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Full text of "The AIDS epidemic in San Francisco: the medical response 1981-1984"

University of California 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 VIII 



Jay A. Levy, M.D. ANIMAL VIROLOGY AND THE DISCOVERY OF THE AIDS VIRUS 



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



Interviews Conducted by 

Sally Smith Hughes, Ph.D. 

in 1993 



Copyright o 2001 by The Regents of the University of California 



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. 

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

All uses of this manuscript are covered by a legal agreement 
between The Regents of the University of California and Jay A. Levy. 
The manuscript is thereby 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 Bancroft Library, 
Mail Code 6000, University of California, Berkeley 94720-6000, and 
should include identification of the specific passages to be quoted, 
anticipated use of the passages, and identification of the user. 
The legal agreement with Jay A. Levy requires that he be notified of 
the request and allowed thirty days in which to respond. 

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

"The AIDS Epidemic in San Francisco: The Medical 
Response, 1981-1984, Volume VIII," an oral history 
conducted in 1993 by Sally Smith Hughes, Regional Oral 
History Office, The Bancroft Library, University of 
California, Berkeley, 2001. 



Copy no, 




Jay A. Levy, M.D., 1996. 



Photograph by Karen Preuss 



Cataloguing information 



THE AIDS EPIDEMIC IN SAN FRANCISCO: THE MEDICAL RESPONSE, 1981-1984, Volume 
VIII, 2001, xix, 159 pp. 



Jay A. Levy, M.D. (b. 1938), "Animal Virology and the Discovery of the AIDS 
Virus": virologist. Education at Wesleyan and Columbia, internship, 
residency, and research at University of Pennsylvania; pre-AIDS career and 
research at the National Cancer Institute, UCSF, and in France; Kaposi's 
Sarcoma Clinic, UCSF, visit to Haiti; 1983 State AIDS research grant; heat 
treatment of blood products and viral cause of AIDS; Robert Gallo at NCI, Luc 
Montagnier and Pasteur Institute group, and Levy laboratory in race to 
identify AIDS virus, and ensuing claims for priority; controversy over AIDS 
antibody tests; cloning and sequencing AIDS virus, Chiron Corp.; naming the 
virus HIV, and research on immune mechanisms and CDS cells in long-term AIDS 
survivors; comments on Robert Gallo, Gertrude (Brigitta) and Werner Henle, and 
William J. Rutter. 

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

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



ACKNOWLEDGMENTS 



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 AIDS Epidemic in San Francisco: The Medical 
Response, 1981-1984: Volume VIII 



PREFACE- -by David and Evelyne Lennette i 

SERIES INTRODUCTION- -by James Chin iii 

SERIES HISTORY- -by Sally Smith Hughes vi 

SERIES LIST xv 

INTERVIEW HISTORY--by Sally Smith Hughes xvii 

BIOGRAPHICAL INFORMATION xix 
INTERVIEW WITH JAY A. LEVY, M.D. 

I EDUCATION AND EARLY RESEARCH 1 
Undergraduate Research at Wesleyan University and Research 

in Paris 1 

Fellowships at the University of Paris, Orsay, France, 1961 2 
Medical Student, Columbia University, College of Physicians and 

Surgeons, 1961-1965 3 

Research in Medical School 4 

Research on Bacteriophage 4 

Research on Burkitt ' s Lymphoma 5 

Research on Reovirus 7 

Internship, 1965-1966, and Residency in Medicine, 1966-1967, 

University of Pennsylvania 8 

Research at the Wistar Institute 8 

Research with the Henles on Burkitt 's Lymphoma 10 

II PRE-AIDS RESEARCH 12 
Staff Associate, National Cancer Institute, National Institutes 

of Health, 1967-1970 12 

Robert J. Huebner 12 

Discovery of Xenotropic Viruses 14 

Second-year Resident in Medicine, University of California, 

San Francisco [UCSF] , 1970-1971 16 

Visiting Scientist, France, 1971-1972 17 

Hopital St. Louis, Paris 17 
Collaboration with Claude Jasmin, Mirek Hill, and Jana 

Hillova, Hopital Paul Brouse, Villejuif 18 

The University of California, San Francisco 19 

Assistant Professor of Medicine, 1972-1977 19 

Research on Endogenous Viruses 19 

Further Research on Xenotropic Viruses 20 

Research on Xenotropic Viruses in Humans 24 

Research on Anti-xenotropic Virus Neutralizing Factor 28 



Visiting Scientist, Weizmann Institute, July 1978- 

January 1979 30 

Visiting Scientist, Institut Pasteur, January 1979- July 

1979 30 

Research Cuts 32 

III THE AIDS EPIDEMIC 

Kaposi's Sarcoma, August, 1981 35 

National Cancer Institute Grant for AIDS Research, 1983 36 

The Kaposi's Sarcoma Clinic, UCSF 37 

Visit to Haiti and the Dominican Republic 38 

San Francisco AIDS Researchers 42 

The State of California Appropriation for AIDS Research, 1983 44 

AIDS Etiology and Heat Treatment of Blood Products 47 
Chasing the Virus 

The Gallo and Montagnier Teams 51 

Immunology Meeting, Japan, July, 1983 

More on the Levy Lab ' s Search for the Virus 

Carlton Gajdusek 55 

Hepatitis B as a Model for AIDS 56 

Levy Misses a Key Meeting 56 

Gallo Reverses His Stand on the AIDS Virus 58 

The French Group's Conclusion: A New Virus Causing AIDS 59 

Levy's First Reverse Transcriptase-positive Viral Isolates, 

Late 1983 61 

Announcing Levy's AIDS-Associated Retrovirus 62 

The UCSF AIDS Specimen Bank 64 

Research on Kaposi's Sarcoma 65 

Immune Deficiency 68 

Seropositivity Without AIDS 68 

Puzzling over Etiology 69 

The Immunofluorescence Assay for HIV 71 
More on RT-positive Viral Cultures, Fall 1983 

Visit to the Pasteur Institute, October 1984 73 
Research on Blood-clotting Factors 

More on Isolating AIDS-associated Retrovirus 76 

Press Conference on the Isolation of ARV, August 16, 1984 78 
Infecting Cell Lines 

More on the Immunofluorescence Assay for HIV 80 
Changing Research Foci 

Discovering the Importance of CDS Cells 85 

Collaborating with Chiron Corporation 86 
Cloning and Sequencing the Virus 

Controversy over the Virtual Identity of HTLV-III and LAV 92 

Mikula Popovic's Use of Pooled AIDS Virus 93 

Controversy over the Cell Line, HUT78 95 

Scientific Controversy and AIDS Research 96 
Giving the Virus an Official Name 

Patenting the Virus 99 

TAPE GUIDE 100 



APPENDICES 101 

A. UCSF News Release "UC-San Francisco Studies Confirm French 

Finding of Retrovirus in AIDS and Demonstrate a Retrovirus 

Could be Passed Through Blood Clotting Factor," May 8, 1984 101 

B. Letter to Jay A. Levy from UC Office of the President, 

Patent, Trademark, and Copyright Office, June 27, 1984 103 

C. "Virus Outpaces AIDS Here, Study Finds," San Francisco 

Examiner, July 1, 1984 105 

D. "HIV Survivors Who Have Beaten Disease," San Francisco 

Chronicle, August 9, 1994 107 

E. "Jay Levy Still Forging Ahead Despite Years of Being Ignored 

by Peers," UCSF News break, February 25-March 10, 1995 108 

F. "Proven Connection- -HIV Causes AIDS," San Francisco 

Chronicle, May 30, 2000 110 

G. Curriculum vitae, Jay A. Levy 112 

INDEX 156 



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 Shilts 1 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 changedalready, 
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 



ii 



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 exponentiallyfrom 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 



IV 



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 



vi 



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 epidemicnot 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 financial- -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 



'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 Shilts 1 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 . 



'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. 



ix 



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 UC Berkeley and 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 picturein this case, the medical and 
scientific aspects of AIDS in San Francisco. Thus the whole (the series) 



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



is greater than the sum of its parts (the individual oral histories), and 
should be considered as a totality. To encourage this approach, we decided 
to bind several oral histories together in most of the volumes. 

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 



xi 



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. A 



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 personalwhich 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. 



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

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



xii 



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



xiii 



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

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 
immediacythrough 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 yearsto 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 conflictpersonal 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 livesof 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. 



*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 



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. 

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 



XV 

December 2001 

THE AIDS EPIDEMIC IN SAN FRANCISCO: The Medical and Nursing Response, 1981-1984 
AIDS PHYSICIANS ORAL HISTORY SERIES: The Medical Response, 1981-1984 

Volume I 

Selma K. Dritz, M.D., M.P.H., "Charting the Epidemiological Course of AIDS, 1981- 

1984." 

Mervyn F. Silverman, M.D., M.P.H., Public Health Director: The Bathhouse Crisis, 
1983-1984." 

Volume II 

Donald I. Abrams, M.D., "The KS Clinic, Lymphadenopathy and AIDS-Related Complex, 

and the County Community Consortium." 

Marcus A. Conant, M.D., "Founding the KS Clinic, and Continued AIDS Activism." 
Andrew A. Moss, Ph.D., "AIDS Epidemiology: Investigating and Getting the Word 
Out . " 

Volume III 

Arthur J. Ammann, M.D. , "Pediatric AIDS Immunologist: Advocate for the Children." 
Paul A. Volberding, M.D., "Oncologist and Developer of the AIDS Clinic, San 

Francisco General Hospital." 
Constance B. Wofsy, M.D., "Infectious Disease Physician, AIDS Educator, and 

Women's AIDS Advocate." 

Volume IV 

Donald P. Francis, M.D., D.Sc., "Epidemiologist, Centers for Disease Control: 

Defining AIDS and Isolating the Human Immunodeficiency Virus (HIV)." 
Merle A. Sande, M.D., "Infectious Disease Specialist: AIDS Treatment and Infection 

Control at San Francisco General Hospital." 
John L. Ziegler, M.D., Ph.D., "Oncologist: Kaposi's Sarcoma and AIDS Research in 

San Francisco and Globally." 

Volume V 

Herbert C. Perkins, M.D., "Director, Irwin Memorial Blood Bank: Transfusion AIDS 
and the Safety of the Nation's Blood Supply." 

Volume VI 

Deborah Greenspan, D.D.S., D.Sc., "Oral Manifestations of AIDS." 
John S. Greenspan, D.D.S., Ph.D., "AIDS Specimen Bank, UCSF." 

Volume VII 

Warren Winkelstein, Jr., M.D., M.P.H., "AIDS Epidemiology at the School of Public 
Health, University of California, Berkeley." 

Volume VIII 

Jay A. Levy, M.D., "Animal Virology and the Discovery of the AIDS Virus." 



xvi 
AIDS NURSES ORAL HISTORY SERIES: The Response of the Nursing Profession, 1981-1984 

Volume I 

Michael J. Helquist, "Journalist of the Early AIDS Epidemic in San Francisco." 
Jeannee Parker Martin, R.N., M.P.H., "The AIDS Home Care Program of Visiting 

Nurses and Hospice of San Francisco." 
Helen K. Schietinger, R.N., M.F.C.C., "Nurse Coordinator of UCSF's First AIDS 

Clinic." 

Volume II 

Gary Stephen Carr, R.N., Ph.D., F.N.P.-C., "Nurse Practitioner at the AIDS Clinic, 

San Francisco General Hospital." 
Angie Lewis, R.N. , M.S., "Nurse Educator in the San Francisco AIDS Epidemic." 

Volume III 

Diane Jones, R.N., "First Wave of the Nursing Staff on the AIDS Ward, San 

Francisco General Hospital." 
Clifford Morrison, M.S., M.N., R.N. , F.A.A.N., "Organizer of the AIDS Ward, San 

Francisco General Hospital." 

Volume IV 

Gayling Gee, R.N., M.S., "Head Nurse at the AIDS Clinic, San Francisco General 

Hospital." 
Grace Lusby, R.N., M.S., "Infection Control Practitioner, San Francisco General 

Hospital." 
Diane Miller, M.P.H., "AIDS Policy and Administration at San Francisco General 

Hospital." 

AIDS COMMUNITY PHYSICIANS ORAL HISTORY SERIES: The Response of Community Physicians, 

1981-1984 

Volume I 

Richard Lee Andrew, M.D., "Psychiatrist and Advocate for Gay Medical Causes in the 

Early AIDS Epidemic." 

James M. Campbell, M.D., "AIDS Clinician and Medical Educator." 
James R. Groundwater, M.D., "Dermatologist Treating the First Kaposi's Sarcoma 
Patient Diagnosed in San Francisco." 

Volume II 

Paul Monahan O'Malley, "AIDS and the Hepatitis B Vaccine Trial in San Francisco." 
Stephen Follansbee, M.D., "Infectious Disease Practitioner in the Early AIDS 
Epidemic." 

Volume III 

Robert K. Bolan, M.D., "Medicine, Activism, and the Gay Community in San 

Francisco. 
William F. Owen, Jr., M.D., "AIDS Clinical Practice in the Private Sector." 



xvii 
INTERVIEW HISTORY--Jay A. Levy, M.D. 



Jay Levy was interviewed for this series because of his role as 
virologist in the small group of physicians and scientists following AIDS 
patients at the University of California San Francisco [UCSF] and San 
Francisco General Hospital [SFGH] in the early days of the epidemic. As he 
describes in the oral history, he began at this time to attend the Kaposi's 
Sarcoma Study Group at UCSF and to establish cell lines for research on the 
disease agent. Only subsequently did the group recognize that Kaposi's 
sarcoma [KS] was only one manifestation of the syndrome which came to be known 
as AIDS. 

The oral history is largely a recounting of Levy's science from his 
undergraduate days through the discovery and early depiction in the mid-1980s 
of the virus which we now know as HIV. The first interview is almost wholly 
devoted to his pre-AIDS research in animal virology, some of it in exotic 
parts of the world. It is a revealing account of mid-century virological 
research and sets the stage for Levy's entry into AIDS science. As he 
explains, it was his decades-long research on viral links to cancer that 
sparked his interest in Kaposi's sarcoma, the skin cancer being reported in 
gay patients by his physician colleagues at UCSF and SFGH as early as 1981. 
He remarks that the discovery of AIDS in hemophiliacs in 1982 convinced him to 
switch to investigating the blood of AIDS patients in his search for a causal 
virus. In the process, he demonstrated that heat treatment destroyed the 
infectious agent in blood clotting factors used by hemophiliacs. The finding 
he took to be evidence that the agent was likely a virus and gave impetus to 
his attempt to identify what he now suspected was a new virus, rather than a 
variant of a known type, as he and others originally believed. 

Although science is center stage in this account, science politics is 
also much in evidence. AIDS has been called the most highly politicized 
disease in history and no episode was more highly politicized than the race to 
isolate and characterize the virus. The contenders were Robert Gallo at the 
National Cancer Institute with its ready access to the abundant resources of 
the National Institutes of Health, the Pasteur Institute group in Paris under 
Luc Montagnier with far more modest support, and Jay Levy in his under- 
equipped and meagerly staffed lab at UCSF. As a participant in the 
contentious race to discover the virus, Levy conveys an insider's view of the 
scientific and political chaos and discord of this period. In the end, 
Gallo 's claim to be discoverer of the AIDS virus was discredited, the French 
group at the Pasteur Institute in Paris acknowledged as the winner, and Levy, 
working with his own viral isolate (AIDS-Associated Retrovirus), credited as 
the second to isolate the virus and the first to confirm the Pasteur group's 
finding. 

But Levy's description of intense scientific competition does not end 
with this episode. He goes on to describe bitter controversy over the patent 
on the AIDS antibody test and the lavish royalties expected to flow from it, 
the multi-party race to clone and sequence the AIDS virus, and the eventual 
agreement to name the virus human immunodeficiency virus, the now-familiar 



xviii 

HIV. All this is set against Levy's long-standing battle, as he sees it, for 
sustained institutional support and recognition. 
The Oral History Process 

Three interviews were conducted in Levy's cramped and colorful office in 
the Cancer Research Institute at UCSF--colorful because several of his 
"primitives" (oil paintings) hang on the walls. With characteristic 
exuberance and enthusiasm, Levy recounted his story, not always adhering to 
standard chronology nor the detached language of science. His colorful and 
outgoing personality can be glimpsed in the pages of this volume. Not 
surprisingly, he was intent on establishing his place in AIDS history, 
particularly in regard to the discovery of the AIDS virus. Much more remained 
to be clarified at the conclusion of the interviews, but Levy felt compelled 
to stop recording and get on with yet another hot research topic, the role of 
the immune system in preventing the appearance of AIDS in long-term survivors 
of the disease. 

Dr. Levy reviewed the transcripts twice, in a few instances taming off- 
the-cuff remarks. The history stands as a distinctively personal view of 
banner episodes in early AIDS history, as well as of less-publicized areas of 
virology. 

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 Richard Candida Smith, Director, and the 
administrative direction of Charles B.. Faulhaber, James D. Hart Director of 
The Bancroft Library, University of California, Berkeley. The catalogues of 
the Regional Oral History Office and many online oral histories can be 
accessed at http://librarv.berkelev.edu/BANC/ROHO. 



Sally Smith Hughes, Ph.D. 

Historian of Science and Project Director 

Regional Oral History Office 
The Bancroft Library 
University of California, Berkeley 
November 2001 



xix 



Regional Oral History Office 
Room 486 The Bancroft Library 



University of California 
Berkeley, California 94720 



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BIOGRAPHICAL INFORMATION 
(Please write clearly. Use black 'ink.) 
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Date of birth 



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Birthplace 



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Father's full name 
Occupation /A-ci 



Birthplace 






Mother's full name 

Occupation 
Your spouse 



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Birthplace 



Occupation 



Birthplace 



Your children 



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Where did you grow up? 
Present coimnunity -^cZe^n 
Education 



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Occupation(s) 




Areas of expertise 



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INTERVIEW WITH JAY LEVY 



I EDUCATION AND EARLY RESEARCH 



[Interview 1: February 16, 1993] 



Undergraduate Research at Wesleyan University and Research in 
Paris 



Hughes: Dr. Levy, let's start with where you were born and educated. 

Levy: I was born on November 21, 1938, in Wilmington, Delaware. I am an 
identical twin, second born. My education was in public schools 
up until I went to college in 1956. I graduated from Wesleyan 
University in 1960 with a major in biology. I almost had a double 
major, because I had almost the same number of units in French 
studies. I became a teacher's assistant in the biology laboratory 
for students, so that made me put my major emphasis in biology. 

At college, I also did research on the anaerobic respiration 
of fungi and what biochemical aspects are involved in regulation 
of this process. It involved very intricate biochemical 
measurements as well as assessing physiological parameters. 
Actually, the topic was not very interesting, but I had no choice 
since Dr. Vince Cochrane was the only professor who was free to 
take a student for a research project. I already knew then I 
wanted to do research. 

Vince Cochrane had a reputation of being a tyrant and he 
proved to live up to that reputation with me! I finally told him 
off on my twenty-first birthday, when he reprimanded me for 
breaking a Warburg vessel during the washing after a long 
experiment. I announced I was treated like a robot by him and did 
not feel comfortable in his lab. I left to celebrate my birthday. 
Ironically, after that everything changed for the better and 



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



Cochrane treated me with more respect, I thought. I even got a 
paper out of this research. 1 But I always say, this experience 
was the easiest way to turn a student off, to work under a man 
like that. He had a nice heart, but was a very strange person in 
the lab. 



Fellowships at the University of Paris, Orsay, France, 1961 



Levy: Then I won Fulbright and French government fellowships to go to 
France in 1961. I went there to take a break and do research. 
Unfortunately, there again, I got into a topic that wasn't the 
most demanding. I studied regeneration of planaria and the 
effects of different heavy metals on the ability of these fresh 
water flatworms to regenerate their heads and tails. 

Hughes: Was that a pet project of one of your mentors? 

Levy: When you were accepted into the fellowship program, you were 

assigned to a laboratory. You didn't have much choice, but I did 
request Paris. So I was assigned to the Laboratoire de Biologic 
Animale at the University of Paris in Orsay. I worked under 
Professor Theodore Lender, who was a former student of Etienne 
Wolff, one of France's most illustrious embryologists and cell 
biologists. 

I had a twenty-minute train ride from Paris to the Orsay lab. 
I thus lived in Paris and commuted. It was a new experience, 
because I did nothing but research the whole time--no course work. 
The first week I got there, Lender told me to go out and find 
planaria. That was my first week's job. I was lucky; I found 
them the first day. But I also was clever; I didn't tell Lender 
until the end of the week, so I had a week to enjoy Paris 
[laughter] and do what I wanted. I love to paint, so I made 
sketches by the Seine. That was such a nice way of getting to 
know Paris . 

Hughes: Are these your paintings on the wall? 
Levy: Yes, these are my "primitives." 



1 V. W. Cochrane, S. J. Berry, F. G. Simon, et al., "Spore germination 
and carbon metabolism in Fusarium solanl. III. Carbohydrate respiration in 
relation to germination," Plant Physiology 1963, 38:533-541. 



