL, Comis, R, Ziegler, JL and Kiryabwire, JWM: Clinical trials of intravenous 5 - (3-
dimethly-1-triazeno)-imidazole-4 carboxamide (NSC 45388) given intravenously in the treatment
of malignant melanoma in Uganda. Cancer Chemother Rep 55:143-39, 1971.

128. Bluming, AZ, Vogel, CL, Ziegler, JL, Mody, J and Kamya, GWS: Immunological effects of
BCG in malignant melanoma: Two modes of administration compared. Ann Int Med 76:405-412,
1972.

129. Bluming, AZ, Vogel, CL, Ziegler, JL and Kiryabwire, SK: Cutaneous reactivity to extracts
of autologous malignant melanoma cells: A second look. J Nat Cancer Inst 48:17-24, 1972.

130. Schein, PS, O'Connell, MJ, Blom, J, Hubbard, S, Magrath, IT, Bergevin, P, Wiemik, PH,
Ziegler, JL and DeVita, VT: Clinical antitumor activity and toxicity of streptozotocin (NCS-85998).
Cancer 34:993-1 000, 1974.

131. Leventhal, BG, Ziegler, JL, Simon, RH and Henderson, ES: The relation of duration of
first remission to survival. In Fliedner, TM and Perry, S (eds.): Advances in the Biosciences,
Pergamon Press, Oxford, Vol. 14, pp. 83-89, 1975.

132. Primack, A, Vogel, CL, Kyalwazi, SK, Ziegler, JL and Simon, R: A staging system for
hepatocellular carcinoma: Prognostic factors. Cancer 35:1354-1357, 1975.

350

133. Vogel, CL, Bayley, AC, Brooker, RJ, Anthony, PP and Ziegler, JL: A Phase II study of
adriamycin in patients with hepatocellular carcinoma from Zambia and the U.S. Cancer 39:1923-
1929, 1977.

134. Levine, AD, Appelbaum, FR, Graw, RG, Jr, Magrath, IT, Pizzo, PA, Poplack, DG and
Ziegler, JL: Sequential combination chemotherapy containing high-dose cyclophosphamide in the
treatment of metastatic osteogenic sarcoma. Cancer Treatment Rept 62:247-250, 1978.

135. Gottdeiner, JS, Appelbaum, F, Ferrans, VJ, Deisseroth, A and Ziegler, JL: Cardiotoxicity
associated with high dose cyclophosphamide. Arch Int Med 141:758-763, 1981.

136. Blatt, J, Mulvihill, JJ, Young, RC, Ziegler, JL and Poplack, DL: Pregnancy outcome
following cancer chemotherapy. Ann Intern Med 69:828-832, 1980.

137. Shamberger, RC, Sherins, RJ, Ziegler, JL and Rosenberg, SA: The effect of
postoperative adjuvant chemotherapy and radiotherapy on ovarian function in women undergoing
treatment for soft tissue sarcoma. JNCI 67:1213-1218, 1981 .

138. Everson, RB, Gad-EI-Mawla, NM, Attia, MAM, Chevlen, EM, Thorgeirsson, SS,
Alexander, LA, Flack, PM, Staiano, N and Ziegler, JL: Analysis of human urine for mutagens
associated with carcinoma of the bilharzial bladder by Ames Selmonella plate assay:
Interpretation employing quantitation of viable lawn bacteria. Cancer 51:371-375, 1983.

MALIGNANCIES/CHEMOTHERAPY/lnvited Reviews

139. Ziegler, JL and Leventhal, BL: Treatment of acute leukemia. In Peschle, C (ed.):
Leukemia, II Pensiero Scientifico, Rome, 1976.

140. Whang-Peng, J, Knutsen, T, Ziegler, J and Leventhal, B: Cytogenetic studies in acute
lymphocytic leukemia. Special emphasis on long term survival. Med Pediatric Oncol 2:333-351,
1976.