Medical Student. Columbia University. College of Physicians and 
Surgeons, 1961-1965 



Levy: When I finished in Paris, I went to medical school at Columbia. I 
had been accepted there in 1960 but took a leave of absence to do 
research in Paris. 

Hughes: Had medical school always been your ambition? 

Levy: Well, at one point, I thought I wanted to be in international 
affairs. In my third year at Wesleyan, I went to see Sigmund 
Neumann, who was head of the Ford Foundation and professor of 
history at Wesleyan and a brilliant historian. Everyone idolized 
him. I was one of those students who looked up to the really 
great professors and enjoyed being around them and hearing them 
talk. 

Neumann got to know me through one of his classes. I said to 
him I couldn't make up my mind between being a doctor and going 
into international affairs . He ' s the only one in my whole life 
who has ever told me what to do, and I don't know why he did it. 
He said, "You can always do international affairs as a hobby. If 
you like medicine, go after that degree." I love that story, 
because what I'm doing now is international medicine. 

Moreover, when I went to Columbia in 1961, I got into the 
International Fellows Program, which was a new program which 
brought people together from all the different disciplines. I was 
the only representative from the medical school. They had law, 
art, journalism, writingit was fantastic. I did my thesis on 
"The Role of International Medicine," and it went very well. 

During all the summers at medical school, as you can see in 
my curriculum vitae, 1 I chose to do research and medicine. 
Sputnik had come out in '57, so there was tremendous thrust on the 
part of the U.S. government to put young people into research. I 
took advantage of that effort. 

Hughes: Had you thought that rather than practice medicine as a clinician 
you would go into research or an academic career? 

Levy: Yes. That's why I did research at Wesleyan even with that 

difficult professor. I wanted to teach and do research at a 
collegethen realized I wanted a medical school career. 



'See the appendix to this volume. 



Research in Medical School 



Levy: As I mentioned, I applied and received fellowships every summer 

during medical school. The first summer [1962], I went to Israel 
and did public health in a clinic at Hebrew University. The next 
summer, I went to Sweden and worked at the Karolinska Institute 
with the famous couple, Elizabeth and Giovanni (Joe) Bertani. I 
worked with bacteriophages, which are viruses of bacteria. I 
studied ways in which one could activate these viruses out of 
bacteria that did not show their presence. I was very interested 
in the possibility that cancers were caused by viruses that 
inserted themselves into the DNA of a cell and set up a state of 
silence or hidden existence but exerted their transforming effects 
on the cell. The lysogenic bacteriophages that can remain silent 
in a host bacterium are a good model, and the Bertanis were 
studying these agents. I recall that at Wesleyan I had read a 
paper by Raymond Latarjet at the Institut Radium in Paris on this 
issue in 1960 in Cancer Research. 1 So I pursued latent viruses in 
relationship to cancer. (My twin brother Stuart later with 
Latarjet in Paris in 1962. Ironically, Luc Montagnier was in the 
lab as a student at the same time.) 

Hughes: Was this before the topic was fashionable? 

Levy: Well, I don't know if it was or wasn't fashionable. It wasn't 
unusual for me to talk about, it, and this theory that viruses 
cause cancer in humans was considered at that time. In the late 
fifties, they knew there were various viruses that caused cancers 
in animal species, so I don't think it was a novel idea. But in 
human cancer, perhaps, the process of lysogeny provided a theory 
of why you couldn't find a virus. I thought it was hidden in the 
cell.' 



Research on Bacteriophage 

Levy: In my second year of medical school, I also did research with 
Herbert Rosenkranz on these viruses of bacteria and discovered 
some interesting things about drugs, like hydroxyurea, that were 
being developed for possible anti-cancer therapy. We chose 
hydroxyurea because it resembled hydroxyamine that activated 
viruses from bacteria. To my surprise, I found that hydroxyurea 



J R. Latarjet, "Viruses in relation to other carcinogenic agents: 
Discussion of Dr. Stanley's paper," Cancer Research 1960, 20:807-815. 



blocked the ability of the bacterium to divide, and it just got 
bigger and bigger. 

That's one of my great examples for students of serendipity, 
because if you looked at the protein content of the bacteria you 
were studying, it went up and up, so I assumed that the bacteria 
were replicating like crazy. But when I plated them, I found the 
number had not changed over an eighteen-hour period. Under the 
microscope, we saw these huge bacteria. So with hydroxyurea, 
while we stopped the bacteria from dividing, they could still 
continue protein synthesis. 1 It was pretty exciting to be 
involved in those early phases of work on hydroxyurea- -now an 
anticancer drug. 



Research on Burkitt's Lymphoma 

Levy: I continued to do research in my junior year of medical school and 
did some work with Harry Rose on vaccinia virus. I wanted to get 
into human virus systems. I was fascinated by Burkitt's lymphoma. 
In 1959, Denis Burkitt had described this tumor in children and 
thought it might be caused by a virus. I wanted to find the virus 
that causes that human cancer. So I did what I advise my students 
to do: I listened to one of Parkinson's laws, which is energy 
expended in one direction can come back in another direction. I 
used to send out letters immediately when I returned from one 
summer trip, in order to find a position for another summer. I 
wanted to go to Africa. The only possibility was a Louisiana 
State University Medical Fellowship, but they were all given for 
studies in Latin America. I wrote the organization anyway and 
told them why they should pick me to go to Africa to do research 
in tropical medicine. 

Hughes: That was their emphasis? 

Levy: Yes, their emphasis was tropical medicine. I wanted to study 

Burkitt's lymphoma. I was lucky. They gave the fellowship to me. 
Well, it had wonderful ramifications. I worked with Denis Burkitt 
in surgery and with Thomas Bell at the East African Virus Research 
Institute in Entebbe, Uganda. In fact, it was the first time I 
worked with animal viruses. For this work, I needed normal monkey 
kidney cells. Therefore, I had to sacrifice a rhesus monkey, take 



1 H. S. Rosenkranz, J. A. Levy, "Hydroxyurea: A specific inhibitor of 
deoxyribonucleic acid synthesis," Biochimica et Biophyslca Acta 1965, 
96:181-183. 



out the kidneys, put the kidneys in culture, and then look in the 
Burkitt tumor cells for viruses that could cause Burkitt's 
lymphoma. Thomas Bell had found a virus called reovirus type 3 
in a tumor, and I was there to see if he was right about this 
virus's involvement in Burkitt's lymphoma. 

That research led me into working with Alexander Haddow, who 
was head of the institute, who I think had discovered more viruses 
than anyone I know by just grinding up mosquitoes. These were 
arboviruses. In some of my studies, I actually climbed trees to 
catch mosquitoes. 

Hughes: This was for research on Burkitt's lymphoma? 

Levy: Yes, in part. Arboviruses are transferred by mosquitoes. 

We thought maybe the virus that causes Burkitt's was 
transmitted by a mosquito, because the distribution of the cases 
mirrors the distribution of mosquitoes in Uganda. We were 
interested in trying to find reovirus type 3 in mosquitoes. The 
experience was unbelievable: I climbed a tree with an African 
counterpart, and we were asked to expose our legs, because Haddow 
and Bell were only interested in the Aedes aegypti mosquito, which 
only bites the lower legs. We were to be paid one shilling a 
mosquito. Each of us collected mosquitoes from the other. My 
African counterpart needed the money more than I did, so he always 
let the mosquito bite him for me to collect it. I found that I 
always hit and killed the mosquito on me when it bit me--and if it 
wasn't living, it wasn't any good for the studies. So he lost a 
little bit of money with me. But it was lots of fun and a new 
experience. 

Hughes : What did you accomplish? 

Levy: Not much with the mosquitoes, although we tried to find a virus in 
them using the monkey kidney cells . I collected sera from 
patients with Burkitt's lymphoma, and, toward another objective, 
sera from normal children. I traveled all over Uganda looking at 
Burkitt's lymphoma cases, but I also did some work with malaria 
transfer through placentas, and I did work in the country with 
nutrition. It was an unbelievable experience- -tropical medicine 
and research, combined with living out, taking care of people in 
the outer parts of Africa, working in clinics and so forth. 



Research on Reovirus 



Levy: I came back to my fourth year at Columbia, and because of my 

interest in reovirus type 3, Ed Curnen, who was head of pediatrics 
and a virologist, offered me space in his lab to work in my spare 
time. So actually I was able to do research in my second, third, 
and fourth years of medical school. 

In that experience, I met Eru Tanabe who was a Japanese 
technician who ran the diagnostic virology lab for Curnen. She 
became my teacher and an unbelievable friend who taught me 
everything that I know about various ways of finding viruses, 
including hemagglutination assays, hemadsorption procedures-- 
every thing. I am very grateful. She and I wanted to prove that 
anti-reovirus type 3 antibodies were increased in Burkitt cases 
versus normal controls . l That meant that we had to run our 
hemagglutination assays around the clock, so we had alarm clocks, 
and we'd sleep in the lab, and we'd wake each other to change 
shifts. Thus we would do the assays alternately. We had to 
finish the study, so when I went to Philadelphia the next year 
[1965], Eru came for a visit, and we did the alarm clock routine 
again and completed the work. My training with Eru was a 
wonderful introduction to the varied fields of virology. 

We proved that we were right. There were more antibodies to 
reovirus type 3 in Burkitt cases than in the controls. Then we 
learned what you have to learn in research, that controls must be 
well selected. The ones I used came from outside the hospital. 
If we had gotten our controls from the hospital, we would have 
seen no difference, because reovirus type 3 was circulating around 
the hospitals! [laughs] 

So that introduction to virologic questions was very 
interesting. I got a lot of experience, and Burkitt 's lymphoma 
got a lot of my attention. And I was right there, at the very 
beginning. Sixty-four, I was in Africa, and '64 the Epstein-Barr- 
Achong paper came out describing herpes virus-like particles in 
Burkitt ' s lymphoma cells . 



'J. A. Levy, E. Tanabe, E. C. Curnen, "Occurrence of reovirus 
antibodies in healthy African children and in children with Burkitt ' s 
lymphoma," Cancer 1968, 21:53-57. 



8 



Internship. 1965-1966. and Residency in Medicine. 1966-1967. 
University of Pennsylvania 



Research at the Wistar Institute 



Levy: When I finished at Columbia, I went to the University of 

Pennsylvania for my internship and residency in medicine. When I 
got to the University of Pennsylvania, I didn't want to stop doing 
research, so I went to the Wistar Institute, which is across the 
street from the medical school and hospital. I was doing an 
internship and residency, two years there, and I had gotten 
accepted at the NIH [National Institutes of Health] to do research 
as a public health officer instead of going to Vietnam. I was to 
work under Robert Huebner, one of the country's leading 
virologists at the time. And that, of course, was a great way of 
putting in military service. 

However, in that first year at Penn [1965], during my 
physical examination at the military unit for induction into the 
army or Public Health Service, I stupidly showed the physician 
that my left foot was deformed because I had osteomyelitis when I 
was a child. Well, that then opened up a whole can of worms, and 
they said they couldn't accept me in the Public Health Service 
because they didn't want anyone with a previous history of 
osteomyelitis, because it might flare up again, and the Public 
Health Service didn't want to pay the cost of treatment. Of 
course, almost immediately the army wrote that it was inducting me 
into Vietnam. So this was just a horrible period for me. I 
wanted so much to go to NIH. 

The University of Pennsylvania was fantastic. It built a 
wonderful case for me on why the Public Health Service shouldn't 
worry about me. I agreed to sign all sorts of waivers, although 
the Public Health Service said there was no such thing as a 
waiver. The person who really did it for me was the former 
surgeon general, Luther Terry, who was the well-known advocate 
against smoking. Luther Terry became vice president of the 
University of Pennsylvania, and I went to see him. He had all the 
connections, and with the help of several department heads at 
Penn, he got me into the Public Health Service, and I was able to 
go to NIH. 

So with that assured, I went to Wistar, and told Hilary 
Koprowski, the director, I wanted to continue my work with 
reovirus type 3 and Burkitt's. He said he didn't want to have a 
new virus in his institute, and that I should talk to Vittorio 
Defendi and learn about lymphocytes. So I went to see Dr. 



Defend!, who was a well-known immunologist/virologist. He agreed 
that I could work with him on lymphocytes. All these things have 
played beautifully into my career, but they were decided by crazy 
quirks of fate. I'm very much a fatalist. 

My medical colleagues at the University of Pennsylvania used 
to call me the Wistar fellow, because I had a beeper and it was 
only fifteen seconds from the Wistar Institute down the steps, 
across the street, into the emergency room or to the ward. So it 
wasn't any different than being on call in your dorm. So I just 
did research at Wistar when I had some free time and used my 
beeper. 

That first week after speaking to Koprowski, I ran into Angus 
Graham, whom my brother had known at Penn. I have a twin brother, 
Stuart, who was a medical student at Penn and did research in 
microbiology, and then moved up to New York for his internship. 
We kind of exchanged places. He went to Mt. Sinai [Hospital], and 
actually inherited some of my patients who were at Columbia, 
because there was a connection between Mt. Sinai and Columbia. 
And I went to Penn and inherited some of his patients. 

I ran into Angus Graham at the Wistar Institute and I said, 
"What are you working on?" He said, "Well, my usual subject: 
reoviruses." I said, "Reoviruses? I didn't think reoviruses were 
in this institute." He said, "They sure are, on the third floor." 
[laughing] That's how I realized that Hilary Koprowski just 
didn't want me to work with Angus Graham, and he assigned me to 
Vittorio Defendi. When I told Hilary about it, he laughed. He 
said, "Why do you want to work with animal viruses? You should 
get into human systems." Sounds providential now. 

Hughes: Did you switch projects? 

Levy: I stayed in lymphocytes and was among the first to describe 

transformed B lymphocyte cell lines. They were first made in the 
early sixties, and we wrote one of the first papers. 1 We weren't 
the first. The lymphocytes were transformed because they had 
Epstein-Barr virus. That finding was ironic since I had begun 
work on that virus with the Henles. 



J J. A. Levy, M. Virolainen, V. Defendi, "Human lymphoblastoid lines 
from lymph node and spleen," Cancer 1968, 22:517-524. 



10 



Research with the Henles on Burkitt's Lymphoma 

Levy: While I was in the emergency room at Penn the first few months, I 
got a phone call from Werner Henle whom I wanted to meet. Now, 
Werner Henle was the thesis advisor of my sister, Ellen [Levy] , 
who's also in research and now a doctor. She was doing research 
on interf eron and was working with Kurt Paucher in Werner Henle ' s 
laboratory unit. Henle and his wife, Gertrude (Brigitta) , were 
among the world's great virologists. 

Anyway, Werner Henle called, and he said that he was giving a 
lecture on Burkitt's lymphoma at Columbia and that he had been 
looking all over for sera from children with Burkitt ' s lymphoma 
versus children that didn't have Burkitt's. So one of the doctors 
in the pediatrics department at Columbia, Hatie Alexander, said, 
"Well, we just had a student who came back from Africa, and he has 
all these sera." "Who is it?" "Jay Levy." "Where is he?" "He's 
at the University of Pennsylvania." That's all part of Brigitta 
Henle 's "blue flower story." The blue flower story is about the 
man who looks all over the world for this famous blue flower, 
comes back to his house twenty years later, goes to the back 
garden, and there it is, growing. 

When the Henles were looking for the virus of Burkitt ' s 
lymphoma, their technician got infectious monofnucleosis] , and 
they had the clever insight to look to see if her white cells 
might be established in culture, and they found Epstein-Barr virus 
in this infectious mono case. They had their African sera through 
my connection to Ellen. 

I went down to Children's Hospital, and the Henles said, 
"We're going to teach you immunof luorescent testing, and if you 
like you can do this research in the late evenings and over the 
weekends." So I worked in the evenings and on weekends at 
Children's Hospital way down in a really miserable part of 
Philadelphia, Bainbridge Avenue, and I handled as well a very 
heavy clinical program as an intern and resident. 

But I was able to pull it off, and I had some nice 
publications with the Henles. In fact, the first one that we 
published, 1 showing differences in antibodies to the Epstein-Barr 
agent, (we didn't know what it was then) got selected in JAMA for 
an editorial. And I'll never forget it, because Mrs. Henle called 



'J. A. Levy, G. Henle, "Indirect immunofluorescence tests with sera 
from African children and cultured Burkitt's lymphoma cells," Journal of 
Bacteriology 1966, 92:275-276. 



11 



me in and said, "Jay, you've made it. They actually call you a 
scientist in this editorial." [laughter] And there it was, 
"Levy and Henle, scientists at the--" Of course, they didn't know 
who the hell I was . 

I worked on the reovirus problem with the Henles as well, and 
actually showed that reovirus could affect EBV [Epstein-Barr 
virus] replication and came up with a good publication in Nature. 1 
And with Vittorio Defendi, I worked on B cell lymphomas, and then 
the two subjects came together, because EBV [ Epstein-Barr virus] 
is involved in both. Very ironic. 



'J. A. Levy, G. Henle, W. Henle, et al., "Effect of reovirus type 3 on 
cultured Burkitt's lymphoma tumor cells," Nature 1968, 220:607-608. 



12 



II PRE-AIDS RESEARCH 



Staff Associate. National Cancer Institute, National Institutes of 
Health. 1967-1970 



Robert J. Huebner 



Levy: After Perm, I went to NIH and I was told by Robert Huebner, who 

was now my mentor, that I was to throw away the work with Epstein- 
Bar r virus --that was in '67 --that I was to work on RNA tumor 
viruses. 

Hughes: Why did he say that? 

Levy: Because he didn't think much of herpes viruses. Actually, he 

didn't want me to work on RNA tumor viruses right away; he advised 
me to work on the adenoviruses, which had been found in the early 
sixties to produce tumors in hamsters by John Trentin. Huebner 
thought' maybe these viruses would be involved in human cancers, so 
they needed reagents to test the hypothesis. They wanted me to 
grow up adenoviruses and polyoma viruses. 

Huebner was one of those enormous giants in virology, made 
all sorts of discoveries, and of course it hits me hard when no 
one knows him anymore. Unfortunately, he now has Alzheimer's and 
is in an institution. But brilliant, and I'll always remember his 
energy. 

Hughes: As I remember, he revitalized the cancer virus story, which had 
been a theme that had waxed and waned since Peyton Rous ' s work 
around 1912. 

Levy: Oh, yes. Huebner was one of the key people to convince Nixon to 
set up the cancer virus program. 

Huebner farmed me out--he was criticized later for having 
all these contracts at different companies--to this company in 



13 



Rockville [Maryland] where they had been working for two years to 
grow up lots of adenovirus and to express viral proteins. Then 
the protein can be concentrated and used for detection assays. 
One can look for antibodies to specific viral proteins in cancer 
patients. They weren't able to accomplish this objective, 
however, with the adenoviruses and the polyoma viruses. 

Huebner said, "You're to work on this problem. You're not 
to work on the herpes viruses." Well, I hadn't finished up my 
last experiments on some of the B cell lines. I tell this story 
because it was so amusing. He'd come in to visit me and he'd go 
to the incubator and he'd say, "What's this? Are they the 
lymphoma cells? Throw them out." I did, but I always had another 
incubator with the cells growing. Finally, I finished up the 
research. He was right. That last paper on established B cell 
lines infected by the herpes virus Epstein-Barr wasn't all that 
important, but I had to complete the work. 

For this new challenge with adenovirus I was able to draw 
from my work with hydroxyurea at Columbia. I said, "Look. If 
hydroxyurea makes a bacterium produce more protein but not divide, 
maybe hydroxyurea will cause the virus to make more and more 
protein but not destroy the cell, because the virus can't 
replicate." And it worked. 

But apparently I was too young to be given credit for that 
discovery. The people at the company who had been working on it 
for a long time became jealous. They started to bad-mouth me. 
I'm not really sure what they said, but I know that they said 
enough that Huebner took me off the project completely. I 
fortunately was still able to publish the paper that showed the 
effect of hydroxyurea. One man even poisoned my animals. So all 
the things you hear about what can go on in labs can unfortunately 
be correct at times. So I'd say that was the second trauma in my 
life, the first being my almost going to Vietnam and not NIH. 

Now I'm at NIH with Robert Huebner, and now I'm in his bad 
favor and I don't know how to tell him otherwise, and I see this 
all as a conspiracy against me, alone and young. I did not know 
what to do. Fortunately I could go see Mike Oxman, who had 
befriended me- -a nice young fellow working with Wallace Rowe. 
Now, Wally Rowe was one of the great virologists working with 
Huebner. He discovered adenovirus and cytomegalovirus . I really 
wanted to work with Rowe, not be off the NIH campus. But you had 
to go where your mentor wanted you. Janet Hartley was also there 
with Rowe, and I admired them both. Mike talked to Rowe, and Rowe 
spoke to Huebner- -that was lucky. 



Levy: But I was soon called into Huebner's office, and I was given what 
everyone later told me was the "annihilation" speech, which led me 
to tears. Huebner said: Who was I to talk against these people I 
was working with? I was a young person, only been at NIH a few 
months; how did I know what was going on? 

Hughes: So this was a theme with Huebner--if the speech had a name, it had 
happened before. 

Levy: Yes, that had happened to other young people who came in. 

The most amazing thing about Huebner is after the whole 
speech is over and I'm absolutely distressed, he then turns to me, 
smiles, and says, "Now, let's go to dinner." I said, "I can't." 
I couldn't! And I left. 

Well, we became good friends after that. Huebner assigned 
me to Wally Rowe. I had glorious times with Wally Rowe and Janet 
Hartley. I'll never forget an early experience. Huebner had a 
mouse that had arrived from Miriam Finkel that was infected with a 
virus that causes bone tumors. Rowe said, "Jay, this is your 
project. You're to get the virus out, and you're to figure out 
why it does what it does . " 

I worked alone, lots of hours, but I had a wonderful time in 
Washington. I was a bachelor; my brother Stuart was there at the 
same time, and we lived together and often had parties for our 
friends. We had a cute little carriage house in Georgetown- -three 
of the most marvelous years. I didn't make much money, but it was 
more money than I'd ever had in my life. The research went well. 



Discovery of Xenotropic Viruses 

Levy: I didn't have many publications until the third (last) year when 

things really hit. It was at NIH that I discovered the xenotropic 
viruses, and that was again serendipity, like the Henles finding 
EBV. There was a mouse called the New Zealand Black [NZB] mouse, 
which I always say is the most published mouse in history. It 
gets autoimmune disease and cancer, and I was interested in these 
diseases. Many had described virus particles in these mice, but 
no one could get the virus out. They all said the virus was 
defective. 

Here I drew from my first independent project with Wally, 
Jan, and Huebner. I had been working with the Miriam Finkel 
sarcoma virus, and other viruses, and I realized that transforming 



15 



genes in tumors can be rescued by helper viruses, by other RNA 
viruses that may induce leukemia or may not. If you mix the cells 
together under the right conditions, you'll rescue the sarcoma 
virus genome in the envelope coat of the helper virus. And then, 
you can look for that transforming virus by cell transformation. 
In other words, you take the culture fluid from mixed cells (the 
transformed and the virus -producing) and add it to a new flat 
monolayer of cells. If the sarcoma virus is rescued, you see foci 
of transformation in culture. Well, I said, maybe the NZB mice 
have such a helper virus; it isn't an infectious virion, but 
perhaps it will rescue a sarcoma virus genome. So I can at least 
show some biologic effect of the NZB virus. 

Hughes: This system had been previously worked out? 

Levy: This system had been worked out by Huebner, Rowe, and Hartley for 
the rescue of sarcoma virus genomes from cells. 

Now another story came into play: Huebner, Rowe, and Hartley 
(I called them the triumvirate) didn't know why you needed two 
particles to get cell transformation in mouse embryo cells or 
chicken embryo cells plated in a dish. I worked with a friend and 
colleague named Robertson Parkman, who was also one of the young 
public health appointees, non-Vietnam group. It was a marvelous 
group. It was highly competitive to get to NIH; if you were lucky 
enough to get there, you met some wonderful future productive 
scientists. 

Robbie was interested in transformation of rat cells. In 
the midst of working with him, I discovered that in mouse embryo 
cells you need two particles for transformation, but in rat cells 
you only needed one particle. 1 And it became clear that the 
reason you needed two particles in mouse embryo cells is that the 
transformed cell died, and you had to constantly produce virus 
progeny to recruit cells into a transformed focus big enough to 
see. In rat cells, the transformed cell didn't die; the rat cell 
grew autonomously into a transformed focus. 

So I said, "This is a great system when I go to find out if 
this NZB mouse virus can rescue a sarcoma virus genome from a 
tumor cell containing that gene. I'll put the fluid from the co- 
cultured cells into mouse embryo cells to see if the NZB-rescued 
virus replicates. And if I put the fluid into rat cells, at least 
I'll know if the NZB virus is biologically active and can rescue 
the sarcoma virus." So if the NZB was a defective virus, it 



! R. Parkman, J. A. Levy, R. C. Ting, "Murine sarcoma virus: The 
question of defectiveness, " Science 1970, 170:326-327. 



16 



wouldn't grow, and I wouldn't see anything in the mouse cells but 
I would in rat cells if I just got a rescue of the sarcoma virus 
genome. Foci of cell transformation would appear. Well, it 
happened unbelievably: I got foci of transformation in rat cells, 
and I didn't get anything in the mouse cells. 

I went to see Wally Rowe, and he didn't think I filtered the 
culture fluid correctly, so I put lots of bacteria in the co- 
culture fluid and then passed it through the filter. Sure enough, 
the bacteria were filtered out, and I got transformation in the 
rat cells. He still didn't believe it, and he had Ted Pincus, who 
was in the lab as well, a good friend of mine, do the experiment 
independently. So Ted did it independently with my coaching. 
Then Rowe believed the observation, and he allowed us to publish 
it on our own. 1 So that is the Levy-Pinkus story on xenotropic 
viruses, but at the time we called the virus the NZB virus. I 
couldn't really get good replication of the NZB virus, but I knew 
this virus would not infect mouse cells even though it came from a 
mouse. I thought it was unique for NZB. 



Second-year Resident in Medicine. University of California, San 
Francisco [UCSF1 . 1970-1971 



Levy: When I left NIH [in 1970], I came to San Francisco to complete my 
residency training. During that year I helped a bit in Tim 
Crocker's lab on chemical transformation of cells. 

Hughes: How had you originally gotten to UC as a second-year resident? 

Levy: John Mills, who was a friend of mine, worked with Bob Chanock at 
NIH on influenza virus. He said, "Jay, you ought to go out to 
California to do your last year of clinical training as a second- 
year residentjust for a lark." [Lloyd Hollingsworth] Holly 
Smith, the head of the medicine department, accepted me. There 
was a group here headed by Tim Crocker doing research on chemical 
carcinogenesis, chemical transformation of human cells, and they 
had money from the Council for Tobacco Research, which is a 
research organization funded by tobacco companies. 

The council asked if I'd be willing to be a consultant to 
them on a grant on cell transformation. Well, that was a great 



*J. A. Levy, T. Pincus, "Demonstration of biological activity of a 
murine leukemia virus in New Zealand Black mice," Science 1970, 170:326- 
327. 



17 



opportunity. I started asking questions about viruses as co- 
carcinogens with chemicals. So I had that wonderful opportunity 
to interact with basic research at the level of co-carcinogenesis 
while I was doing my second-year residency. 



Visiting Scientist. France. 1971-1972 

Hopital St. Louis, Paris 

Levy: Then in May [1971] I went off to France on an invitation to teach 
retrovirus techniques to Michel Boiron's group in Paris. 
Interestingly, when I got to the Hopital St. Louis, they were 
looking at transformation of human cells with a mouse retrovirus. 

Hughes: And they didn't know any retrovirology? 

Levy: They knew some, but they wanted me to do special assays with them. 
Well, I began working there, and in the midst of looking at 
transformation of human cells, I began thinking about the NZB 
virus and wondering whether it could infect human cells . But I 
didn't do anything with this idea for a year, and no one took up 
the NZB story. In fact, I was not beloved by many in the 
scientific community, especially Frank Dixon, who worked as well 
on the NZB mouse and said, "Levy has a rat virus." 

Hughes: Which was a retrovirus? 

Levy: Yes, they're all retrovi-ruses , but that was in 1970 when they were 
known as RNA tumor viruses . 

Hughes: Did people believe that retroviruses could not infect human cells? 

Levy: Yes. 

Hughes: But you didn't believe that? 

Levy: I wasn't buying into any of the dogmas. 



18 



Collaboration with Claude Jasmin, Mirek Hill, and Jana 
Hillova, Hopital Paul Brouse, Villejuif 

Levy: After six months with Boiron in which I studied transformation of 
human cells by an unusual mouse virus (because we incorrectly 
thought it was unique) , I then went to work with George Mathe at 
the Cancer Institute in Villejuif, which is a very well-known 
research center. There, I worked on transformation of cells as 
well. The lab I went into was Claude Jasmin's, who's a very close 
friend and France's leading oncologist now. We were peers, and 
Claude turned his lab over to me and asked if I would direct it. 
He had tuberculosis and had to leave for six months for the 
mountains. So I directed his lab and worked on Friend leukemia 
[virus], which is a mouse leukemia virus. Most of my studies, 
however, dealt with inhibitors of the mouse virus and not so much 
with Friend virus. 

During this time, I began trying to transform cells with 
DNA. It was a brand-new technique that had been discovered by the 
couple, Mirek Hill and Jana Hillova from Czechoslovakia. I became 
friends of theirs. They extracted DNA from cells that were 
infected with the avian RNA tumor virus, Rous sarcoma virus, which 
is a retrovirus--that is, it makes a DNA copy of itself in the 
cells and then integrates into the cell chromosomes. They showed 
that you could take that integrated DNA from the cell and put it 
into another cell through transformation and you got back the 
whole virus again. In those days, that was unbelievable. Nature 
turned their paper down twice. I helped them to rewrite it. It 
was just that the editors of Nature didn't believe it. 

Hughes: What was the basis of that disbelief? 

Levy: Dogma was if you took DNA and you put it into cells, the virus 

couldn't be alive, couldn't regenerate itself. How did it happen? 
You need an infectious virus. Here, you just put the DNA of the 
virus in, and out came the entire virus. Today, it seems like, 
"Of course it works." In those days, "no." Today we are using 
pure DNA for vaccines , and that rather recent discovery was not 
believed at first. 

Anyway, I wanted to do the same procedure in a murine 
system, which was more complicated. But the difference in the 
mouse system was, we didn't have a competent virus, a transforming 
virus. We had the transforming gene, but then we couldn't get the 
virus to replicate out. So it was very tough to see if you had 
transferred the viral DNA. 



19 



This approach was based on transfer of a virus via DNA into 
a recipient cell. If replication of the virus took place, it was 
easy to find since it would spread through the culture. If it 
transformed the cells, you could detect it. This procedure is the 
beginning of oncogene research that was pioneered by Bob Weinberg. 
He put tumor cell DNA into mouse 3T3 cells and found 
transformation. I started working on it in 1971 because I thought 
it was an exciting observation and wanted to prove it in the mouse 
system, but I couldn't. 



The University of California, San Francisco 

Assistant Professor of Medicine, 1972-1977 



Levy: When I came back from France in 1972, I was given a position at 
UCSF in the Cancer Research Institute by David Wood, who was a 
great mentor. He's now eighty-eight years old. He was then the 
head of the institute. Sid Salmon, who's a very well-known 
oncologist working with tumor cell resistance, and Marty Klein, 
who is a hematologist and was co-director of the institute, 
realized they needed a virologist in the cancer institute, and 
they asked me if I was interested. 

So in 1971 during my residency Dr. Wood called me in, 
offered me this lab space, and offered to renovate it for me. I 
said, "I'll be back in two months." In two months, he wrote me, 
"Stay in France, because it's not ready yet." And then two months 
became a year, and that was the most unbelievable year I've ever 
had. We already discussed it. 



Research on Endogenous Viruses 



Levy: Now in 1972 when I came back to UCSF after that year in France, my 
goal was to try to figure out why the DNA transformation wasn't 
working better. Mistakenly, I was trying to save the long pieces 
of DNA, to really make the method work better than what the Hills 
had done. The Hills had more primitive approaches, and they would 
just grind the viral DNA up and bring it back and forth through 
needles. When I did it, I made very small DNA. 

Hughes: Why did you get short lengths of DNA? 



20 



Levy: I was extracting the DNA, purifying the DNA, and then putting it 
through a small needle, and this breaks the DNA up automatically. 

Hughes: So you didn't use restriction enzymes. 

Levy: No, I didn't. When I came back from France, I rejoined my 

interactions with Mike Bishop ' s group with Harold Varmus . We were 
good friends. We'd interact a lot when I just arrived at UCSF. 
The association began in 1970, before I had my own lab, when I was 
just a resident. Huebner knew them, and I think when one of 
Huebner's fellows came to UCSF, they invited me to join their 
group and to be in the journal clubs and meet their fellows. So 
for a long period of time, I had tremendous interaction with 
Mike's and Harold's groups. I heard lots of stories about the 
discovery of oncogenes, from not only Mike but also from Dominique 
Stehelin, who was the one who did much of the research and was the 
first author on the paper, though it was Mike and Harold's idea. 

In any case, Harold also wanted to get the DNA system 
working in his lab and agreed to help by measuring the DNA so we 
could use the right lengths. It was annoying that he had a French 
woman working on it as well but others said that was Harold. I 
didn't really appreciate that competition. But Harold did work 
with us, and so he's a co-author on the paper, which was the first 
paper to confirm the Hill and Hillova research. 1 But we were 
never cited much, because Howard Temin did the same thing, 
published it in a Cold Spring Harbor journal, and for some reason 
everyone referred to that paper. Our paper in Virology was the 
first confirmation of the Hill paper and showed that you needed 
low molecular weight DNA to get it to work. 

The person who was the first author in the Temin paper was a 
researcher named Geoff Cooper who then went on to do a lot of this 
work in oncogenes. So again our work really was part of that 
trend to look for transforming genes. Actually, I have never 
thought about that until our discussion here. 



Further Research on Xenotropic Viruses 



Levy: So anyway, when I came back in 1972 and I opened my lab, I had a 
little group. Besides the DNA work, I started revitalizing the 



'J. A. Levy, P. M. Kazan, H. E. Varmus, "The importance of DNA size 
for successful transfection of chicken embryo f ibroblasts, " Virology 1974, 
61:297-302. 



21 



NZB story. It's wonderful how things happenwe were trying to 
figure out why the NZB mouse has this virus , which was called the 
NZB virus. And Beatrice Mintz, who is a very well-known 
scientist, had formed what we call tetraparental mice. They have 
four parents. She took eggs of two couples and just pelleted them 
together and put them into a foster mother. By that procedure, 
she got offspring that had a certain percentage of NZB and a 
certain percentage of C57 Black in their genetic background. 

Norman Talal, who was head of immunology at the Veterans 
Hospital here, and who was a friend of mine at NIH, said, "Jay, I 
have these animals, and you can do some work with them." I said, 
"I would like to see how easily we can get virus out of the 
tetraparental mice: if there's only 10 percent NZB or only 5 
percent and so forth." 

So we got tissue from these animals, and did the sarcoma 
rescue and found the NZB virus again. And in the midst of it, I 
said, "Let's see if we can get it to go into human cells." And 
sure enough, we got transformation of human cells with the rescued 
virus. What was even better is that I got virus replicating in 
the human cells. It doesn't replicate very well in the rat cell 
so I couldn't get much virus progeny. So now I had a replicating 
NZB agent. 

In the midst of doing all this work, I found that there was 
one animal that gave me virus, and it wasn't supposed to have any 
NZB genes in it. It was supposed to be completely C57 Black. So 
I got another C57 Black mouse, and sure enough, I got virus out of 
that one. This was another serendipitous discovery. 

Let me tell you about NZB mice. If I had considered better 
their origin I might not have been so surprised about the C57 
Black observation. Marianne Bielschovsky derived the NZB mice 
from a wild mouse colony at her institute in New Zealand. I 
visited her in New Zealand before she died. My biggest regret is 
that she willed me all her books, but I never received them from 
her lab. She became a good friend. You know that movie, "Harold 
and Maude"? That's what we were. She and I bummed around 
together all over Dunedin, and she showed me the places. It was 
really cute. Her husband Franz had died and in many ways I could 
see she enjoyed visitors. 

She told me how she made these mice. She just had random 
mice that had been collected in New Zealand (you couldn't import 
any into New Zealand), and whatever was left, she used. 
Eventually out comes this mouse with an autoimmune disease. 



22 



Well, in retrospect that meant the NZB virus had to come 
from some wild mouse. So I should have thought to myself, 
"There's nothing unique about NZB. Other mice strains must have 
this agent." But I didn't take that leap. I was too set in 
looking at NZB. But it didn't matter, because in the midst of 
doing the work, I found C57 Black mice had this virus. And I 
said, Well, if they have them, what about the NIH Swiss? That's a 
mouse that was said to have no RNA tumor virus at all, according 
to the dogma. Then, I got the virus out of NIH Swiss. That was a 
big step. 

About this time, Wally Rowe calls me on the phone and he 
says, "Jay, you know the NZB virus that you isolated?" (Wally was 
always very critical; I always thought I had to prove myself to 
Wally Rowe.) I wasn't sure what he would say. "People are now 
doing work on NZB here, and there are rumors that George Todaro is 
finding the NZB virus grows in rabbit cells." 

I said, "Wally, I'm sitting on a big discovery. Now I have 
the virus in C57 Black and NIH Swiss mice." He said, "Well, you 
better write this up." Then I said, "Well, not only do we know it 
grows in human cells and rabbit cells and all these other cell 
types as well, but it does not grow in mouse cells. It's probably 
a universal virus, and must be inherited since it cannot infect 
the mouse." He encouraged me very much, and I feel that was fate 
at my door. 

So I wrote it up immediately, and we didn't know what to 
name the virus. 1 Riding back in the car from a Gordon conference 
the summer of 1973, I was talking it out with my brother, and we 
were trying to figure out a name. Since I love Greece and I love 
Greek people--! think I was Greek in one past lifetime--! drew 
from the Greek xenos for "foreign" and tropic for "turning," and I 
said, "Let's call them xenotropic viruses." And we did, and the 
name stuck. It's a virus that comes out of a species and does not 
go back into the same species; it goes into foreign species. 

Then I chose to name the virus that comes out of one species 
and likes to go back into the same species. We called them 
ecotropic viruses, which comes from the Greek word oikos . home, as 
in ecosystem, ecology. So I had the pleasure of naming the two 
major species of retroviruses in animals. Then Suraya Rasheed and 
Murray Gardner in southern California and Janet and Wally at NIH 
discovered a virus in a wild mouse that will grow both in mouse 
cells and in foreign cells. Wally asked me to name it. So I took 



'J. A. Levy, "Xenotropic viruses: Murine leukemia viruses associated 
with NIH Swiss, NZB, and other mouse strains," Science 1973, 182:1152-1153. 



23 



the Greek amphos . for both, like amphibians, and called them 
amphotropic viruses. So those are the three virus groups. And 
they all are different; they have different envelope coats and so 
forth. 

Well, that now put my laboratory on the map. I was here a 
year, and we had xenotropic viruses, and there was tremendous 
excitement. There was newspaper coverage but I never capitalized 
on it. I never said, "Now I should do this to advance our 
reputation." I just continued to work in my lab on it. Someone 
else would have really publicized it and maybe assured themselves 
of better security than what I had. 

Hughes: Why didn't you? 

Levy: Not part of my nature, and it was not how I was trained. 

Scientists stayed in their lab; they didn't go after publicity. I 
was embarrassed by the publicity. Not that I didn't like it, but 
I was embarrassed by it. 

The paper was published December 2, 1973, in Science. I was 
visiting my sister in the Dominican Republic. I picked up the 
newspaper, and on the front page it said in Spanish, "New 
Discovery on Viruses that Has an Application to Human Cancer." I 
said to my sister, "Once again, someone claiming they have the 
cure for cancer." [laughing] Then I discovered it was my article 
they were discussing! It was picked up by the newspaper reporter 
David Perlman and written up. I wasn't even around! They even 
interviewed the [UCSF medical school] dean, Julius Krevans, who 
really was nice but never that supportive of me. Yet here he was 
on the TV talking about this work. I was then thirty-five years 
old. 

I grew up with the Rowes and the Henles and the Huebners-- 
well, Huebner was a little more f lamboyant--who said as a 
scientist, you do the work, and you allow people to read about it, 
and you're not the one to talk to newspapers and make big 
publicity out of it. In fact, when the newspaper article came out 
on NZB, Wally Rowe wanted to know how it came about, and I didn't 
know if he was upset or not. I said it was by chance; I had 
nothing to do with it. Well, he had heard it on the radio, NPR 
[National Public Radio], I think. 

Hughes: Why wasn't Krevans supportive of you? 

Levy: I have no idea. 

Hughes: It was nothing to do with science? 



24 



Levy: Well, yes. UCSF had Mike Bishop and Harold Varmus working on 
avian retroviruses . They didn't need someone in mouse 
retroviruses. This campus isn't big enough. So I was an extra. 
Huebner and the Henles used to argue that Mike and Harold did 
molecular studies and were not looking at the biology and 
pathogenesis, but it didn't matter to this school. They had one 
retrovirus group. 



Research on Xenotropic Viruses in Humans ## 

Levy: I then plunged into looking for characteristics of these 

xenotropic viruses, and at the same time got a grant, through the 
help of Bob Huebner, to look for xenotropic viruses in human 
tissues. After all, that was what we really wanted to see: there 
must be a human xenotropic virus . People thought maybe that ' s why 
you can't get the human cancer virus, because when you try to grow 
it in human cells, it won't grow; you have to put it animal cells. 
So several groups embarked on taking extracts of tumors and 
putting them into all sorts of different animal cells. 