141. Ziegler, JL, Magrath, IT, Gerber, P and Levine, PH: Epstein-Barr virus and human
malignancy. Ann Int Med 86:323-336, 1977.

142. Ziegler, JL, Adamson, RH, Barker, LF, Fraumeni, Jr., JR: Workshop on hepatitis B and
liver cancer. Cancer Res 37:4672, 1977.

143. Ziegler, JL: Clinical trial methodology. Cancer Clinical Trials 1:89-91, 1978.

144. Ziegler, JL: The present state of development of cancer chemotherapy. Federation Proc
38:93-98, 1979.

145. Ziegler, JL: Long-term effects of cancer chemotherapy in children. Drug Therapy 7:80-86,
1979.

146. Ziegler, JL and Muggia, F: Long-term sequelae of cancer chemotherapy. In G Mathe and
F Maggia, (eds.): Recent Results in Cancer Research 74:312-315, 1980.

147. Muggia, F and Ziegler, JL: Comments on the carcinogenic, mutagenic and teratogenic
properties of anticancer drugs. Ibid. 74:305-311, 1980.

148. DeVita, VT, Oliverio, VT, Muggia, FM, Wiemik, PW, Ziegler, JL, Goldin, A, Rubin, D,
Henney, J and Schepartz, S: The drug development and clinical trials programs of the Division of
Cancer Treatment, NCI. Cancer Clinical Trials 2:195-216, 1979.

351

149. Ziegler, JL: Immunotherapy of childhood solid tumors. In Recent Advances in
Management of Children with Cancer, Tokyo, pp. 275-279, 1 980.

150. Ziegler, JL: Cancer and the prostaglandins. In Current Concepts Monograph Series,
Upjohn Co., Kalamazoo, Ml, 1982.

MALIGNANCIES/CHEMOTHERAPY/Chapters in Books

151 . Ziegler, JL: Management of Burkrtt's lymphoma. In Pochedly, C (ed.): Management of
Cancer in Children, Publishing Sciences Group, Inc., Acton, MA, 1975, pp. 187-202.

152. Bluming, AZ, Vogel, CL and Ziegler, JL: Screening of systemic adjuvants of immunity. In
Mathe and Werner (eds.): Recent Results in Cancer Research, Springer- Veriag, New York, 1974,
Vol. 47, pp. 415-420.

153. Ziegler, JL: Childhood cancer - lessons for the oncologist. Opening lecture, Perugia
Quadrennial International Conference: Tumors of early life in man and animals, 1978.

154. Hutt, MSR and Ziegler, JL: Tumors in the tropics. In Strickland, GT (ed.): Hunter's
Tropical Medicine, WB Saunders, Philadelphia, 1984, pp. 81-93.

155. Ziegler, JL: Neoplasms. In Warren, KS and Mahmond, AAF (eds.): Tropical and
Geographical Medicine. McGraw-Hill, New York, 1984, pp. 52-60.

156. Parkin DM and Ziegler JL: Malignant Diseases. In Strickland, G.T., (ed). Hunter's
Tropical Medicine, 8th edition. WB Saunders, Philadelphia, 1997 (in press)

HODGKIN'S DISEASE/Original Work

157. Ziegler, JL, Morrow, RH, Bluming, AZ, Pass, L, Templeton, AC, Templeton, C and
Kyalwazi, SK: Clinical features and treatment of childhood lymphoma in Uganda. Int J Cancer
5:415-425, 1970.

158. Olweny, CLM, Ziegler, JL, Berard, CW and Templeton, AC: Adult Hodgkin's disease in
Uganda. Cancer 27:1295-1301, 1971.

159. Henderson, BE, Ziegler, JL and Templeton, AC: Acute necrotizing encephalitis in a
patient with Hodgkin's disease. East Afr Med J 48:592-600, 1971.