We went after the human placenta for this virus, because Sy 
Kalter had shown that there were virus-like particles in human 
placentas. We thought that since NZB mice had these viruses in 
placentas, they could be expressed in humans. We should look at 
tissues from autoimmune patients for a human virus. And that's 
another dramatic time. 

I was looking for a placenta from a woman with lupus 
[erythematosus] , and one came in almost immediately. I remember 
going over to the VA Hospital, coming back, and actually passing 
Julie Krevans on the steps. Julie, very friendly and all, said, 
"What's going on?" I said, "Julie, this is my attempt to find the 
xenotropic virus in humans. I've got this lupus placenta." I 
have no idea what he thought. 

One of the things I did was to send some of the placenta 
tissue down to Ellen Dirksen, who had been in the Cancer Research 
Institute at UCSF but left after they didn't appreciate her work. 
She did some very nice studies on epithelial cells in the lung and 
in the trachea and was a superb electron microscopist. Anyway, 
she found the virus -like particles in human placentas and we 



25 

published the confirmation of Kalter's work, 1 but she found them 
in normal placentas as well as in lupus placentas. Now we 
considered these agents possible viruses of normal development. 

To isolate a human virus I had what I called zooion lines-- 
obviously from the word "zoo". We took various cell lines from 
all different animals. Since I was working in xenotropic viruses, 
our liquid nitrogen freezer was literally a zoo. You would walk 
into this lab--I wish I had pictures of it and we'd have fish 
cultures growing on top of the incubator, because they grew at 20 
degrees [centigrade]. We had some animal cell cultures inside at 
37 degrees, and then we had mosquito cultures on the shelf, 
because they did better at 17 degrees. And all of them were being 
inoculated with xenotropic viruses. 

Some researchers had raised the issue that xenotropic 
viruses might bring harm to humans if infected, but we were able 
to prove that it would be very difficult to get humans infected, 
especially since human blood lyses the virus. So we weren't put 
under the pressure to have special safety precautions that you now 
have with HIV. Nevertheless, we worked with the human placentas 
and, when possible, with human fetuses in a small eighty-square- 
foot room renovated for me from a former hot room used at the 
Cancer Research Institute. 

Our lab was flourishing in the mid-seventies. I was always 
fighting for space, and Julie Krevans was the one who handled it. 
He gave me space, and then the next person who saw him, he gave it 
to him. So we always said you had to see Julie Krevans last in 
order to make sure you got it. I remember we had a chair outside 
the lab in the corridor, and we would have people sitting on the 
chair waiting to come into the lab to use the hood- -we only had 
one hood- -and it was very, very hot. The university didn't 
believe in air conditioning. They finally allowed us to get an 
air conditioner. 

By the way, the paint in the lab was brand-new. In 1970 
when I first built this lab, I didn't want to have it painted in 
yellow and green, which were the institutional colors. When I 
called color experts to find out what are the colors that are 
conducive for work, what do you think they said? Yellow and 
green. And I said, "Well, I can't stand them." So we got 
chartreuse and violet and sky blue, and made a very exciting lab. 
And then after we did it, other labs came in to see it, and they 



'E. R. Dirksen, J. A. Levy, "Virus -like particles in placentas from 
normal individuals and patients with systemic lupus erthematosus , " Journal 
of the National Cancer Institute 1977, 59:1187-1192. 



26 



all started doing it; they changed the face of labs in the 
university. Well, we were really the first, I think, and we 
needed special permission. 

Then Julie Krevans gave me the room across the hall to do 
work and we expanded into that space. I had a lot of money to 
work, and we were going after the human xenotropic virus. We 
were also trying to insert the xenotropic virus gene into 
ducks ; we were inoculating duck eggs . We went up to Petaluma 
Farms and got duck eggs, brought them back, hatched them. We 
kept the ducks on the roof of the animal tower, and I had a 
woman technician, Oksana, to care for them. We wanted the 
ducks to lay eggs and have the eggs fertilized so we could put 
the xenotropic virus gene into the fertilized egg. I'm loaded 
with funny stories about how you try to get a duck to fertilize 
the egg. This was a very exciting and fun period. 

I was working with a xenotropic virus of mice and hoped 
that it would have some relevance to humans, but it didn't look 
like it was the cause of autoimmunity or cancer. We began to 
derive a theory that these were viruses of normal development, 
and that they were needed in the placenta. And that was a way- 
out idea. We published a few papers on that theory, and 
actually talked a lot on it. And I think people just said, 
"Ah, relatively young, naive guy, just ideas--." 

Hughes : Your theory was unpopular because people thought all viruses 
were pathogens? 

Levy: They thought all viruses are pathogenic. They didn't care 

about the fact that you have bacteria in your gut to help you. 
To think that a virus might be helpful was unheard of. 

In pursuing this interest I conducted work with JoAnn Leong 
up in Oregon in the mid-seventies. She had been a postdoc with me 
for six months and then went to Oregon to begin her career. We 
have remained close colleagues and friends. Thus I would fly up 



27 

to Oregon every other month to work on placentas. Jay Nelson, 
who's now a wonderful molecular biologist, was a student with 
JoAnn. In a way, he was with both of us. Essentially, we 
would get a placenta and work it up for virus over a long 
weekend. 

Now, in Oregon in those days, finding a woman that had 
fourteen children wasn't unusual, so getting placentas was easy 
as can be. I would arrive there on Friday and we put the word 
out we wanted a placenta, and we had it. We then extracted the 
placenta to look for virus, and we searched by measuring 
reverse transcriptase in the placenta, which is the enzyme for 
retroviruses . 

Hughes: That was a recognized technique for identifying retroviruses? 

Levy: By that time. But we had to work out all the procedures. 

Reverse transcriptase in the placenta was very labile, and you 
sometimes saw it and sometimes you didn't. We did maybe eighty 
placentas. It would be all-nighters. We'd start on Friday 
morning, and we'd go straight through until Saturday at noon, 
and do the whole thing. 

Hughes: You went to Oregon because the placentas were readily 
available? 

Levy: Right, but mostly since JoAnn Leong and I had begun the work in 
my lab, and we decided this would be a collaborative work. 

Also, I did not have any ultracentrifuges nor money to buy 
this equipment. Her lab could do the molecular work. This 
becomes important with HIV research since I did not have an 
ultracentrifuge at the time I needed it. I had none of the 
molecular techniques ongoing in the lab. Everything I did was 
biology: how the viruses infect; how can you manipulate them? 
It was not the kind of subject that attracted students, because 
they wanted fast results, and fast results came with molecular 
approaches. The Herb Boyer (recombinant DNA] techniques 
weren't quite there. Reverse transcription was there to work 
on, but not with as advanced technology as there is today. But 
still, a student could work with Mike or Harold and get a 
result much quicker than coming to my lab. So I always had a 
hard time finding postdocs, and Mike would sometimes send me 
the list of people that he didn't take. One did come to my lab 
and was disappointed she was not with him, so it didn't work 
well. 



28 
Research on Anti-xenotropic Virus Neutralizing Factor 

Levy: JoAnn had come from Mike's lab to work with me in biology and 

pathogenic systems. While she was here, I put her on an exciting 
project. We found that in the serum of mice, there was 
neutralizing activity against the xenotropic virus. Other people 
had also seen it, and they had reported the finding of high 
titers of antibodies to xenotropic virus. 

It didn't make sense to me: Why would an animal make an 
antibody against something it inherits in its genes? I always 
say it was naivete, because I thought I had a new finding. I 
felt the animal should not be making antibodies. And I remember 
saying that maybe it's not an antibody. 

Sir Macfarlane Burnet was here at the time, and I met him. 
I told him about xenotropic viruses and about our antiviral serum 
factor. I'll never forget what happened. He looked at me and 
said in his Australian accent, "Well, that would be terribly 
novel." [laughter] And we went after it. 

And here's another lucky event: I had met a scientist named 
Ron Barnes in England. He worked on NZB and mouse viruses. I 
didn't have the procedures for doing a lot of 
immunoprecipitation of antibodies and he offered to help. He 
did it for me in England and sent the material here, and we 
tested them. The results were exciting. The antibodies in the 
mouse serum had no antixenotropic virus activity, and the non- 
antibody fraction did. I'll never forget, I was so excited. 
This was two years after the discovery of xenotropic viruses. I 
had another new thing to report that was nonconventional and 
anti-dogma. 

Huebner was visiting at the time and I brought him into my 
small office. I recall he sat on this desk- -well, at that time, 
it wasn't as nice a desk. But it was in the same room. And I 
said, "I have some very important information to tell you, and I 
would like you to submit it to the [Proceedings of the] National 
Academy of Sciences." In those days, you did that to protect 
yourself, because other people might rush in and try to take the 
discovery away. This way, he could direct it to trustworthy 
people. He was equally impressed. At the same time, he had 
grown fond of me, partly, I felt, because his wife, Harriet, who 
was formerly his secretary, was such a very good friend of mine. 

In any case, what was nice about Huebner was once he 
submitted the paper, then he told everybody about it, and they 
didn't dare take it away. And that's what he did for me for 
xenotropic viruses, too. I give him credit for getting everyone 



29 

to accept the term, because he went around calling everything, 
"xenotropic, ecotropic," and everybody just accepted it. You 
need people to get the word out, and I wasn't the one to do it-- 
at least then. 

Hughes: Well, not only people, but people of the stature of Huebner. 
Levy : Right . 

I knew very good immunologists at NIH, whom I called and 
asked, "I would like you to prove I'm right on this 
observation," and they did it, and came up with the same 
finding. Thus I could note in the article that they confirmed 
the observation. This became known as a neutralizing factor. 
No one knew what it was biochemically. Then JoAnn and I did all 
sorts of really very primitive biochemical and protein assays, 
and we proved the neutralizing factor was a lipoprotein. With 
that finding I joined with John Kane in the Cardiovascular 
Research Institute here, and we proved it was an apolipoprotein. 
What an interesting timeto learn antibody purification 
techniques and then all about lipoproteins. I tell my students 
that is where science can be so exciting- -never dull. Then I 
got invited to lipid and cardiovascular meetings, because this 
finding was the first example that a lipoprotein had some 
biologic activity aside from transporting lipids. 

So in '75, '76, '77 we tied in the neutralizing factor in 
the mouse with the xenotropic viruses. And now xenotropic 
viruses were being found in cats, in deer, in mink, and they 
became a theme. So while working on the placenta virus we were 
looking as well for neutralizing factors in human serum. But 
none were found. 

All of this work came about up to 1977. I was asked to 
write a review of xenotropic viruses , which took a lot out of 
me. It was through Werner Henle, and it was a very good review, 
and I got lots of praise for it, particularly from him. A lot 
of things happened that year. I had been wanting to be an 
associate professor, and since I didn't have any great strong 
advocates--Dr. Wood had retired; I was inherited by the 
department [of medicine]. Anyway, finally I got it with the 
wonderful statement that it was about time that I received this 
promotion. And I got married to Sharon in that year [September 
1977]. 



30 

Visiting Scientist, Weizmann Institute, July 1978- January 
1979 



Levy: All this happened at the end of the seventies, and I decided, I 
need a sabbatical. I received money through the Eleanor 
Roosevelt Foundation and another fund to go to Israel [Weizmann 
Institute] to work on T-cell leukemias with Nechama Haran-Ghera. 
I had met her at the Gordon conference in 1973 and really 
appreciated her approach to research using live animal models. 
For five months in Israel I learned about T-cell leukemogenesis. 
I was there to work on viruses that could induce these tumors , 
and it was a very interesting time. We showed how the mouse 
virus could affect the immune system of the animal and thus lay 
the basis for leukemia development- -not a too distant cry from 
HIV. 

I also had a very active lab in San Francisco. I bet I had 
about fifteen people. There were no fax machines. Mail would 
come to Israel three weeks later. By the time I got it, I'd 
forgotten the questions I'd asked. I got hepatitis while I was 
there from eating the wrong food, and then I was out for about 
five weeks. It was terrible but I have great memories of my 
time there, and Sharon and I remain very active in Weitzmann 
Institute events. 



Visiting Scientist, Institut Pasteur, January 1979- July 1979 

Levy: After Israel then we moved on to Paris, where I couldn't drink 
wine for three months because of the hepatitis. I worked with 
[Francois] Jacob on embryocarcinoma cells. This was again a 
different subject for me. I wanted to show that viruses could 
affect differentiation. I was, as I said before, directed at 
looking at viruses in cancer and normal development. So I 
studied T-cell differentiation and leukemogenesis and how viruses 
would manipulate that system. 

Then, I wanted to go to the Pasteur Institute to study the 
effects of retrovirus on embryogenesis. Also I was happy to work 
with Jacob and experience the Pasteur Institute. And I loved 
Paris ever since I spent the year there in 1960. I decided in 
1960 that I was going to return to Paris every decade and spend 
time learning and teaching. Well, it hasn't worked out because of 
AIDS, and I just haven't been able to get away. I went to Paris 
in '60-'61, '71-'72, and then '78-'79, when I spent eight months 
there. It was very difficult then, I have to say. They weren't 
used to working with viruses. In fact, Jacob didn't want viruses 



31 



in his lab, so I had to take my embryocarcinoma cell cultures from 
his lab across the center quad to Jean-Claude Chermann's lab in a 
small makeshift one-story building. 

Now, Jean-Claude Chermann--the name will later become 
important- -had been a friend of mine, because in 1971 and '72, 
when I had been with Jasmin for six months in Villejuif , Jean- 
Claude was often around. At the time I had described a factor 
that NZB cells make that inhibits murine retrovirus replication. 
I thought that this substance might have something to do with the 
block in xenotropic virus infection. But it didn't. However, 
this factor still stands today as one of those substances, not an 
interferon, that is antiviral. But I didn't get very far with it. 

Jean-Claude had seen something similar, so we interacted, 
but initially on his research subject. He and Dani and Sharon and 
I would socialize in Paris. He actually established reverse 
transcriptase assays in my lab in 1973 or '74. We used the 
procedure, especially for searching for the placenta virus. Up 
until about '78 or '79 the reverse transcriptase assays, which 
were very good, were a major biochemical approach used for our 
work. 

In "78- '79 when I was at the Pasteur, Luc Montagnier was the 
head of the lab where Jean-Claude worked. In fact, Luc had been a 
student with my brother Stuart in Raymond Latarget ' s lab in the 
early sixties. You recall I was also influenced by Latarget and 
his ideas on cancer viruses. So I knew Luc because they were 
colleagues together. Luc was interested in interferon, and Jean- 
Claude and Francoise Barre-Sinoussi, who was a very good friend of 
mine as well, were interested in viruses. So I interacted with 
them with my embryocarcinoma cells. When I proved that you could 
actually influence development with retroviruses, we published 
it. 1 I was very pleased that Jacob agreed to be on the paper. He 
really did not want much to do with viruses . 

Hughes: Because they were infectious? 

Levy: Yes. He wanted the lab clean. When I showed him that every mouse 
cell has a virus [laughing], he still just smiled wryly and I 
traveled to Chermann's lab. 



'J. A. Levy, H. Jakob, D. Paulin, F. Kelly, J.-C. Chermann, F. Jacob, 
"Productive infection of embryonal carcinoma cells with ecotropic mouse 
type C viruses and subsequent arrest of differentiation," Virology 1982, 
120:157-170. 



32 



I worked very hard at the Pasteur, I think harder than 
most of the French researchers there. I didn't end up with a 
lot of papers, but I ended up at least proving what I came to 
do. I wanted to learn about embryocarcinoma cells; I wanted to 
learn about differentiation and how viruses could affect it. 



Research Cuts 



Levy: I came back to this lab in '79 and set out to revitalize it; 

wrote up all my grants. Then 1980 hit, Reagan was elected, and 
all my grants failed. I was reduced from fifteen people to me, 
a part-time secretary, Michelle Ramirez (who by the way was 
most important). Dr. Wood told me: "Your secretary is one of 
your most important people. Don't ever give her up." Anyway, 
I ended up with four people. I had a student and a postdoc on 
her own salary. Everyone else had to go. 

Then I got a letter from the dean, [Robert H.] Crede, 
saying, "Dear Dr. Levy, since you have no more money for your 
support, if you do not find any funds within a year, you must 
leave the university." I found that letter so cold, callous. 
Not even, "We thank you for all the money you brought in and 
what you've done for us in the past." 

I then talked to Marty Petrakis, who was head of contracts 
and grants here; she was a good friend. She said, "Jay, this 
is the saddest part about this place. They don't care a thing 
about what you've done in the past." With her, I tallied up 
all the money I had brought the universityit was close to $2 
million but the overhead didn't matter either. The school 
agreed they would pay my salary for one year. 

My wife was the best thing that ever happened; Sharon was 
fantastic. I was so depressed; I couldn't believe this was 
happening. It happened to me first among my research 
colleagues. It happened to the others later. Some left 
science completely. Sharon said it was one of my most creative 
periods. If so, it was also very difficult. It can, however, 
be your most creative period, because you have to sit back and 
figure out what you're going to do. 

I could be a physician but I didn't think I really wanted 
to do it, though I knew I'd be a good one. I have a nice way 
with people, because I enjoy taking care of them. But I wanted 
the excitement of research. So I wrote grants. I have a file 



33 

on that project. I must have sent out a hundred grant 
applications. Letters. Met with foundations. 

Fortunately I had a friend whom I met through Ellen 
Dirksen, the electron microscopist. This woman worked at the 
National Science Foundation. And I'll never forget what 
happened: In 1980 or '81, I applied for a grant on 
embryocarcinoma cells. It was for $39,000 for three years. 
This lady knew that I was in terrible financial shape, and she 
fought for me, and I got the grant. I got the news at the same 
time that I got an award notice that I was given a month grant 
to return to the Weizmann Institute to finish up some work on T- 
cell leukemia with Haran-Ghera. Then I got another grant for 
another small amount of money from some local people, so that I 
was able to get by. My luck had finally changed. That history 
brings us up to August of '81. 

Let me say in retrospect that 1976 -'80 was also difficult 
for me emotionally since I had as the new head of the Cancer 
Research Institute Stephen Shohet. 

Hughes: Why? 

Levy: Because he just wanted his own people. I had a Research Career 
Development Award [1972-1977] that Julie Krevans had sponsored 
me for, which was nice of him. That really was a commitment by 
the university to me. 

I remember when Steve Shohet in '76 said he couldn't even 
spell "virus." He was nasty, tried everything to get rid of me, 
and forced me out of the room across the hall that we were 
using. He kept it empty, but we always snuck back and used it. 
Just terrible behavior. You just can't believe the atmosphere 
of this place in '76- '77. Well, I'm sure it's true at a lot of 
places. 

And then to have Julie Krevans when I went to see him say 
to me, "Well, Jay, he's the director of the institute. If he 
wants to get rid of you, he can." Think about how insecure that 
would make one feel, when I had a fine research group. So I 
have never really felt a great security at this university, but 
I kept working. 

I'm telling you this because I actually don't know why I 
continued here. Maybe part of it is to just prove that I don't 
care what they do, we're going to get this research done anyway. 
Xenotropic viruses weren't that important to them. If my 
research turned out to be exciting, great: they'd take the 
credit, thank you very much, goodbye. And the neutralizing 
factor is a very unique observation. Our research in biologic 



34 

systems has always been novel and adventuresome. That made it 
fun. 

Hughes: Were your financial troubles in the early eighties related to 
the fact that Nixon's war on cancer was petering out? 

Levy: Well, Reagan got in and said that government was not going to 
support research. You had to go to the companies for support. 
He cut the budget. I wrote Dick Rauscher at the American Cancer 
Society and said, "I'm going to have to close my lab. This is 
terrible." I wrote him about the neutralizing factor. He got 
me $50,000 to continue. So that helped. Those kinds of grants 
really help people through the tough times. But many did not 
survive and left science. 

The reason I'm building this up is to show that the 
atmosphere here was not great. Steve Shohet was the director of 
the Cancer Research Institute; he seemed to be an unhappy person 
and obviously did not like the job. They then got rid of him in 
the six-year review, and they brought in Ed Cadman, who was 
better and was more supportive of me. Nevertheless, even then 
the institute did not recover the importance it had under David 
Wood. 



35 



III THE AIDS EPIDEMIC 



Kaposi's Sarcoma, August, 1981 



Levy: Paul Volberding came to do his oncology fellowship here while I 
was in Paris and Israel. He had done work in retroviruses in 
Minnesota. He spent two years working with me in '79 and "80. In 
1981, he moved to San Francisco General to become an oncologist. 
He saw the problem of getting money for research. 



Levy: Then in August of '81, Paul calls me and says, "Jay, we have 

Kaposi's sarcoma [KS] occurring in homosexual men. It's a small 
number of cases, but we'd like you to come over [to San Francisco 
General Hospital] to grand rounds and discuss it, because I think 
this is an opportunity for you to look at human cancer." 

Judy Luce, an oncology fellow with me then, and I went over, 
and Don Abrams talked about the case; Don was then a fellow. I 
got up and explained why, if Kaposi was caused by a 
cytomegalovirus (the leading idea for a virus causing this 
cancer), you couldn't get the virus out. I went back to the fact 
that if a DNA virus was causing the cancer, it would be locked in 
and wouldn't express the total particle. Back to 1962 and 
lysogeny and bacteriophages. It's the same story, because if the 
virus replicates out of the cell, it kills the cell. I said it 
might be a defective cytomegalovirus and that we would like to 
work on this problem. But I had no money. 

Hughes: Why were they even thinking viruses? 

Levy: Well, Burkitt's lymphoma had been linked to a herpes virus, EBV 

[Epstein-Barr virus]. Kaposi's sarcoma in Africa had been linked 
with cytomegalovirus by Gaetano Giraldo. There has been a close 
association with cytomegalovirus with this cancer, but no one can 
prove it as the cause. So Kaposi's sarcoma was now suddenly 



36 



occurring in these young men, where usually it's in much older 
Mediterranean people and in Africa. It was an opportunity to move 
into human cancer, and we needed to get the tumors out and grow 
them. I had no money. That was in August of '81. 

Then it became clear that Kaposi's was really hitting as an 
epidemic. In San Francisco, Pneumocystis [carinii pneumonia] was 
not as emphasized then in association with AIDS. In February of 
'82, Marc Conant called me and said, "I've got a case of Kaposi's; 
do you want to get started on your growth of Kaposi cells? Come 
on over." I went over, and I met Dan Turner. Dan Turner was a 
young, vivacious, handsome guy. He had a KS lesion on his foot. 
Marc took it off, gave it to me. I came back here, and it was the 
first Kaposi's tumor that we established in cell culture. That 
was in early '82, and I subsequently established about thirty cell 
lines in this early period. 



National Cancer Institute Grant for AIDS Research. 1983 



Levy: In the beginning of '83, end of '82, a group of us at the 

university decided to write a grant to work on AIDS. The NIH had 
announced that requests were being considered. Paul decided to 
put the grant together with John Ziegler. I give a tribute to 
Paul; Paul had just been my fellow, remember. He had a name that 
no one could pronounce, and he was going to go for this first 
grant on AIDS. He was an unknown in research, and we all were 
saying, "Paul, it's not good for you to be head of this research 
grant; it should be John Ziegler." Ziegler had worked in cancers 
in Africa; he was well known to NIH. Paul said, "No. I'm going 
to see a lot of these cases at San Francisco General. If I'm 
going to do this, I want to be co-investigator." And there was 
nothing we could do. Today, if you can't pronounce his name, it's 
not because you haven't thought about it. So he became the co- 
investigator with John Ziegler on the grant. 

Hughes: I have heard it postulated that it was that grant that established 
the hierarchy of the San Francisco AIDS workers; 1 that it gave 
Volberding the edge. 



the oral history in this series with Andrew Moss. This and many 
of the other oral histories in the AIDS series are available online at: 
http://www.lib.berkeley.edu/BANC/Biotech/ . 



37 



Levy: Absolutely. But who else was around? I mean, it was Paul calling 
me in to see Kaposi's sarcoma in '81, then Marc Conant seeing 
patients and then starting the Kaposi's Sarcoma Clinic. 



The Kaposi's Sarcoma Clinic. UCSF 
[Interview 2: February 22, 1993] ## 

Hughes: Dr. Levy, last time we talked about your first encounter with the 
AIDS epidemic. What we should do now is record your memories of 
how the KS Clinic was founded and set up. 

Levy: In February, 1982, as you recall, I saw Dan Turner in Marc 

Conant 's office, and began to work on Kaposi's sarcoma. Marc 
Conant invited me to what had just been opened [in September 1981] 
as the Kaposi's Sarcoma Clinic 1 over in the [UCSF] Clinics 
Building. The study group was held, I think, at lunchtime every 
Thursday, or every other Thursday. I would go there representing 
a basic researcher and virologist. 

There weren't very many of us at first. I think John Mills 
was there, Dan Stites, several epidemiologists. Selma Dritz would 
come. It was an excellent format for describing what was going on 
in KS, this new disease. I can remember having discussed with Don 
Abrams whether lymphadenopathy, swollen lymph glands, was part of 
this syndrome or not. We discussed whether other viruses could 
cause lymphadenopathy and did we know if homosexual men got 
swollen lymph glands. I believe that I said that I thought 
lymphadenopathy probably was related to the new disease. 

I can recall Larry Drew arguing for cytomegalovirus as a 
possible cause. At that clinic evolved the separation of our two 
approaches, where I wanted to go for a new agent and Larry was 
looking for a mutant of a known agent as the cause of AIDS. 

Hughes: Why did you suspect a new agent? 

Levy: We hadn't seen Kaposi's sarcoma, and later Pneumocystis disease, 
occur at this level, ever before. 

Hughes: In this age group? 



: Levy and others use the term "clinic" to embrace both the KS Clinic 
and the KS Study Group, which followed the clinic. 



38 



Levy: Yes, in this age group, and like an epidemic or a minor epidemic 
in cities, among people that were of certain backgrounds and risk 
groups and sexual persuasions. We had some very good discussions 
in the Kaposi's Sarcoma Clinic. 

This clinic was an excellent opportunity to have this 
information exchange, and I do not know why it stopped. Partly, 
money ran out. Partly, people after a time didn't attend as 
often, although I always went. But you met everybody who was 
anybody in public health and working on this new disease. I was 
really one of the only basic researchers, along with Larry. Larry 
didn't come as often as I, because he's at Mt. Zion and I think 
had a more difficult commute . 

Hughes: What was the usual format? 

Levy: Marc or his assistant would set up lectures, and you'd hear a 

lecture or two. I can't remember; I think sometimes it was two. 

Hughes: Which were sometimes by outside people? 
Levy: Some outside visitors came. 
Hughes: Were there patient presentations? 

Levy: No. You had people discuss various aspects of KS or a related 

topic. They wouldn't present a problem, but they might use a case 
to illustrate one of the points they were making. While we 
focused at first on KS, later it was on lymphadenopathy and AIDS 
in general. 



Visit to Haiti and the Dominican Republic 



Levy: I went to Haiti at the end of '82 to look into the possibility 

that the virus that causes AIDS, as it was then called then, might 
have originated in Haiti. You may recall that fingers were 
pointing there. I also went to the Dominican Republic where I had 
been doing work with Ellen Koenig, who is my sister and is a 
virologist. We had been looking at AIDS in the Dominican Republic 
as a third-world country. Since the country has Haitians working 
in the sugar cane factories, I thought that we might see a 
difference in the disease among the two populations . We collected 
blood in 1982- '83 and then with the discovery of HIV could trace 
the onset of infections in the Dominican Republic. And that 



39 



turned out to be a rather major observation, published in JAMA. 1 
We found a high rate in Haitians and a very, very low rate in the 
Dominican homosexual community. 

For collecting the blood in that country, I would go dressed 
in a white jacket with Dr. Koenig and her public health coworkers 
to gay bars and hotels, bleed the men, and keep the blood, because 
in '82, '83 we didn't know what the cause of AIDS was but felt it 
could be a virus. Every December at the holiday season, I go down 
there. We set up this collaboration with the national laboratory 
and it turned out to be very interesting. We could watch HIV 
enter the Dominican Republic and spread, as I was able to do as 
well in Zimbabwe, which is another story. 

Hughes: How was HIV entering Haiti? 

Levy: It was entering with tourists and Haitians. It was quite clear 
that the concentration of cases in Dominicans was in the port 
cities, and we showed that fact in our first paper. 

Hughes : Gay men were bringing in HIV? 
Levy: It was mostly gay men. 
Hughes: From the United States? 

Levy: Wherever, but most likely, yes. We didn't think the infection of 
Dominicans came from Haitians; they don't mix very much, although 
you have a few Haitian prostitutes . Ellen went on to prove that 
most of the prostitutes in the Dominican Republic are negative for 
HIV. It's the international prostitutes who are infected, being 
moved around the world. That was one of Ellen's comments: "Stay 
away from international prostitutes." 

In December 1982 I arranged to go meet Bob Elie in Haiti, 
who was my host. It was really an amazing trip. Because I was 
going to Haiti, I called Berkeley and asked if there was anyone 
there in Haitian studies and met a young Haitian teacher named 
Michel Laguerre who was a history of Haiti scholar. He had a lot 
of contacts in Haiti with a very intellectual group. One of his 
friends, Max Blanchard, became a friend, and I serve with him on a 
Haitian-American committee in San Francisco. 

So I went to Haiti armed with all these contacts, and I met 
many of them. One was a famous historian and lecturer, and I had 



'R. E. Koenig, L. G. Brache, J. A. Levy, "HIV in the Dominican 
Republic," Journal of the American Medical Association 1987, 258 :A7. 



an incredible time. In fact, I even met with the minister of 
health. My hotel was empty because AIDS had been just talked 
about and no tourists came. I think I spent four days, and there 
were meetings all the time. I met some of Michel's friends and 
the head voodoo priest. I photographed a voodoo ceremony and 
raised the question of whether the virus could come from chickens, 
because they drink chicken blood. 

At that time, Jane Teas had her African swine fever virus 
article published in Lancet, which captured the imagination of 
lots of readers and the gay community. And Jane was here in San 
Francisco, talking about it. I decided to examine further the 
idea though I thought it was a bit far-fetched. While in Haiti I 
checked on the pigs that were supposed to be infected by this 
virus, and although all the pigs had been ordered killed, there 
were plenty of pigs left in Haiti. No one bothered to kill them 
all. In the voodoo ceremony, they smear themselves with pig 
blood. So I looked around for swine fever virus as a possible 
cause of AIDS and learned some very interesting things while I was 
there. For certain the swine fever virus did not seem 
responsible. 

One reason was that most of the wild animals were gone; they 
had all been eaten. The second was that there had been in 1977 a 
conference of gays in Haiti, and a lot of gay people had come down 
from New York for this conference. After all, Haiti was a great 
spot for gay vacations . The poverty there had lots of young boys 
acting as prostitutes. There apparently were some there when I 
was there, but it wasn't as evident. There was a hotel that had a 
lot of famous homosexuals staying there. I saw the hotel; I can't 
remember the name of it. I also learned that one guy had given a 
party in which rhesus monkeys were featured, running around wild 
at the party. So that led me to think again about viruses 
spreading from an animal to humans, or--I always laugh--the other 
way, too. 

I came away with a wonderful appreciation of Haitian 
culture, despite the short visit. The voodoo priest was 
wonderful; really it was a privilege to be there for a special 
voodoo ceremony, and I was permitted to take many photos. Years 
before I had been in Haiti with friends and actually went to a 
voodoo ceremony that we paid for. It was like $10 and went on for 
three days. We saw the first six hours and then excused 
ourselves, but it went on forever. So I had a feeling for it and 
met some voodoo priests then. I came back to San Francisco and 
gave a talk on this visit at the KS Clinic. It was really very 
well received. I had marvelous pictures, which I still use. I 
said then that I thought perhaps in '77 the virus was brought to 
Haiti via New York. 



Al 



I continued my connections with Haiti, but it became 
impossible to do research with them. I tried very hard, even 
tried to get blood samples from them and found that the best way 
of doing it was getting the blood from Haitian sugar cane workers 
in the Dominican Republic. They go back and forth over the 
border. So that's where I did most of my work in the Caribbean. 
I looked at the Caribbean as a third world country for us to 
study. I maintain some wonderful Haitian friends here in the 
city. I still see Max Blanchard, who is a prominent Haitian 
businessman hereor he may be a lawyerand, as I mentioned, I'm 
an advisor to the Haitian-American Foundation that strives to 
bring up the level of attention to Haiti. 

I tell you that story because it adds a certain dimension to 
my own life, but it also gave me insight. You go there; you see 
it. As a result of that experience, I went to Africa at my own 
expense so I would not be just hearing about it and reading about 
it; I would see it myself. And that added tremendous dimensions 
to my appreciation of the HIV problem. 

Hughes: Did these trips add to your science? Was what you were doing in 
the laboratory affected by where this virus originated? 

Levy: Well, at that time, I thought these trips might give me a hint as 
to what animal cells to culture the virus in, and ways in which it 
could be transferred. But as a medical person trained in 
virology, I'm also very interested in epidemiology and disease 
transmission. So I cover quite an area when I look at 
pathogenesis. I'd like to know how a virus gets transmitted as 
well as how it causes the disease. 

Hughes: Now, why did it have to be a virus? Why were you convinced that 
it wasn't another type of infectious agent? 

Levy: I was convinced it was a virus because in early '82 there was the 
case of immune deficiency in a hemophiliac who received only blood 
products, not blood transfusions, and all the Factor VIII material 
is filtered. So it therefore became really rather silly when a 
prominent researcher published in the New England Journal of 
Medicine in 1983 that a fungus could cause this disease. 1 That to 
me was ruled out. Also, it couldn't be a bacterium, because 
bacteria are also blocked by filtration. The cause had to be a 
virus . 



'K. W. Sill, T. Folks, K. T. Kwon-Chung, J. Coligan, and W. L. Maloy, 
"Cyclosporin immunosuppression as the possible cause of AIDS," New England 
Journal of Medicine 1983, 309:1065. 



42 



Hughes: Was a viral etiology pretty well accepted in the KS group? 
Levy: No. Some people thought it was amyl nitrate. 

The Peter Duesberg story that Peter still maintains was 
considered: hypersexuality, drugs. 1 Males have this one enzyme in 
their T cell and homosexuals may have more of it, et cetera. 



San Francisco AIDS Researchers 



Levy: I have to say, without romanticizing the time in San Francisco, it 
was a small cadre of people who got together and took this disease 
seriously when the university couldn't give a damn. And we as an 
outside crowd really went after it to try to get an answer. There 
were people who shared information. There was no one who demanded 
top attention. You had great personalities that to this day 
remain in wonderful rapport, which highlights this AIDS program on 
the campus. There is only one group, which has recently come to 
UCSF, that has not made any efforts to collaborate, and that's the 
Gladstone [Institute of Virology and Immunology] group. They kind 
of came after everything, and they're kind of staying separate. 
The group from the early days has maintained tremendously close 
association. I'll get on the phone and call Larry Drew or John 
Greenspan or Andrew Moss or John Ziegler or Marc Conant. 

Hughes: What you're describing is a cooperative situation. 

Levy: It was partly because we each came from a different discipline. 
If there were two prominent virologists, perhaps we would have 
been at each other. Larry's a good virologist, but he took herpes 
as the cause. I took the probability of a new virus. 

Hughes: This choice of research areas just happened to be what you each 
were interested in? 

Levy: They became partitioned in the Paul Volberding grant application 
to the National Cancer Institute [NCI] in 1982. That's where it 
was decided. Larry said, "I'll take cytomegalovirus , " and I said, 
"I'm taking a new agent." So if I found a herpes virus, it went 
to Larry. If he found something new, it came to me. Anyway, that 
was the principle. 



*For more on Duesberg 's views on AIDS, see the oral history in this 
series with Warren Winkelstein. 



Hughes: And that went on down the line? 

Levy: Everyone had their turf. There were problems when people felt 
they didn't get the credit or that someone was encroaching on 
their research area. And I, and John Greenspan 1 as well, would 
very often negotiate settlements so that we could retain very 
close rapport, and it worked. Always worked. 

Hughes: Why was it you two? 

Levy: Partly maybe because I've been around a long time, and I was after 
the virus, and after I found the virus, I became important for 
everybody because I did all the [HIV] antibody tests for them. 
And maybe because we took it seriously. We felt that everyone 
should get along, and this should be a part of what we do. We 
took pride in the fact that our group was different from UCLA, New 
York- -there everyone was grabbing and trying to get the credit. 
And that spirit of cooperation here, as I said, maintains today. 

So from the KS Clinic, we devised this grant application to 
NCI, and we defended it in May of 1983. It was a very exciting 
period of time. What I had was thirty-three KS cell lines and the 
review committee liked my work and the algorithm for finding the 
AIDS virus. I could not isolate any virus in a serious way; I had 
no ultracentrifuges. What became famous from Randy Shilts's 
book, 2 my old flow hood did not have a filter that would pass 
inspection, and it was to cost $1,500 to buy a new filter. 

Well, as I mentioned to you, in 1980 I lost all my money 
when Reagan came in, so I had no money to upgrade my facility, no 
less go after an infectious agent, but I took on the challenge. 
And I had at the time very few people. Judy Luce was here; an 
undergraduate student from University of San Francisco, Tony 
Hoffman; a secretary, Michelle Ramirez; and Martha Szoenyi, who's 
been with me for seventeen years and is the woman who maintains 
the lab supplies, cleans up, et cetera. 

Later I was able to accept John Morrow on a fellowship from 
England, but he began working on autoimmune diseases, which was 
part of a big research effort looking at viruses and autoimmunity 
--a confirmation of my NZB studies, neutralizing factor of 
xenotropic viruses. John took on the challenge of isolating an 
AIDS agent in small animals --and later primates. Here again I 



'See the oral history in this series with John Greenspan. 

2 Randy Shilts, And the Band Played On: Politics, People, and the AIDS 
Epidemic, New York: St. Martin's Press, 1987, pp. 173-174. 



44 



used my contact with a former virology colleague, Sy Kalter, who 
arranged for me in 1984 to have chimps in which to inoculate our 
virus, ARV-2 [AIDS-associated retrovirus-2] (second isolate). I 
find this another example of how previous work in the field came 
together with the contacts I had from former years. In 1983 I 
also accepted a postdoc, Leslie Tobler. She began working in the 
small room which we had for the human virus research. 



The State of California Appropriation for AIDS Research. 1983 



Levy: I went to the dean, Julie Krevans, who is the chancellor now. I 
asked for money in '82, just $1,500, and he said, "Well, you have 
to apply; I can't give it to you." 

Hughes: This was for the filter? 

Levy: Yes. I applied, but it took months, so Marc Conant called the 
state legislators, and they got on the chancellor. Then the 
chancellor called Marc in and gave him hell for going above his 
head. 1 But it got me my filter. 

Hughes: Did you go down to the Los Angeles meeting with [California State 
Assembly Speaker] Willie Brown? 

Levy: Yes. There were a group of us. We heard through Marc Conant that 
Willie Brown was going to submit an AIDS appropriation bill to the 
legislature. So I got up at five o'clock in the morning, took a 
cab to the airport, met Art Ammann, Dan Stites, John Greenspan, 
Paul Volberding, and Murray Gardner from UC Davis, and we flew 
down to L.A. to Willie Brown's office. We got there at eight 
o'clock in the morning, and we were to work on a budget. There 
were six secretaries with word processors assigned to us. Now, at 
the time, I had never even seen a word processor. There were some 
very nice people there from UCLA, Irvine, and San Diego, but I was 
the more senior person. I headed the virology group. 

Hughes: What virology group? 

Levy: Well, all the people interested in looking for a virus [in 
association with AIDS]. 

Hughes: All those campuses had ongoing AIDS research in place? 



Conant 's viewpoint, see his oral history in this series. 



Levy: They were getting started. We were well ahead of them; we really 
were. 

We set up a budget to go after finding the virus. I set up 
my own budget, which was about $190,000--most of it being for an 
ultracentrifuge to do the enzyme assays I needed. You could not 
get funds for machines from NIH. I couldn't get money for 
salaries, no less machines, and that really was important to me. 

At the L.A. meeting we came up with this budget, and they 
counted it all up as $2.9 million. Well, you could have picked me 
off the floor. I said, "No way. We'd better get that down below 
$2 million--$1.2 million or somethingor we'll never get it." 
And the others said, "Jay, you're wrong. The legislature is all 
hepped up to do this; this is a major issue. The legislature has 
a lot of pressure on it from homosexual groups, and so forth. 
You'll be surprised. This is not a lot of money; it will go 
through, and you will be able to get started." So sure enough, in 
June 1983, the bill passed. 

Now there are some interesting political aspects to this. I 
was playing squash with John Ziegler, because we had a regular 
squash game, and he said to me, "Dave Golde is saying that he is 
going to prevent us from getting the money unless he gets just as 
much money as you." Dave Golde had been here as a fellow in 
hematology and oncology when I was already an assistant professor 
and for some reason developed an envy. He seemed above coming to 
that meeting with Willie Brown, so he didn't have any request for 
money, and no budget. 

The 'legislators wanted to take money away from other people 
so that Dave Golde wouldn't mess it up, and I insisted to John 
that I would not give in: Dave Golde should not get this funding; 
we should call his bluff. There was no way he was going to 
challenge the state, and it would be more embarrassing to him. 
I'll never forget that. That was really unbelievable. I was 
furious. But it indicates what goes on here. So in July of 1983, 
the bill was voted on and approved. Golde didn't get his funds. 

I had just published the Lancet paper where I said that AIDS 
was an opportunistic infection, 1 and it had gotten a fair amount 
of publicity. So I had established myself as thinking about the 
AIDS problem and also the cause of Kaposi's. So it wasn't like I 
was an unknown. 