160. Olweny, CLM and Ziegler, JL: Hodgkin's disease. Uganda Practitioner 4:52-57, 1971 .

161 . Olweny, CLM and Ziegler, JL: Treatment of Histiocytic lymphoma in Ugandan adults. East
Af r Med J 48:535-591, 1971. "

162. Ziegler, JL, Pass, L, Bluming, AZ, Magrath, IT and Templeton, AC: Chemotherapy of
childhood Hodgkin's disease in Uganda. Lancet 2:679-682, 1972.

163. Magrath, IT, Ziegler, JL and Templeton, AC: A comparison of clinical and histological
features of childhood malignant lymphoma in Uganda. Cancer 33:285-294, 1974.

164. Olweny, CLM, Katongole-Mbidde, EJ, Kiire, C, Lwanga, SK, Magrath, IT and Ziegler, JL:
Childhood Hodgkin's disease in Uganda. A ten year experience. Cancer 42:787-792, 1978.

352

165. Sherins, RJ, Olweny, CLM and Ziegler, JL: Gynecomastia and gonadal dysfunction in
adolescent boys treated with combination chemotherapy for Hodgkin's disease. New Eng J Med
299:12-16, 1978.

HODGKIN'S DISEASE/lnvited Reviews

166. DeVtta, Jr.. VT, Glatstein, EJ, Young, RC, Hubbard, SM, Simon, RS, Ziegler, JL and
Wiemik, P: Changing concepts: The lymphomas. In Salmon, SE and Jones, SE (eds.): Presented
at Second International Conference on the Adjuvant Therapy of Cancer, Grune & Stratton, Inc.,
Tucson, pp. 15-20, 1979.

167. Berard, CW, Greene, MH, Jaffe, ES, Magrath, IT and Ziegler, JL: A multidisciplinary
approach to Non-Hodgkin's lymphomas. Ann Int Med 218-235, 1981.

HODGKIN'S DISEASE/Chapters in Books

168. Carbone, PP, DeVita, VT and Ziegler, JL: Intensive care of patients with malignant
lymphoma. In Clark, et al. (eds.): Oncology 1970, Year Book Medical Publishers, Chicago, 1971,
Vol. IV, pp. 532-537.

TROPICAL SPLENOMEGALY SYNDROME/Original Work

169. Ziegler, JL, Cohen, MH and Hurt, MSR: Immunologic studies in tropical splenomegaly
syndrome in Uganda. Brit Med J 4:15-17, 1969.

170. Stuiver, P, Ziegler, JL, Wood, JB, Morrow, RH and Hurt, MSR: Clinical trial of malaria
prophylaxis in tropical splenomegaly syndrome. Brit Med J 1:426-429, 1971.

171. Patel, AH, Ziegler, JL, D'Arbela, P and Somers, LK: Familial cases of endomyocardial
fibrosis in Uganda. Brit Med J 4:331-334, 1971.

172. Hamilton, PJS, Stuiver, PC and Ziegler, JL: Splenomegaly in tropical splenomegaly
syndrome: A five-year follow-up. J Trop Med Hyg 74: 230-232, 1971.

173. Ziegler, JL and Stuiver, PC: Tropical splenomegaly syndrome in a Rwandan kindred in
Uganda. Brit Med J 3:79-82, 1972.

174. Ziegler, JL: Recent advances in tropical splenomegaly syndrome. Uganda Medical
Journal 1:72-73, 1972.

175. Ziegler, JL, Voller, A and Ponnudurai, T: Malarial antibodies in tropical splenomegaly
syndrome in Uganda. Trop Geogr Med 25:282-285, 1973.

176. Ziegler, JL: Cryoglobulinemia in tropical splenomegaly syndrome. Clin Exp Immunol
15:65-78, 1973.

177. Woodruff. AW, Ziegler, JL, Hathaway, A and Gwata, T: Anemia in African
trypanosomiasis and tropical splenomegaly syndrome in Uganda. Trans Roy Soc Trop Med Hyg
67:329-337,1973.

178. Tabor, E, Ziegler, JL and Gererty, RJ: Hepatitis B E antigen in the absence of hepatitis B
surface antigen. J Infect Dis 141:289-292, 1980.

TROPICAL SPLENOMEGALY SYNDROME/Chapters in Books

353

179. Ziegler, JL: Tropical splenomegaly syndrome. In Strickland, GT (ed.):
Immunoparasitology: Principles and Methods in Malaria and Schistosomiasis Research. Prager
Scientific Co., New York, 1982, pp. 87-98.

CARCINOMA OF THE BLADDER/Original Work

180. Gad-EI-Mawla, N, Hamsa, R, Caims, J, Anderson, T and Ziegler, JL: A Phase II trial of
methotrexate in carcinoma of the bilharzial bladder. Cancer Treatment Rept 62:1075-1076, 1978.

181. Gad-EI-Mawla, N, Hamsa, R, Chevlen, E and Ziegler, JL: A Phase II trial of bleomycin in
bilharzial bladder cancer. Cancer Treatment Rept 62:1109-110, 1978.

182. Gad-EI-Mawla, N, Hamza, R, Chevlen, E and Ziegler, JL: A Phase II trial of adriamycin in
carcinoma of the bilharzial bladder. Cancer Treatment Rept 63:227-228, 1 979.

183. Gad-EI-Mawla, N, Chevlen, E, Hamza, R and Ziegler, JL: A Phase II trial of cis-
diamminedichloroplatinum (II) in cancer of the bilharzial bladder. Cancer Treatment Reprt
63:1577-1578, 1979.

184. Gad-EI-Mawla, N, Ziegler, JL, Hamza, R, Elserafi, M and Khaled, H: Phase II
chemotherapy trials in carcinoma of the bilharzial bladder. 5-fluorouracil, cyclophosphamide,
ifosphamide, and vincristine. Cancer Treatment Rpt 68:419-421, 1984.

185. Gad-EI-Mawla, N, Ziegler, JL, Hamza, R, Elserafi, M, Khaled, H: Randomized Phase II
trial of hexamethymelamine versus pentamethylmelamine in carcinoma of the bilharzial bladder.
Cancer Treatment Rpt 68:793-795, 1984.

CARCINOMA OF THE BLADDER/lnvited Reviews

186. Chevlen, EM, Awaad, HK, Gad-EI-Mawla, N, Ziegler, JL and Elsebai, I: Cancer of the
bilharzial bladder - a review. Int J Radiol Oncol Biol & Phys 5:921-926, 1979.

CARCINOMA OF THE BLADDER/Chapters in Books

187. Gad-EI-Mawla, N and Ziegler, JL: Chemotherapy of cancer of the bilharzial bladder. In
Elsebai, I (ed.): Bladder Cancer, Vol. II, CRC Press, Boca Raton, 1983, pp. 133-138.

MEDICAL EDUCATION/Original Work

188. Kanas, N and Ziegler, JL: Group climate in a stress discussion group for medical interns.
Group 8:35-38, 1984.

189. Ziegler, JL, Kanas, N, Strull, MW and Bennett, NE: Stress in medical internship:
Experience in a weekly discussion group. J Med Educ 59:205-207.

190. Ziegler, JL, Strull, WM, Larsen, RC, Martin, A and Coates, TJ: Medical staff conference:
Stress and medical training. West J Med 142:814-819, 1985.

1 91 . Ziegler, JL. Curricular essentials for Makerere University postgraduates in Medicine.
Uganda Med J, 8:24-33, 1991.

192. Ziegler, JL. Medicine in Africa. Cambridge Medicine 10:20-22;1993

193. Ziegler JL: Music and Physic. Cambridge Medicine 10:23-26;1994
MEDICAL EDUCATION/lnvited Reviews

354

1 94. Ziegler, JL: Cardiology in the Renaissance. J Lancet 84:89-96, 1 964.