'J. A. Levy, J. L. Ziegler, "Acquired immune deficiency syndrome 
(AIDS) is an opportunistic infection and Kaposi's sarcoma results from 
secondary immune stimulation," Lancet 1983, ii: 78-81. 



I remember Rudi Schmid coming up to me at a dinner at Steve 
Shohet's house (after Cadman took over the cancer institute) and 
saying, "Jay, it's very good what happened, and don't worry, 
you'll get your money in time. But we can't just have the state 
money for AIDS research given like that." Someone else had also 
said, "There's going to be trouble, because Rudi Schmid is not 
going to allow us to have the money. He's going to seize it and 
make us all go through a review." 1 

Hughes: Which was not the legislature's idea? 

Levy : No . 

Hughes: They wanted the funds to go immediately to the AIDS researchers? 

Levy: That's right. I had to go off to a meeting, and during that 

period of time, Art Ammann came out very adamant against Rudi and 
was in the newspaper about this. 2 Shortly thereafter, Art left 
the university. 3 

Rudi Schmid was very demanding. I went down to see Dick 
Littlejohn, who was his assistant and vice dean, and said to him, 
"Dick, this is wrong." Dick and I had known each other from 
social events. He said, "Jay, Rudi is adamant about this but I 
think you'll get some money." 

Hughes: Schmid was adamant that AIDS funds should go through university 
channels? 

Levy: That it should be peer reviewed. Now, we kept saying, "We're not 
fly-by-night researchers; we are major people in research; we've 
gotten grants before, and we need this money to get going right 
away." Eventually in September I received money (three months 
late) to buy my ultracentrifuge so we could begin doing reverse 
transcriptase assays for detecting the virus. That machine did 
not get purchased until October, 1983. 

At the time, I was anti enveloped virusesherpes and 
retroviruses--being the cause of AIDS, mostly because I did not 
think they could survive the treatments used to make Factor VIII 



*For Schmid 's viewpoint, see his oral history in Archives and Special 
Collections, UCSF Library. 

2 Randy Shilts, "UC Assailed for Delay on AIDS Funds," San Francisco 
Chronicle, August 25, 1983. 

3 See the oral history in this series with Arthur Ammann. 



47 



for hemophiliacs. 1 In mid- '83 I was thinking along the lines of a 
parvovirus or small DNA virus. I like parvoviruses, because 
they're hard to grow. 

My grant from the state of California was to isolate the 
AIDS virus in animals . So when the grant came through in July of 
'83, John Morrow was here looking at xenotropic virus expression, 
nutrition, and autoimmune disease, and Larry Kaminsky joined me as 
a dermatology fellow. Now I could hire some technicians. But the 
grant gave me, for the whole year, only $19,000 for supplies. 
That hardly would pay for much. 

I called the NIH and I told Jack Gruber, whom I had known 
for years in cancer, that there was not enough money. I said, "It 
is so little money that when the press asks me, 'Is there enough 
money for AIDS research? ' , I am going to have to tell them, 
'Absolutely not.'" He said, "Are you threatening me?" I said, 
"Take it as you will. I'm called by the press all the time." He 
blew up, apparently called everybody, and he said, "I am working 
like crazy to get you more money and don't mess it up." Within a 
week, I had $20,000 more for each year. That's the way NIH seemed 
to work. 

Now, Jack was tied to the National Cancer Institute, and I 
can tell you that that group was tied to Gallo, and that whole 
area of research [AIDS] was cordoned off for Gallo, and not much 
support for anybody outside. At that time, 1982-1983, Bob Gallo 
and I were good friends, but he had all the money he wanted, and I 
had no money. So I always was hoping Gallo would help me, and I 
did various things at his advice, like writing a letter to 
Congress in defense of Vince DeVita so he would be maintained as 
the head of the NCI. I never got even a letter of thanks from 
him. 



AIDS Etiology and Heat Treatment of Blood Products 



Levy: Meanwhile, I had come up with this great idea, 1 thought. I had 
worked with mouse retroviruses, and I knew they were very 
sensitive to acid. If you lyophilized them, freeze-dried them, 
you could keep them living, but they lost some infectivity. I 



'Stephen Follansbee, M.D., remembers receiving at one of the KS Study 
Group meetings a document giving Levy's reasons why the AIDS agent was 
probably not a retrovirus. See Follansbee 's oral history in this series. 



48 



felt that the procedures for making Factor VIII would probably 
kill them. How then could a retrovirus give AIDS since the chance 
of this virus surviving Factor VIII preparation would be low? 

I called Bruce Evatt at CDC [Centers for Disease Control] to 
find out whether all hemophiliacs with AIDS had received whole 
blood, because if they had, then my idea wouldn't work. They 
could get the virus from blood transfusions. Well, I found out 
that no, there were some hemophiliacs who only got Factor VIII 
concentrate, and they had AIDS. Everyone then was rushing to look 
at Factor VIII concentrates by DNA hybridization in search of a 
virus--! mean, what were they going to look for? --but they were 
looking. And they were trying to culture the virus. 



Levy: To examine this idea, in the fall of 1983, I contacted five 

companies manufacturing Factor VIII. Armour, Abbott, Highland, 
and one other said that they couldn't work with me. I wanted to 
have them prepare the mouse retrovirus according to their 
procedure and see what happened to it. 

Hughes: Why did they say they couldn't work with you? 

Levy: They said their procedure was under a patent and they couldn't 

reveal it not that they'd have had toand they just didn't want 
to work on this project. 

I wanted to figure out what this virus was, and the only 
clue I had was that it was passed in a product (Factor VIII 
concentrate) that had been subjected to acid, pH changes, 
filtration, pelleting, centrifugation, all these procedures. So I 
thought, This virus has a physicochemical property that may not be 
characteristic of a retrovirus, and I ought to figure out first if 
I should just forget about the retroviruses as a cause of AIDS. 
So I contacted the companies, and Cutter, a subdivision of Miles 
Laboratory, was the only one that said, "We'll do it with you," 
and that was George Mitra and Milt Mozen. So we set up some 
experiments. The phone calls were in the fall of '83. I had even 
written up a letter for submission to a journal saying 
retroviruses might not cause this disease, but it was never 
published. 

Everyone else who had said it could be a retrovirus, like 
Gallo and [Myron] Essex and all, hadn't given this [heat treatment 
of Factor VIII] any thought. Although I had the idea, I had to 
prove to myself that it was right or wrong, so I needed to do it 
[purification of Factor VIII] exactly the way the companies did 
it, and Cutter agreed to do it. So we set up some experiments at 



49 



the end of ' 83 with the mouse retroviruses , and they were ongoing 
for several months. 

Hughes: At Cutter? 

Levy: Yes. I sent the mouse virus over to Cutter in Berkeley; they 

prepared the Factor VIII material, brought it back here, and we 
tested all the fractions; we measured how much virus was left 
after purifying the Factor VIII. And those studies ended up in 
March of '84 revealing that the virus survived in the freeze-dried 
product. ' 

Having observed this result, we agreed to test heat 
treatment as a means of eliminating the virus. We found that it 
took up to seventy-two hours at sixty-eight degrees C. to kill off 
all the mouse virus added to the plasma sample and remaining in 
the lyophilized product. We then went to the National Hemophilia 
Foundation and asked them immediately to ask that heat treatment 
be the accepted therapy. They refused. 

Hughes: Why? 

Levy: They said, "You did it with the mouse virus and not with the human 
virus." This is my second biggest regret in AIDS; the first is 
that I didn't go to Park City in February 1984. I would have been 
ahead of the NIH as I would have known about the emphasis on 
retroviruses and heard Jean-Claude's [Chennann] talk. 2 The second 
is that I didn't go to the National Hemophilia Foundation [NHF] 
meeting. I was in Europe. Milt Mozen went, and Milt came back 
and said, "Jay, no, they don't want to do it." Peter Levine, then 
head of NHF, wouldn't advocate it, we thought because it required 
too much money and the evidence was not conclusive. It would have 
cost millions of dollars to recall all of the blood products and 
have them heated. 

Hughes: But AIDS is a fatal disease! 

Levy: At the time, even I didn't think that many hemophiliacs would get 
contaminated product. We didn't know how widespread HIV was in 
blood products. In fact, if we had heated blood products in "84, 
we would have protected a number of peoplebut not the vast 
majority. They had already been infected with HIV. 



J J. A. Levy, G. Mitra, M. M. Mozen, "Recovery and inactivation of 
infectious retroviruses added to Factor VIII concentrates," Lancet 1984, 
ii:722-723. 

2 See below for more on this topic. 



50 



So now we had to repeat all that work with HIV, and then 1 
had a hard time getting the human virus work published by Lancet. 
They said, "You're just repeating the mouse work!" But we finally 
got it published, I think in '85, as a letter. 1 

The CDC [Centers for Disease Control] did the same thing we 
did, and they came up with a similar but not as quantitative a 
result. But to this day, the work that we did showing three days 
of heat treatment is needed is the only treatment of blood 
products that protects against blood product transmission of HIV. 
There are people who have been infected by products heated for two 
days at sixty degrees, not sixty-eight degrees. In this regard, I 
feel good that we made an impact on hemophiliac care. 

Hughes: Was heat treatment a recognized technique in virology? 
Levy: It had just been developed at Cutter. 
Hughes: For what? 

Levy: For hepatitis B, and it worked okay, but not consistently, I don't 
think. 

Hughes: What was the theoretical basis? 

Levy: They were afraid that if you heated the concentrate too long, 

you'd kill the Factor VIII. So you had to work out conditions in 
which you would not inactivate Factor VIII but you would kill 
virus. Which they did. 

Hughes: Was heat ever thought of as a possible treatment for AIDS 
patients? 

Levy: You can't heat the blood. You'd kill the white cells. So it's 
only useful for plasma. 

Hughes: In the pre-antibiotic era, hyperthermia was used to raise body 
temperature with the idea of killing micro-organisms. 

Levy: Yes, with syphilis. And some people said this might work for HIV, 
but it has not. 

Interestingly, the only recognition I received in those 
early years for all the work I did in HIV came from the heat 



M. A. Levy, G. A. Mitra, M. F. Wong, M. M. Mozen, "Inactivation by 
wet and dry heat of AIDS-associated retroviruses during Factor VIII 
purification from plasma," Lancet 1985, 1:1456-1457. 



51 



treatment process. I got the Murray Thelin Award [1986] from the 
National Hemophilia Foundation for finding a way of making blood 
products safe. 

Hughes: Did you go to the blood bank meeting in Atlanta in January '83? 
Levy: No. I was unable to attend. 1 



Chasing the Virus ## 

The Gallo and Montagnier Teams 

Levy: Now, I was in Paris in October of '83 for my brother's wedding. I 
had had my sabbatical with Jacob at the Pasteur in 1979, and I had 
maintained close contact with Jean-Claude Chermann and Frangoise 
Barre-Sinoussi, and I was now quite proud of them. I have to say 
that in some ways I didn't think that the European labs were as 
well-equipped to have gotten a foot in the door in this disease. 
And I was pleased for them to have been in the forefront of 
looking for the AIDS virus . They always had been trying so much 
to make a name for themselves, Jean-Claude particularly, and 
Frangoise too. So I was really proud of them. I wrote them a 
letter before I came, saying congratulations and expressing my 
pleasure to see them involved. But, I felt they were wrong. They 
published in Science in April 1983 that they had isolated an HTLV 
[human T cell leukemia virus] -like virus. 2 And Gallo also 
published that he had isolated an -HTLV-like virus. 3 

I got some nasty comments from Bob Gallo: "Jay Levy, who 
does he think he is, talking against this retrovirus?" Because I 
put together the fact that HTLV is cell-associated, and so you 
would never get enough to make plasma infectious as we knew it 



'For comment on this and other events associated with blood 
transmission of HIV, see the oral history in this series with Herbert 
Perkins . 

Z F. Barre-Sinoussi, J.-C. Chermann, et al., "Isolation of a T- 
lymphotropic retrovirus from a patient at risk for acquired immune 
deficiency syndrome (AIDS)," Science 1983, 220:868-871. 

3 R. C. Gallo, P. S. Sarin, et al., "Isolation of human T-cell leukemia 
virus in acquired immune deficiency syndrome (AIDS)," Science 1983, 
220:865-868. 



52 



could be. Moreover, HTLV is not cytopathic; it transforms cells. 
So it didn't fit the AIDS picture. I said, "It's impossible that 
this be the virus. If HTLV s there, it's a passenger; the 
patients are immunosuppressed. We're going after the real virus." 

Hughes: The realization that Gallo was on the wrong track prompted you to 
go after what you're calling the real virus? 

Levy: Not at all. Because from '82 I was looking for the virus, right? 
So what difference did Gallo 's publication make? No, if anything, 
I was pleased to see they were completely off on the wrong track 
by sticking to HTLV. I was going to take the right track, but 
with a hell of a lot less money than they had. 

So then I went to Paris, and I wrote to the Pasteur 
Institute group saying, "I'm coming," and they invited me to Luc 
Montagnier's Saturday morning lab meeting to hear more about LAV 
[lymphadenopathy- associated virus] . Well, I was very impressed 
that he got the whole lab in on Saturday morning, and was pleased 
to be able to go to the meeting as well. 

Hughes: He had started those Saturday sessions because of AIDS? 
Levy: I guess. Perhaps it was a usual session for his lab. 



Immunology Meeting, Japan, July, 1983 

Levy: But I have to backtrack a bit to, say that in July of '83, I went 
to the international immunology meeting in Kyoto, Japan. At that 
meeting, I spoke on nutrition and autoimmunity-- totally unrelated 
to AIDS. But there was the uproar: "What about this new disease?" 
Japan was asking, "What is AIDS? What is AIDS?" There was so 
much commotion over it that Susan Zolla-Pazner, who was an 
immunologist in New York and now a good friend of mine, organized 
a press conference there to discuss where we were in general to 
finding a cause, and I went to it. She did a sensational job. I 
didn't know her then; I wrote to tell her that she did such a good 
job handling the questions. She is very bright. 

There was a young French guy--I think it was Marc Alizon-- 
who got up and talked about the HTLV that they had isolated. He 
didn't speak English that well, but I didn't recognize that. What 
I did recognize was that he said that the one thing clear in his 
studies was that antibodies to this virus were found only in 
French people. Everyone took that statement as exclusive, and 
thus few took him seriously. 



53 



So in October 1983, when I met with Luc, Jean-Claude, and 
Francoise and they described their virus, I was surprised they had 
something that potentially could be the AIDS virus. As John 
Crewdson correctly reported, I came back to the hotel and I said 
to my wife, "Sharon, I think they may have it." 1 I've got to say, 
I felt they had a good head start. I didn't even have my 
equipment, and I felt bitter that I wasn't given the opportunity 
to really go after the virus. I couldn't do reverse transcriptase 
assays in my lab to look for this virus because no one would let 
me use an ultracentrifuge to spin down material from AIDS 
patients. 

I said to the French group at the time, "Well, you know, 
this is a big surprise to me because when your young fellow 
[Alizon] got up to speak in Japan in July, it sounded like you 
just had a French virus." And they all laughed and said that was 
because of his [poor English] language, and he got a little 
embarrassed. I said, "Well, look, if this is so, I'm going to be 
the first group to confirm you, because I don't think that the 
NIH, which is Gallo and Essex, is onto it." And they said, 
"You're absolutely right; they think it's HTLV. We've been 
telling them they're wrong; they don't believe us." The French 
group told me how LAV grows preferentially in CD4 cells, and it 
kills the cells. And they had an immunofluorescent test to look 
for antibodies in the blood. It showed the virus in the cultured 
peripheral white cells. But the problem was, the white cells kept 
dying. 



More on the Levy Lab ' s Search for the Virus 



Levy: So when I came back to the lab in October, we had gotten the 

ultracentrifuge, because Rudi Schmid allowed us $50,000 from the 
State of California grant. So we began doing our RT [reverse 
transcriptase] assays. It was the undergraduate student Tony 
Hoffman, a chemistry major at USF [University of San Francisco] , 
who did the reverse transcriptase assays. He was one of the few I 
could keep in my lab since he was not paid. 

Hughes: He knew the assay when he arrived? 

Levy: No, I had learned it, and the method was part of our lab protocol, 
and we perfected it. In fact, after working on the initial 



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



54 



procedure, Tony improved the technique and, in October 1983, we 
found some RT positives, but we also found some controls that 
looked kind of positive. We had to work out the parameters that 
would give us really accurate results. At the same time, in the 
back of my head was the question, "Is this a retrovirus? Would a 
retrovirus be in Factor VIII products?" I was waiting for the 
data from Cutter Labs. 

By the end of November [1983], we had some real positives; 
but we also had some negatives (from AIDS patients); we didn't 
have a virus that was growing like crazy. We could only say: We 
have a virus candidate, but we can't say it's the cause of AIDS, 
because we aren't finding it in all the AIDS cases. It was a 
situation where I had so many patients coming in; we had so few 
people to work; we were doing so much; there was only a certain 
amount of things we could get to. 

Hughes: Where were the patients coming from? 

Levy: Many from Paul Volberding, but to tell you frankly, several of 
them came right to this door because Harry Banghardt, one of my 
classmates from Wesleyan University where I went to college, was a 
doctor, and he had a lot of friends who were gay, and they were 
infected. I have to say that Harry, who later died from suramin 
treatment of HIV infection, brought me some of the most 
interesting cases, including the one that gave me high virus 
replicative activity in November-December [1983]. Then we knew we 
had something. We also thought the virus was similar to what the 
French had. 

Hughes: Why did you think so? 

Levy: Because it was killing lymphocytes. I then called Fransoise, and 
I said, "Send me some serum and fixed infected cells on slides, so 
we can see if it's the same virus." She sent the serum, and we 
did the immunofluorescence assay, and we found that the serum 
recognized some of the viruses we isolated but not all. So we 
felt maybe our virus was different from that of the French. Then 
I began thinking, We have a different one. They have a different 
one. This may be just a passenger virus in an AIDS patient, and 
we haven't found the real cause. So we continued to isolate 
viruses, checked the sera for antibodies to our agent and to 
slides fixed with the BRU (the French) agent. I called Fran<joise 
and told her, "We've got some cross-reactivity, but not with all 
[viral] isolates." 

And then in March 1984 when I found that the mouse 
retrovirus survived Factor VIII purification, I realized that we'd 
better concentrate on this human agent with RT activity. We'd 



55 



done all this animal workguinea pigs, mice, rats, hamsters- 
inoculating in the brain, in the gut, bleeding them, checking 
them. I had a UCSF medical student looking at peripheral blood to 
see if there was any depression in white cells in the blood. It 
took an incredible amount of energy, something that I just don't 
think I could do again. We attacked the problems from many sides 
and again with very few people to help. 

We had to travel ten miles to the animal facilities, because 
for safety precautions they had to be in a lab separate from the 
campus. I had to get separate biohazard hoods in which to work. 
Fortunately, the state funds paid for this. I was right next to 
Stan Prusiner's prion experiments with animals; that's where they 
put us with the AIDS work. And despite using many animals we 
didn't have any results that looked good. 

I also called Sy Kalter in San Antonio at the Southwest 
Texas Foundation. I looked on this as being an opportunity to 
call on all my friends, everybody I knew from earlier virology 
days. He had a primate colony. I said, "Look, I want to send you 
blood to put into primates. I would like a chimpanzee." He got 
permission at the last minute, and then it was taken away. So the 
best we could do was to put it into baboons. 

Hughes: Why was permission taken away? 

Levy: The institute didn't want to give up the chimps. Sy was getting 
near retirement, and they took control away from him. 



Carlton Gajdusek 

Levy: I also got a call from Paul Brown, who worked at NIH with Carlton 
Gajdusek, the Nobel Prize-winner for slow viruses. Brown asked 
would I be willing to work with Gajdusek to isolate the AIDS virus 
in chimpanzees? I took him down to meet Ed Cadman, our new 
director of the Cancer Research Institute, who I thought was 
supportive. I wanted Ed to hear it, because I was nervous that I 
would be doing all this work and then I would lose control of the 
project. 

Hughes: Lose control to whom? 

Levy: To Gajdusek. I would send all the bloods to him and then never 
hear from him again. It would be tough. 



56 



I called Werner Henle as well, who was one of my mentors, 
and he said, "Jay, you have to be very careful because you will 
lose control." So I wrote a letter to Gajdusek saying that I'd be 
happy to collaborate, but that I expected that we would be very 
forthright about it, and that it would be my project working with 
him; we would work together on it. I never received another 
letter from him, and never heard from Paul Brown again. 
Apparently he went to Gallo and to Montagnier, and he did work 
with them. They published an article in which Gajdusek was the 
first author, so I thought my concern was reasonable. 

Hughes: Why were you moving into primates? 

Levy: Because I wanted to see if I could find the AIDS virus in a 
chimpanzee, which is the closest relative to man, and get a 
disease; then I might isolate the virus that way. That's the only 
way you can get hepatitis B virus. I knew this was the only 
method that led to isolation of some human viruses. 



Hepatitis B as a Model for AIDS 



Hughes: Hepatitis B keeps cropping up in people's conversations. Why was 
it picked as a model for AIDS? 