195. Ziegler, JL: The Uganda Cancer Institute. Uganda Practitioner 3:17-19, 1970.
MEDICAL EDUCATION/Chapters in Books

196. Ziegler, JL: The design and planning of controlled clinical therapeutic trials. In Bucalosi,
et al. (eds.): II Linfomi Maligni, Casa Editrice Ambrosiana, Milan, 1974, pp. 181-182.

197. Ziegler, JL and Kanas, N: Coping with stress during internship. In Scott, C and Hawk, J
(eds.): Heal Thyself: Health of Health Professionals. Bruner-Mazel, San Francisco, 1985, pp. 173-
184.

LYME DISEASE/Original Work

198. Benach, JL, Bosler, EM, Hanrahan, JP, Coleman, JL, Habicht, GS, Bast, TF, Cameron,
DJ, Ziegler, JL, Barbom, AG, Burgdorfer, W, Edelman, R and Kaslow, RA: Spirochetes isolated
from the blood of two patients with Lyme disease. N Eng J Med 308:740-742, 1983.

ARTICLES RECENTLY PUBLISHED OR IN PRESS (1995-)

199. Ziegler JL, Katongole-Mbidde E., Wabinga, H, and Dollbaum CM. Absence of sex-
hormone receptors in Kaposi's sarcoma. Lancet 345:925;1995

200. Ziegler JL and Katongole-Mbidde E. Childhood Kaposi's sarcoma in Uganda:Analysis of
100 cases and relationship to HIV infection. Int J Cancer 65:200-203; 1996

201 . Ziegler JL. Cutaneous anergy in the legs of Ugandan patients with Kaposi's sarcoma.
J Roy Soc Trop Med & Hyg. 90:1743-4;1996.

202. Chang Y, Ziegler JL, Wabinga H, et al. Kaposi's sarcoma-associated herpesvirus and
Kaposi's sarcoma in Africa. Arch Int Med 156:202-204; 1996

203. Gao, S, Kingsley L, Zheng W, Parravicini, Ziegler JL, Newton R, et al. KSHV antibodies
among Americans, Italians, and Ugandans with and without Kaposi's sarcoma. Nature Med 2:925-
928; 1996

355

INDEX--The History of the AIDS Epidemic in San Francisco: The
Medical Response, 1981-1984, Volume IV

Note to Index: When an organization or entity is known primarily by its
acronym and referred to primarily by its acronym in the text, it is indexed
under the acronym. Otherwise full titles are given, followed by the
acronym. Examples: HIV [human immunodeficiency virus], NIH [National
Institutes of Health]; but General Accounting Office [GAO]

Abrams, Donald I., 129, 136, 141,
153, 162-164, 193, 211, 214,
227, 233, 240, 246, 248
Acer, David, 135, 156-158
ACT UP [AIDS Coalition to Unleash

Power], 150
Adult Immunodeficiency Clinic,

UCSF, 220, 236-236
Africa

AIDS in, 115-116, 142, 173,

199, 227, 237, 255
AIDS in Zaire, 69-70
Kaposi's sarcoma in, 221-225
malignancies in, 203-204, 211
Uganda, 165, 203-204, 219,

221, 253-254

Agency for International
Development, U.S., 2
Agnos, Art, 104, 175
AIDS [Acquired Immune Deficiency
Syndrome], 9, 50-53, 94-95,
122-123, 255
an autoimmune disease (See also

immunosuppression) , 269-271
defining and characterizing,
74-76, 75, 76, 89-93, 91,
153-155, 175-176, 212-213,
238
diagnostic criteria (See also

CDC), 74-76, 238, 240-241
early cases and perceptions,
70-72, 126-127, 139, 179,
206-208, 215-217, 237-239
incubation/ latency period, 57,
59, 75, 129, 226-227, 244,
257

AIDS (cont'd.)

naming the disease or the
virus, 55, 93-94, 155.
See also AIDS opportunistic
infections; AIDS patients,
care of; epidemiology;
etiology of AIDS; HIV [human
immunodeficiency virus]; risk
groups for AIDS; women, AIDS
in
AIDS antibody test. See HIV

antibody test
AIDS dementia, 257
AIDS drugs, 150

accelerated approval of,

199-200
AZT, 274
BCG [Bacille Calmette-Guerin] ,

269

Compound Q,
cyclosporin,
pentamidine,
steroids use,

151-152
269
186

186

trimethoprin sulfa, 186, 198
AIDS education and prevention,
72-74, 82, 106, 109, 271-272
AIDS opportunistic infections,
18, 244-246, 258
amebiasis, 225
Burkitt's or AIDS-associated
lymphomas, 211-212, 215,
217, 237-238, 240, 250
candidiasis, 237
cytomegalovirus, 16, 202, 211,

242

hairy leukoplakia, 234
herpes zoster, 215

356

AIDS opportunistic infections
(cont'd.)
lymphadenopathy, 41, 233, 237,

259, 270

Mycobacterium avium, 239, 254
Pneumocystis carinii pneumonia,
16, 89-90, 125, 136, 139,
146, 148, 179, 186, 198, 207,
215, 231, 240

toxoplasmic encephalitis, 179
toxoplasmosis, 179, 207, 254.
See also cryptococcal diseases;
Epstein-Barr virus; Kaposi's
sarcoma

AIDS patients, care of, 74, 163,
174, 194-195, 239-241, 274
alternative therapies, 272
chemo- and radiotherapy,

238-239, 252

holistic approach, 148-150
multidisciplinary approach,

167-168, 251-252, 274
organizational and delivery
aspects, 166-167, 169-171,
170, 233, 258-259
physician-patient relationship,

196-198

quality of life issues, 195
SFGH course in, 201.
See also medical community; San
Francisco model of AIDS care;
SFGH; UCSF; VA
AIDS testing. See HIV antibody

test

AIDS Treatment News, 137
AIDS virus. See HIV [human

immunodeficiency virus]
Alpha Therapeutics, 62
Altman, Larry, 52, 89, 198-199
amebiasis, 225
American Cancer Society, 208-209,

244, 266
Ammann, Arthur J., 61, 63, 127,

214-216, 256, 268
amyl nitrite ("poppers"), 19, 35,
155

And the Band Played On

book (Shilts), 20, 35, 81,

106, 141, 158
HBO film, 28, 106
Andrieu, Jean-Marie, 269
animal models in AIDS research,

29-30, 34, 38, 41, 119, 168
antibody test. See HIV antibody

test

antigen mimicry, 270
antioxidants, 272
Armstrong, Donald, 71
Aronson, Stu, 80
ARV [AIDS-associated retrovirus],

Atlanta, CDC, 30-33, 32
autoimmune disease, AIDS as,

269-271
AZT (AIDS drug), 274

BAPHR. See Bay Area Physicians

for Human Rights [ BAPHR]
Barre, Francoise, 37-38, 41-42
bathhouse issue, 70, 74, 99,
138-140,
153, 165
civil liberties versus public

health, 139-140
closure, 140, 172-173, 247-248
reopening, 140
Bay Area Physicians for Human

Rights [BAPHR] , 150
BCG [Bacille Calmette-Guerin] ,

269

behaviors, at-risk, 13-14, 24,
70-71, 71, 74, 98, 126, 139,
226, 249

Belgian AIDS cases, 69
Bellevue Hospital (New York), 202
Bennett, John, 28
Bishop, Michael, 181
Bissell, Montgomery, 121
blood banks, blood screening,
62-63, 94-95, 107, 216, 241
blood safety issue, 95
CDC meeting on blood safety

[Jan. 1983], 61-63, 70-71
resistance to screening, 63-66

357

blood banks, blood screening

(cont'd.)