Levy: Because it was transmitted at a high rate among homosexual men; 
it's passed sexually; it affects the immune system, and it 
certainly would survive Factor VIII purification. 

Hughes: Were there any ways in which that model misled you? ' 

Levy: Yes. It misled you in that it was soon found that some people, 
like children, got AIDS and they didn't have hepatitis B 
antibodies. The hepatitis B model just didn't hold up. The CMV 
model held up longer than any of the others. Nevertheless, many 
investigators thought antibodies to hepatitis B core antigen might 
be a surrogate marker for AIDS virus infection. 



Levy Misses A Key Meeting 



Levy: In February of '84, there was a meeting, organized by Bob Gallo, 
at Park City, Utah in which they were to discuss AIDS. As was 
usual for Gallo meetings, I wasn't invited and did not have any 
funds to go on my own. At that meeting, Jean-Claude Chermann 



57 



presented the data on what he now called LAV. Susan Landau was 
working with me part-time on the project. She's a co-author on 
the ARV paper. She said, "I'm going to Park City with my husband 
to ski; I'll look in on the meeting." I said, "Okay, great. At 
least I'll have somebody to report on the meeting." Susan came 
back from the meeting, and this was my big mistake: I should have 
gotten her to take notes. She said, "Jay, it's no big deal. They 
were talking about HTLVs and -Is and -Us and -Ills, and 
everything that we have talked about. There was nothing new." 
Apparently, every time Jean-Claude Chermann started talking about 
his virus [LAV], Gallo got up and said, "It's a contaminant; you 
don't know what you're talking about," and really downplayed the 
French results that he did not believe. 

Suddenly in March [1984], there was a big turnabout, and 
then Gallo rushed four papers into publication. In fact, one 
thing Abe Karpas from England showed, which I was amazed at, was 
that Gallo had submitted a paper in January to Science, which 
appeared with the other papers in May, in which words had been 
changed! In January, the virus was HTLV-I. In May, it suddenly 
became HTLV-III. In other words, he completely did a turnabout, 
and changed everything around, and put the four papers together 
for Science. 

Now, you can ask why he had four papers in Science: Because 
Bob Gallo had incredible power. You can then see why he was so 
feared; nothing could touch him. He did whatever he wanted. 
Anyone that did him bad, you were out of the picture. He ran it 
like an autocrat, tyrantwhatever you could call him. It was a 
dangerous situation for science; he controlled it all. And that's 
why he could do what he did and almost get away with what he- did. 

How could I fight him in a university that doesn't even want 
to have a press conference to draw attention on our work? I 
published in Science 1 [on the isolation of the AIDS virus] and 
did get some publicity, 2 but not to the point of saying, "Jay 
Levy ' s group found the AIDS virus . " Forget it ! Gallo ' s 
announcement had already been in every newspaper and magazine 
around the world! It wasn't as if I could have a press conference 



'J. A. Levy, A. D. Hoffman, S. M. Kramer, et al., "Isolation of 
lymphocytopathic retroviruses from San Francisco patients with AIDS," 
Science 1984, 225:840-842. 

2 "UC-San Francisco studies confirm French finding of retrovirus in 
AIDS and demonstrate a retrovirus could be passed through blood clotting 
factor," UCSF News /Public Information Services, May 9, 1984. 



58 



in May and say, "Yes, but we have the virus as well." He 
published before we did. 1 

So if I had been there in Park City, I think I would have 
heard the French data a little bit better, and I would have taken 
our results more seriously and gotten the paper out faster- -before 
the Factor VIII data came through. However, I still think that 
not having the Factor VIII data would have made me reluctant to 
write it up as the AIDS virus. 

Hughes: So the effect would have been the same? 

Levy: It might have been the same, except I think by March [1984], I 
would have quickly put the paper together, and I probably would 
have published in the same issue with Gallo. 

Hughes: Now, this is pure speculation, of course, but what if you had had 
the filter for the hood and the ultracentrifuge earlier than you 
did? 

Levy: We would have had the virus a year earlier. There's no question 
in my mind. It was so easy to find. We were a lab dedicated to 
finding viruses. We still are. There weren't very many left; 
everyone was put out of business by Reagan's economic program in 
'80. There's no question in my mind about that. And more the 
ultracentrifuge than the hood; the hood was important, but that 
was only $1,500. The ultracentrifuge was $50,000, and I had to 
wait much longer for that money. Even if I had had the centrifuge 
in June as planned by the state legislature, I would have isolated 
the virus earlier. 



Gallo Reverses His Stand on the AIDS Virus 



Levy: I've got to backtrack: in April of '83, just before the Science 

papers from the French and from Gallo came out, I was invited to a 
meeting at NIH to discuss AIDS. Richard Krause, then head of 
NIAID [National Institute of Allergy and Infectious Disease] , 
organized it. At that meeting, there were many people who were 
involved in AIDS research, including Tony Fauci. And I remember 
never having met Tony before, and they said, "Oh, this is one of 
the new young immuno legists coming up the ranks at NIH; very 
bright guy." He and I hit it off very well from the beginning. 



'Gallo 's papers on the AIDS virus were published in Science in May 
1984; Levy's paper was published in Science in August 1984. 



59 



I talked quite openly about the types of viruses which might 
cause AIDS . They had people talking about the epidemic of canine 
parvovirus that occurred in '77. Could this be the canine 
parvovirus causing AIDS? There was some evidence that perhaps it 
was a parvovirus, which of course I was looking at. 

Hush was around that Gallo had found an HTLV in association 
with AIDS--it didn't bother me at allbut there was a big hush 
about it. So they demanded that his associate [Edward] Gelman 
talk about it. I think he said that he had evidence of the virus 
in the white cells. Frankly, I didn't believe it. 

Hughes: Who is Gelman? 

Levy: He worked with Bob Gallo. 

It was clear that NIH looked to Bob Gallo to solve this 
[AIDS] problem. He was their leading virologist, and he had the 
resources--$ll million or more a year. So from all over the 
world, people were sending specimens to his lab. 

Hughes: Since the AIDS agent is cytopathic, why did Gallo link it to HTLV? 

Levy: Exactly my question. They said, "Well, it might not be HTLV, but 
it's HTLV-like; it may be a cytopathic counterpart." And when 
they isolated HTLV-III, they said it cross-reacts with HTLV-I, but 
that is false. The viruses Gallo isolated in 1983 were HTLV, so 
their role in AIDS did not make any sense. Bob Gallo has this way 
of being able to make an observation and draw public attention to 
it. It actually has some positives, because he can put forward an 
issue, even if the data aren't that great. So he got all this 
attention on HTLV, and it was wrong. So did Max Essex. And it 
misled a lot of people. That was the bad part of it. 



The French Group's Conclusion: A New Virus Causing AIDS 

Hughes : One difference between what Gallo was doing and what you and the 

French were doing is that you and the French had a more open-ended 
view of what the AIDS agent might be? 

Levy: Yes. I think that Gallo was convinced that it had to be a 
retrovirus, because he wanted to put more attention on 
retroviruses, since he found one (HTLV) and it wasn't getting much 
attention. 



60 



The French wanted anything, and they were retrovirologists, 
so when they found this retrovirus, they thought it was brand new. 
They didn't approach it like I did, which was to ask, "Could it 
possibly be just another contaminant?" It was a new retrovirus; 
at least it looked that way. But I didn't know that. 

Hughes: Why did the French assume that it was a new virus? 

Levy: Because they knew it kills lymphocytes. They told me it did not 
cross-react with HTLV, although that was inferred in the Science 
paper. There were differences between the AIDS virus and HTLV. 
Now we know that the cross reactivity was written in by Bob Gallo 
when he was the reviewer on that paper. Luc Montagnier didn't 
have the courage, apparently, to say it was wrong. I have the 
feeling Montagnier was uncertain as to what was the truth, and 
maybe it was Framjoise and Jean-Claude who really knew they were 
onto something important. But anyway, for some reason, there was 
a "greying" of what was really true. 

Hughes: I read that the first electron micrographs of LAV were difficult 
to interpret. 1 Do you remember that? 

Levy: Well, I didn't see any of the electron micrographs --oh, yes, when 
I went to the Pasteur Institute I saw them, and they looked okay 
but it was difficult to know if the agent was new. But I know 
that Bob Gallo thought, and others thought as well, that this 
virus [LAV] was a contaminant, that the French were famous for 
contaminating cultures with viruses from other sources. 

They said there was some cross-reaction with the horse 
lentivirus, equine infectious anemia virus, which was I must say 
dear to my heart. I had done a lot of sleuthing about the equine 
infectious anemia virus years ago when I first suggested it could 
be a retrovirus. And Gallo thought it was a contaminant. I think 
he even said so at one point. I think he said it to me. I did 
wonder about whether equine infectious anemia was a possibility as 
a cause of AIDS. That's why I thought, Well, if we don't find 
something like this in our patients, it could be a contaminant. 



'John Crewdson, "The great AIDS quest," Chicago Tribune, November 19, 
1989, section 5, p. A. 



61 



Levy's First Reverse Transcriptase-positive Viral Isolates, 
Late 1983 



Levy: When, at the end of '83, I did get the first isolate that I 

thought was right, I found out that the guy from whom the virus 
was cultured had been traveling in France. I suddenly thought, 
Uh-oh, maybe he picked up this virus, and it's not the AIDS virus. 
And I couldn't find him, because he was on vacation for a couple 
of weeks. Well, what unfolded was isolations, RT positives, but 
also many negatives. Now I know why we had many negatives. We 
were attempting to isolate virus like other people were doing, 
which is far from being the ideal. 

Hughes: Please explain. 

Levy: Well, because we were not putting fresh, normal white cells into 

the cultures. We would just take a person's white cells, put them 
in culture with a mitogen, and wait for the virus to come out. 

Hughes: You mean white cells from infected people? 

Levy: Yes. 

Hughes: So the people were already unhealthy? 

Levy: Well, yes, they were feeling some symptoms. And what we now know 
is that there are in many infected individuals lymphocytes that 
can suppress HIV, so you wouldn't find it in a culture alone. But 
we only learned that by chance in '84 when we asked why some blood 
cultures did not release virus. 

Also, from October of '83, when I came back from France and 
had my ultracentrifuge, to March of '84, which is six months 
later, I had with me just a student, a technician, and a secretary 
doing this work. We had about twenty positive cultures. We were 
confident. We concentrated on one culture, which happened to be 
from a patient whom I actually saw through Harry Banghardt. I had 
seven milliliters of the patient's blood; that's all. And this 
virus came out with such activity that it was just unbelievable. 

Hughes: Was it just luck that you had concentrated on that particular 
specimen? 

Levy: No. It was just that, when cultured with the white cells, the 

virus grew like crazy, and we found antibodies to it in peripheral 
white cells. I said, "Well, this is a really good prototype," and 
that became our ARV-2. We had an earlier one we called ARV-1, and 
there were other cultures that might have been positive. We 



62 



didn't count them, because we didn't grow them for a long time. 
That one [ARV-2] we concentrated on. 



Announcing Levy's AIDS-Associated Retrovirus //# 

Levy: So Gallo has his press conference [April 23, 1984], and he didn't 
mention the French. "Live at Five" [a television news program] 
asked me if I'd comment. This was in April, I think. I went down 
and said, "We have similar viruses too." So that was my first 
announcement that we had the virus . 

In early May, Gallo 's four papers came out. I was to give a 
lecture at a joint meeting of the American Society for Clinical 
Oncology and the American Association for Cancer Research [AACR] 
on viruses and autoimmunity and immune disorders, and I chose that 
moment (May 9, 1984) to show all our data on our AIDS virus, which 
we called AIDS-associated retrovirus, ARV. And these were 
beautiful data. We had EM [electron microscope] pictures, and 
everything was there. I remember Marty Hirsch coming up to me 
after the meetinghe was a co-speaker--and saying, "Jay, I can't 
get over all the data you have. Why haven't you spoken about it?" 
Though it was written up in a Canadian newspaper, and the San 
Francisco Examiner (Richard Harris, May 9, 1984) and San Francisco 
Chronicle (May 10, 1984), I said, "If I did, I wouldn't have the 
paper accepted for publication." Journals do not like publicity 
before a paper is published. I wanted to get it published in 
Science. 

So I wrote the paper up in May, and sent it to Science, and 
it got reviewed, and it got accepted within a month. 1 There was 
one point during the review when I was afraid it wouldn't be 
accepted. One editor had said, "Well, why do we need another 
paper on the isolation of the AIDS virus?" And I said, "This is 
in San Francisco, and the isolation is totally independent." And 
the paper then sailed through the review process. 

Hughes: Did it make a difference that yours was a different isolate? 
Levy: Well, the reviewers didn't know that. 
Hughes: Oh, because nothing had been sequenced. 



*J. A. Levy, A. D. Hoffman, et al. , "Isolation of lymphocytopathic 
retroviruses from San Francisco patients with AIDS," Science 1984, 225:840- 
842. 



63 



Levy: Right. So Gallo's papers came out, and of course the news was all 
over the world. I asked the university whether we should have a 
press conference. Oh, no, they didn't want any press about this. 
This isn't the way we do things. 

Hughes: What was the thinking there? 

Levy: Well, it was Rudi Schmid. He didn't like any publicity on AIDS; 

it's not the way you do it. Also I think the school was afraid to 
have any attention given to this disease for fear it would 
compromise chances of getting good housestaff. Many young people 
might avoid an AIDS medical school. Also in general, a scientist 
should wait until the paper is published. So I waited until 
August; the paper did not come out quickly like the Gallo papers. 

Hughes: Was his reviewed faster than yours? 

Levy: Yes. It was submitted in March, accepted in April, and published 
in May. Mine was submitted in May, accepted in June, and 
published at the end of August. So I lost out in being considered 
in the same group of discoverers. But deep down, I felt that 
eventually my contribution would be understood and that the 
scientific community would see that I worked independently. The 
room I worked in you can see is a tiny little room. I was able to 
do it with very limited funds and staff. I actually grew the 
cells myself. And there is something to say for that. 

I did say in my paper that I never had the advantage of 
having the French virus in my lab. I had heard from Luc 
Montagnier that he had sent the virus to Gallo, and in the back of 
my mind I thought, Well, once you have their virus, you know how 
to grow it, you can get it much faster. I had to work completely 
independently. So I say in my Science paper that this is the 
first independent confirmation. I also realized that in the Gallo 
paper, they made no mention of having the French virus. 

I also wrote Bob Gallo and asked him for his rabbit serum 
against his HTLV-III, to see if that cross-reacted with mine, and 
I never heard from him. Later he actually told me that when he 
got the letter, he was so angry that I was involved in this 
research, he decided he wasn't going to answer me. 

Hughes: You make quite a point of the fact that ARV could not have been 
contaminated by LAV-- 

Levy: That's right. 

Hughes: --because you deliberately didn't receive any virus samples from 
the French. 



64 



Levy: Exactly. If you're going to confirm somebody, don't bring their 
virus into your lab because how would you know the difference? 
That's very important. 

Hughes: Did you foresee that having LAV in the lab was going to be a 
problem for Gallo? 

Levy: No. I knew that my problem would be to just stay on top and let 
others know, "Look, I was there also." 

When Gallo started calling himself a co-discoverer of the 
virus, that really got me upset. If he was a co-discoverer, then 
I was a co-discoverer. Gallo says he isolated his virus at the 
end of '83. There's no evidence that he did. Yet, in my lab we 
have it documented in our lab books that the viruses were isolated 
in late 1983. 

After my lecture at AACR in May [1984] where I presented the 
data on ARV, I was invited to a meeting in Denver by Marvin Rich 
to talk about the virus. They had invited Gallo, Montagnier, and 
me. That June, I was to go to southwest Texas to inject my 
viruses into a chimpanzee, and I decided, "I'm not going to that 
meeting; I'm going to inject my chimpanzees." In retrospect, it 
was interesting that someone back then actually did try to bring 
us together. I don't think it would have made any difference if I 
had gone. Historically, I think I would have still been treated 
as, "Oh, you too?" 

Hughes : Is that the way it really has been? 

Levy: Yes. They will say, "You're one of the three," or they'll say, 

"You're the third person to isolate the virus. When really, I was 
probably the second. In fact, I know I was the second. Because 
I'm the only one who had a different virus. 



The UCSF AIDS Specimen Bank 
[Interview 3: July 25, 1993] #// 

Hughes: Dr. Levy, please comment on the AIDS specimen bank. 

Levy: It was decided, probably by Marc Conant, that we had a rich source 
of material from AIDS patients for people worldwide, or at least 
nationwide, and that we should organize a specimen bank that would 
take care of storing the specimens. We had to figure out who 
could take care of it. The only one who had space, who had a 



65 



freezer available and was willing to do it or could be coaxed into 
doing it, was John Greenspan. He set up the specimen bank, and I 
don't know who was on his committee. We did discuss how much 
plasma to collect, what tissue to collect, how should it be 
handled, and so on- -John should really fill in those details. 1 

Hughes: How did that tie in with what you were doing? You started out 
with the Kaposi's sarcoma problem. 

Levy: We did not rely on John's tissue bank, because I had fresh 

specimens from Marc Conant or from Paul Volberding. Where it 
became more important to us was some years later when we began 
doing work with John on oral manifestations of AIDS, when the 
tissue from hairy leukoplakia patients and so forth was sent up to 
us through that facility. 

Hughes: How actively was the tissue bank used? 

Levy: John knows that. The bank is expensive to run, and he has had to 
justify it for a long time. He's been successful. There was 
very, very active use of it in the first years of the epidemic. 
Now, as the disease has spread, I don't know if people have as 
many demands on it. 

I can recall that if we wanted specimens or sera from 
patients with Pneumocystis , we could just call John and he would 
send us 0.1 milliliters of it quicklyvery easy to get the 
samples. It was of great benefit in those early days when you 
wanted to have well-characterized material. But I think others 
who didn't have as much access as we did to fresh material from 
patients took advantage of the bank more than we did. 



Research on Kaposi's Sarcoma 



Hughes: You mentioned last time that Dr. Conant gave you some biopsy 

material from Dan Turner in February 1982. What did you do with 
it? 

Levy: Marc called me and he said, "Jay, I have a KS patient in my 

office. Do you want to come on over?" So I went over and met 
Dan. Marc removed a Kaposi lesion from the leg of Dan Turner and 
I took it back to the lab. Since I was so limited in staff, I did 
all the work, which was essentially wash the tissue, cut off all 



'See Greenspan's oral history in this series. 



66 



the material that I thought was not the tumor but was adventitious 
tissue, connective tissue. Then I decided on my own that the only 
way to get the cells to grow in culture was to try to create a 
micro-environment so that if the cells produced any factors that 
would help it grow, they would be produced locally and might stay 
if I didn't have them diluted out by the medium. 

So I decided I would cut it up, mince it with scissors and 
forcepsthis was only a one-millimeter biopsy; it really required 
micro-procedures--and then I put it all under a very thin cover 
slip. I pushed the cover slip down on the tumor tissue, then 
added the growth medium. The growth medium finds its way 
underneath the cover slip and it's kept there. The cells after 
two weeks grew out from the biopsy. We developed thirty- three 
different cell lines by that technique. After a lot of work to 
try to find the agent for Kaposi's, which was not successful, we 
were sidetracked to the finding of the AIDS virus, so we froze 
those [KS] cells away. We still have them frozen. They never 
formed tumors when inoculated in nude mice, so we weren't sure 
they were malignant. 

One of the reasons I was looking at the growth factors for 
KS was that I published a paper with John Ziegler in '83 in 
Lancet 1 , saying that Kaposi was probably like a hormone -dependent 
tumor and needed factors to get it to grow. Well, two weeks ago 
we again cultured a Kaposi's sarcoma tumor. I want to revitalize 
that project. I still want to look for an agent. The cells have 
grown. It really is fun, ten or eleven years later, to redo the 
research and have it work so nicely. I now have a few people 
helping me. 

Hughes: In 1982, were you looking for an infectious agent in Kaposi's? 
Levy: Yes, I was. 
Hughes: Why? 

Levy: In those days, I didn't know that Kaposi's was caused by something 
that killed the immune system. I thought it was an agent that was 
spreading around, causing malignant tumors. So I concentrated on 
Kaposi's sarcoma. Once we realized that it was an epi-phenomenon, 
a result of immune deficiency, then we started looking for the 
agent of the immune deficiency. 



'J. A. Levy, J. L. Ziegler, "Acquired immunodeficiency syndrome is an 
opportunistic infection and Kaposi's sarcoma results from secondary immune 
stimulation," The Lancet 1983, ii, 78-81. 



67 



Hughes: At some point, you switched from tissue to blood. 