See also HIV antibody test;
Irwin Memorial Blood Bank;
transfusion AIDS
Blood Products Advisory Committee,

Bo, Li Ching, 15
Bolan, Bob, 248
Brandt, Edward, 50-51, 87
Braude, Abe, 181
Brown, Willie, 104, 159, 179-180,

182-183, 189, 214, 235
Burkitt, Dennis, 202
burnout, 193
Bush, George, 105, 263
Bye, Larry, 73

Cabradilla, Ci, 32, 46, 78
California Medical Association

[CMA], 96, 102-103, 112
California Public Health Hospital

Association, 190
California Nurses Association,

103

California propositions, 103
California, State of

Assembly Ways and Means

Committee, 182, 185, 189
Department of Health Services,
101-103

Office of AIDS, 105-106
Campbell, Tom, 182
cancer, 203, 207, 252
viral theory of, 12
and viruses, 210-211.
See also Kaposi's sarcoma;
National Cancer Institute
[NCI]

candidiasis, 237
Carbone, Paul, 203
Cardiff, Robert, 181, 185
Carlson, Jim, 185
Carmen, Charles, 99
CD4 lymphocytes, 243, 259, 270

CDC [Centers for Disease Control
and Prevention], 21, 49-50, 96,
108, 111, 132-134, 215, 221, 243
in Africa, 69-70
AIDS diagnostic criteria,

74-76, 238, 240-241
Atlanta office, 30-33
blood safety recommendations
[Jan. 1983], 61-63, 70-71
Center for Preventative

Services [CPS], 81, 82
Division of Viral Diseases, 32
Epidemic Intelligence Service

Program, CDC, 2, 10
funding issues, 18, 20-22, 28,
32, 54, 68-69, 83, 100-101,
106-109
General Accounting Office

audit, 84-86
health care worker

recommendations, 135-136,
156-157
Pasteur Institute and, 36-37,

77
Phoenix Laboratory, 11, 13,

18, 29-31, 37
politics affecting, 21, 76,

86, 100, 105-107, 156
relationship with NIH, 79-81
Sexually Transmitted Diseases

Division [STD], 16-17, 84
Task Force on AIDS, 17-18.
See also epidemiology; Francis,

Donald P.

Centers for Disease Control and
Prevention. See CDC
Cesario, Tom, 181
Chabner, Bruce, 207
Charles, Sandy, 257
chemotherapy, 238-239, 252
Chermann, Jean-Claude, 41-43, 45,

58, 77

Chin, Jim, 73, 103
Chung-Bo, Liu, 80
Cimons, Marlene, 89
civil rights, and public health,

98-99

clay (kaolin) soils hypothesis of
KS etiology, 220-225

358

Clement, Michael, 146, 154,

193-194
Clinton, William (Bill),

administration, 22, 68, 106
Clumeck, Nathan, 142, 172
CMA. See California Medical

Association [CMA]
Coates, Tom, 73
cofactors, AIDS, 112-113, 218,

241, 265
Cold Spring Harbor Meeting on HTLV

[Sept. 1983], 38-39
commercial or market factors,

114-115, 169

Compound Q (AIDS drug), 151-152
Conant, Marcus, 73, 102, 125,

128, 141, 159-161, 165, 179,

208-209, 229, 232, 234, 236,

255-256, 259, 267
condom use, 86, 106
Conte, John E. , 128
Cooke, Molly, 132
County Community Consortium, SF,

162, 193, 246-769
Cowan, Morton J., 216
Crewdson, John, 79, 187
cryptococcal diseases, 207, 244
cryptosporidiosis, 254
meningitis, 89, 179, 215, 221,

239
Curran, James [Jim], 16, 28, 43,

50, 72, 82-84, 106, 111, 132,

241
cytomegalovirus, 16, 204, 211,

242
cytometry, flow, 61, 259

Dacey, Ralph, 119-120
Dannemeyer, Bill, 76, 91, 97,

100, 103, 110
Darrow, William, 17, 84
Day, Lorraine, 129, 166
de Banfort [Red Cross], 64
death and dying, 149-150, 195
Delaney, Martin, 137, 150-152
dementia, AIDS-associated, 257
dermatology, 250.

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