Levy: Yes. That came about when we were able to get a good filter in 
our hood, because we could then bring HIV-infected blood in here. 
We also needed an ultracentrifuge as well as other equipment to 
work on blood, and none of that came through until the Willie 
Brown initiative that gave us the money in June of '83. And then, 
as you know, Rudi Schmid seized the money, wouldn't let us have 
it, so I didn't have any money until September to purchase the 
ultracentrifuge. And then when I got the ultracentrifuge, I had 
to negotiate to get a room to put it in, which was that tiny 
closet across the hall there. We put the ultracentrifuge in 
there, because no one would let me bring AIDS material into any 
other lab. Subsequently we found the reverse transcriptase in the 
cultured blood cells and were able to isolate the virus we called 
AIDS-associated retrovirus. 

Hughes: Do I understand that you limited yourself to the KS problem mainly 
because of difficulties in getting the equipment you needed to do 
virus isolation? 

Levy: There were two reasons. One was, first we thought that Kaposi's 
held the answer to this disease in young men, because we first 
thought it was an epidemic of Kaposi's sarcoma. And then later, 
because we didn't have any equipment nor place to do the work on 
blood, we couldn't approach the culturing of white cells to look 
for an agent. 

Hughes: If it was an epidemic of Kaposi's sarcoma, how did you explain 
Pneuiaocystisl 

Levy: Pneumocystis was not very prominent on this campus. And while it 
was seen, it wasn't emphasized as much as Kaposi's. At first, it 
didn't enter into the thought process, frankly. 

Hughes: So to you, in those early days, AIDS was Kaposi's? 

Levy: Yes. It wasn't even called AIDS, as of course you know. It was 

epidemic KS and then gay-related immune deficiency. We're talking 
early '82. 

To recapitulate, in August of '81 I see my first U.S. 
Kaposi's sarcoma patient, with Paul. Now I'm waiting to work on 
it. I have no money, no hoods, nothing to do it, and finally we 
get some help. And I immediately go to the Kaposi's. It must 
have been a few months later that it became clear, or more 
evident, that this syndrome comprised not just a tumor, but an 
infectious disease causing immune deficiency. But then we 
couldn't do anything at first except to concentrate on Kaposi's. 



68 
Immune Deficiency 

Hughes: When did immune deficiency enter into your thinking? 

Levy: At the end of 1982, I put together this hypothesis in Lancet that 
said that AIDS was an opportunistic infection which took advantage 
of a compromised immune system. A lot of people have been trying 
to see if that's true, but it isn't true. 

I originally thought that in individuals whose immune system 
was somewhat altered--!. e. , babies, gay men who have used drugs, 
IV-drug peoplethe AIDS agent in most cases would be fought off, 
but there would be a group of people that would succumb. My 
thought was that the immune deficiency created an imbalance in the 
immune system, causing some elements of the immune system to 
overreact and produce cytokines that worked on increasing growth of 
endothelial cells, which are the origin of Kaposi's sarcoma. So I 
called AIDS a disease of hypo- and hyper-immune response. I still 
believe that. It's just that the hyper-response which keeps 
emerging as an idea--autoimmune-type--isn' t as prominent a problem 
as we might have expected. But Kaposi's sarcoma could be a result 
of a hyperactive immune system trying to respond to a deficit that 
has occurred because other elements of the immune system don't 
work. 

Hughes: You suggested in this paper that the immune deficiency preceded 
what we now call AIDS . 

Levy: Right. I thought that we would see lots of infected people that 
had fought off this agent because I came from a background of 
virology where that is true for most virus infections. Epstein- 
Barr virus causes mononucleosis in only a small percentage of 
people who get EBV. Paralytic polio is observed in only 1 percent 
infected. I discussed this point at the AACR [American 
Association of Cancer Research] annual meeting in Canada on May 9, 
1984, where I also announced our virus, ARV. I said that we 
expected that this agent might be found without disease, and we in 
fact were the first group to show healthy people had the virus but 
no symptoms . 



Seropositivity Without AIDS 

Levy: Interestingly enough, that was a small part of my 1984 Science 
paper. And then Marty Hirsch's group went on to publish an 
article on just one person who was clinically healthy who had the 



69 



virus . In other words , I learned sometimes you put so much into 
one article that the readers can't keep track of what you have 
covered. So in this case we said it in our paper, and then later 
other people came in and said, "Well, do you know seropositive 
people can be healthy?" Well, we knew that in the beginning. My 
only disappointment was and still is that there are not many 
infected people who do not get ill. It's interesting as I relate 
that to you that the long-term survivors of HIV infection have now 
become the major focus of my research. 1 

In 1984, I started studying healthy individuals who we felt 
were infected for two years. It had by 1984 almost become the 
dogma that everyone infected got AIDS. That concept is so naive. 
In those early days, we thought two or three years was long-term 
survival. Who would have thought of a disease- -and this is the 
problem with Peter Duesberg--that would take a long time to kill 
or to cause symptoms? There are very few, very few diseases that 
take as long as AIDS does to manifest themselves. Perhaps cancer 
could be another example. 



Puzzling over Etiology 



Hughes: Explain how that observation relates to Peter Duesberg. 

Levy: Peter Duesberg says he's never heard of an agent that takes so long to 
cause disease, so HIV can't be the cause of AIDS. He thinks that he 
knows so much about viruses that he's right, but he has to accept the 
fact that there are models in animals that show a slow development of 
disease. Many of these viruses are known as lentiviruses, "lenti" for 
"slow". But Peter doesn't want to move from the animal model to 
humans . 

Well, I'm not as blocked in that thinking. I'm a medical person; 
I know about pathogenesis. I know it takes ten or twenty years for 
cancer to develop. Some of those cancers are caused by viruses. So 
we shouldn't be surprised, except that this [HIV] has a different 
aspect; it is a lytic virus, not one that transforms, and it is an 
agent that attacks the immune system. 

I think what's very important in research is that you have 
to be able to change your concept when it looks like it's 
different. I've already told you, my concept was AIDS was 



'Jay A. Levy, AIDS, 1993 7: 1401-1410. 



70 

Kaposi's sarcoma. And you said, "Why not Pneumocystisl" We see 
Pnewnocystis in cancer, so I chose to think of that as, oh, sort 
of an epiphenomenon of a cancer virus. 

CD4/CD8 ratios were brand new. I mean, no one was doing the 
CD4 analysis regularly. If we had, we might have been able to 
say, "Wait a second, the immune systems are abnormal." But I 
might have then responded, "Of course, a cancer virus is causing 
this immune problem," and stuck to KS. It was something I had 
been working on; I had lot of clinical material. 

What I cannot remember is when I suddenly made the switch to 
say, "The causal agent is in the blood." I think it had to have 
been the end of '82 because in 1983, when I read of Montagnier's 
finding virus in the blood, I already knew that's where you should 
be looking. But we couldn't get the virus assays going because of 
our lack of equipment and funds. We were already growing some 
white cells in culture. We could just grow them and look for 
changes in them, which we did. But most of our subjects were not 
so sick. 

Hughes: Weren't you also aware of AIDS in hemophiliacs? 

Levy: Yes. 

Hughes: Didn't those cases indicate that the virus had to be in the blood? 

Levy: Well, by that time, I already knew. End of '82, early '83, I knew 
it was in the blood, and that this disease [Kaposi's sarcoma] was 
an epiphenomenon. 

Hughes: When did you get state funds? 

Levy: May '83. So we said already in that grant that we would look in 
blood. So we had to have known in January of '83 that this virus 
was in the blood. And I could not work on it, because I didn't 
have the equipment nor funds. 

Hughes : Were you involved with lab studies in connection with the patients 
who presented at the KS Clinic? 

Levy: I know occasionally we were asked to do the antibodies for ARV, 
but that would be the beginning of '84. 

Hughes: You mean once you had the HIV antibody test? 
Levy: Yes, right. 



71 
The Immunofluorescence Assay for HIV 

Hughes: What about your immunofluorescence test? 

Levy: That was developed for the first time in '84, after the agent was 
isolated. We found the agent, and then developed the assay. 

Hughes : What is to be said about how it was based scientifically? 

Levy: Well, first, we had to find the agent in the blood. Once we had 
the equipment to do reverse transcriptase assays to look for the 
virus, we were at the time separating white cells by Ficoll/ 
Hypaque separation, which was the classic way of doing it based on 
density. The granulocytes go to the bottom of the tube and the 
lymphocytes are at the interface of the material. Red cells go 
down to the bottom as well. After you remove them, you have all 
your lymphocytes, macrophages, free of red cells. 

You put the white cells in culture with interleukin-2 [IL- 
2]. Interleukin-2 is a growth factor that had been discovered at 
NIH as being important for growth of white cells. We began to 
study what occurs over time. Now, in those early studies, we 
worked with Dan Stites, Conrad Casavant, and Tom McHugh, because 
we did not have our own machine to look at CD4 and CDS cell 
ratios. So they were doing that for us, and many of our early 
publications were done because they helped us. 

Hughes: Was the machine a cell sorter? 

Levy: It's not a cell sorter; it's a flow cytometer that shows you what 
types of cells are there. 

Hughes: How recent was that technology? 

Levy: That was a brand-new technology. It was developed by Len 

Hertzenberg and his wife Lee, and it revolutionized the ability to 
quickly look at subsets of white cells. What happens is the 
antibody attaches to its antigen on the surface of the cell. It's 
either f luorescinated or has rodamine or one of the other 
fluorescent dyes. In some cases you use another antibody to pick 
up the attached antibody. And then you put the cells through a 
machine with laser beams, and it tells you what percentages of the 
cells are of a particular type. It was expensive to do that 
procedure then. The antibodies were expensive. 

Hughes: Was there just one machine at UCSF? 



72 

Levy: I think there were two. There was also a separate one in a core 
facility. We worked with Dan Stites, and that was a big help to 
us, to be able to watch over time what happens to the white cells 
in a subject. 

Hughes: Is flow cytometry the only way of obtaining numbers of CDA and CDS 
cells? 

Levy: You could do it with a microscope by immune fluorescence. That's 
what they do in third world countries. You find how many cells 
show fluorescence with specific antibodies. We didn't do that. I 
know we tested it, though, because we did some fluorescent 
testing. I remember going back to Steve Shohet's lab where 
Margaret Clark was, and we looked at labeling of the cells with 
fluorescent antibodies versus the flow cytometer method. 



More on RT-positive Viral Cultures. Fall 1983 

Levy: You put cells in culture with IL-2, then you watch them over time. 
You remove fluids and assay for reverse transcriptase. At first, 
we didn't start taking fluids out as early as three days since 
it's expensive to do reverse transcriptase [RT] assays. So we 
took them out at about nine, twelve, and fifteen days. This was 
probably October or early November [1983] that we were getting 
some RT-positive cultures. But we couldn't be sure that this 
wasn't a cellular factor, because the reverse transcriptase assay 
is a most sensitive technique, and it can also pick up cellular 
enzymes. So we had to put the virus back into culture and check 
on its infectivity. 

Hughes : Cellular enzymes can be confused with the RT? 

Levy: Right. Any DNA polymerase can use the template that we used. I 
had already worked in that area when we were looking for an 
endogenous human retrovirus, and we kept coming up with cellular 
polymerases. So I knew that I'd better not jump to a conclusion 
on one assay. So we had to isolate and grow an agent. That took 
us about a month. So by December, I guess, we began thinking more 
along the lines that we had the AIDS agent. 



73 



Visit to the Pasteur Institute. October 1984 



Levy: Now, as you remember, I was in Paris in October of 1984, and, as I 
said, I went to see my friends at the Institute Pasteur because 
Jean-Claude Chermann and Francoise Barre-Sinoussi had been 
associates of mine in 1979 when I did a sabbatical in Paris with 
Frangois Jacob. All the virus studies had to be done in their lab 
for safety reasons. I have known Jean-Claude since the early 
seventies. He was under Montagnier. I only saw Montagnier once 
during that period, near the end of my sabbatical stay, when I 
went and described my research, which was on embryocarcinoma cells 
and virus infection. 

Hughes: You mean that Montagnier wasn't really deeply involved with the 
lab work? 

Levy: He wasn't deeply involved with Chermann' s work, because Montagnier 
was not working on retroviruses ; he was working on interferon. 

I know we went through this, but I went to Paris to 
congratulate them for the isolation of the AIDS virus, because it 
was not a major lab in retroviruses--in the world. In France, 
they were okay. And I was pretty proud of the fact that they had 
a paper in Science in April [1984], and that they were showing Bob 
Gallo that they could also find viruses like Bob Gallo was finding 
viruses. But Bob Gallo 's virus was HTLV, which I was adamantly 
convinced was not the cause- 
Hughes: At what stage? 

Levy: Oh, at the very beginning. I was interviewed, and Bob Gallo was 
furious with me for saying it wasn't the cause. 

Hughes: Go over the reasons. 

Levy: It couldn't be a cause of this disease, because HTLV is not 

produced by the cells in sufficient quantity that you could have 
sufficient virus in blood products to infect hemophiliacs. 
Hemophiliacs become very important for my way of thinking. 

Hughes: Whom Gallo never paid attention to? 

Levy: I don't know, but he never seemed to pay attention to them. He 
was somewhat lucky, because he could have missed the agent even 
more, because he didn't consider the fact that some hemophiliacs 
never got a blood transfusion, that they had platelet transfusions 
and Factor VIII and Factor IX and got this disease. Thus if HTLV 
is so cell-associated, it could never be the cause. Now we find 



74 



out, he changed the abstract of the French to sound like their 
virus was HTLV. 1 So it misled a lot of us, which is one of the 
things the country's concerned about. 

Hughes : Including you? 

Levy: Absolutely. I talked to you about going to the meeting in Japan, 
and hearing about the French agent, and kind of laughing because 
Alizon said antibodies to it were only found in French patients. 
Which was really due to his language problem. He didn't mean to 
say it. Then later, the more I heard, the more I realized that I 
had been misled by everything I had read in our press, that indeed 
this [LAV] looked different from HTLV. 

Hughes: I pulled you away from telling the other reasons why you thought 
the causal agent couldn't be HTLV. 

Levy: HTLV is highly associated with T cells; it does not kill T cells; 
it transforms them. So how could you explain the CD4 cell loss? 
And the virus would have to have been produced in very, very high 
amounts to have been recognized as being transferred among 
homosexual men by sexual routes. It can be passed from women. 
But most of the time, HTLV is passed by milk. So when I told the 
French, "Your agent is HTLV and could not be involved," they 
responded, "No, that's not the case," and they started telling me 
how LAV grows in high titer, how it kills CD4 cells, and has a 
preference for growth in CD4 cells. 

I said to the French, "Look, if you're right, once we get 
set up, we should be able to confirm you right away." They said, 
"Oh, you can have our agent." I said, "Oh, no. If I confirm your 
finding, it will be totally independently. Otherwise, no one will 
believe it." 

So I came back to UCSF; we finally got an ultracentrifuge; 
we started doing it, and we isolated a retrovirus . But we didn't 
recover this virus lots of times. We only got it out, oh, maybe 
10 percent, 15 percent. We weren't yet capable of isolating the 
virus in an efficient manner. We now know why. 

That lack of consistent recovery is the initial basis of 
Peter Duesberg's theory. I had lunch with Peter during those 
early periods, and I said, "You know, we can't get the virus out 
of a lot of people." He still holds on to that information. I 



1 F. Barre-Sinoussi, J.-C. Chermann, F. Rey, et al. , "Isolation of a T- 
lymphotropic retrovirus from a patient at risk for acquired immune 
deficiency syndrome (AIDS)," Science 1983, 220:868-871. 



75 



strongly felt the data indicated that we just weren't good enough 
technique-wise to get out the virus; Peter read it as, it's 
because the virus is not there. 



Research on Blood-clotting Factors 



Levy: But I also was concerned that this retrovirus might not be the 
cause. Maybe it was a passenger in an immune deficiency state, 
And what threw me was the Factor VIII. How could a retrovirus 
survive all that purification procedure for clotting factors? 



Levy: I believed the method for obtaining and lyophilizing Factor VIII 
would destroy the [viral] envelope and kill the virus. I asked: 
Cytomegalovirus? Herpes viruses? They're not passed by Factor 
VIII or Factor IX; they're enveloped viruses. A retrovirus would 
also be affected. 

Hughes: Retroviruses are killed in the purification process. 

Levy: Yes. But I also realize now there's nowhere near the quantity of 
these viruses in the blood as is true of HIV. I actually wrote up 
a little paper, which was not published, in which I said, "Is a 
retrovirus involved? If it is, it's got to go through all these 
purification procedures, and it seems logical that it might not be 
the cause, and we should be looking for another agent." 

I had learned that a researcher can come up with ideas but 
has got to prove them. So I decided to see if a retrovirus could 
be the cause of AIDS by doing experiments in which plasma 
specimens would be spiked with the murine retroviruses . That one 
has the same chemical properties of the AIDS virus but would be 
easier to work with in large quantities. As I told you, I called 
around to five companies purifying Factor VIII. Only oneCutter 
--agreed to do it with me; the others said because of patent 
rights, they didn't want to get involved, and they should have big 
regrets now. 

Hughes: I don't understand how patent rights fit in. 

Levy: They didn't want me to know how they purify. Actually I didn't 
care what they did to purify the factor. 

Well, Cutter said, "We're happy to do it." Cutter came over 
and I gave them the murine virus. They spiked the plasma and did 



76 

the separation studies. This experiment was set up at the end of 
'83. We began studying it in January and February of '84. It was 
a lot of work. In March of '84, there was evidence that virus was 
surviving the purification. I was very surprised. It didn't 
survive 100 percent, but if there were a lot of virus in blood, 
you knew it could survive. So it fulfilled my view of Koch's 
postulates; everybody with AIDS could have gotten this type of 
virus. 



More on Isolating AIDS-associated Retrovirus 



Levy: So we really then began emphasizing research on HIV or ARV--the 
AIDS-associated retrovirus, as we called it. We concentrated on 
this one agent. I had EM [electron microscope] pictures taken and 
antibody studies extended. March [1984] was quite an active 
month. 

Hughes: Was there an electron microscope here? 

Levy: No, I took it to Lyndon Oshiro, who for years had been working 

with me on EM studies. I view AIDS as being that one opportunity 
to call in all the people that were here working with me in the 
early days of virology. I had actually organized a group in the 
San Francisco area when I first arrived in the seventies to 
interact on a regular basis. We called the group the Tumor and 
Virus Group of the West. Walter Nelson-Rees came up with the name 
so we'd have the acronym TuViGrouWe. That group met every two 
months at different placesBerkeley, Stanford, and hereand it 
combined people in many different areas of virology, including 
tumor virology. 

Hughes: Isn't Oshiro over at--? 

Levy: Berkeley, State Labs [State of California Department of Health and 
Human Services] . 

Lyndon and Paul Arnstein were part of this group. Paul 
later was the one doing all my inoculations of Kaposi's sarcoma 
tumors into nude mice to see if they'd grow. And Lyndon 
collaborated on EM studies. Interestingly, the lyophilization 
work on retroviruses that I did later with Factor VIII and ARV was 
actually done earlier with mouse retroviruses with Howard 
Fieldsteel who was at the Stanford Research Institute. Then we 



77 



studied this means of preserving retroviruses. 1 So what you're 
really seeing, Sally, is that suddenly many things I'd done before 
came together for this challenge. And I found myself turning to 
papers that were seemingly unrelated to AIDS. Even when we were 
trying to prove that HIV was not associated with any other 
diseases, I called my former colleagues and mentors. For example, 
the Henles helped me on some antibody studies. 

Gallo has had papers that were wrong and I think misled 
scientists. For example, he had a paper in Science that said that 
the origin of HTLV-III, as he chose to call it, was located in 
Uganda around the Lake Victoria basin, because he found these 
antibodies to the virus in children there but curiously not in 
adults. Now, how could the virus be in children and not in 
adults? It didn't make any sense. It seemed like the Gallo group 
didn't consider a mechanism; they just reported the data, and the 
results were later proven wrong. 

We evaluated 300 serum specimens from all over Africa that 
the Henles had stored. We used the immunof luorescence assay 
[IFA], not the ELISA [enzyme -linked immunosorbent assay] 
technique. The Henles actually were at a meeting and presented 
those data, and Bob Gallo said, "Well, Jay Levy probably didn't do 
the assay correctly." The Henles responded, "Well, no. He's done 
a lot of IFA assays and knows how to do them. We taught him." 
Well, the reason for Gallo 's claim of HTLV-III in children was 
nonspecific sticking of antibody to the ELISA plates. It was all 
wrong. A Science paper! 

So we return to my earlier comments: As I -mentioned, I 
worked in Africa on Burkitt's lymphoma. Now, that experience came 
into my research on AIDS. I knew Africa; I knew the problems in 
Africa, and I had sera from Africa to use for these studies. 
Thus, when I returned to Africa in 1987, I wasn't surprised at the 
living conditions in the hospitals. My colleagues who had never 
been there before said, "Oh, this is terrible." I was not 
surprised as I had already seen this. So many things in my past 
came together with the present. 

If I had been more like a Bob Gallo and jumped rapidly to a 
conclusion, I probably would have published in December of '83 
that we had a retrovirus similar to that of the French. At the 
present state of my career with no tenure position, I couldn't be 
that quick to a conclusion. If wrong, it could hurt my 



'J. A. Levy, A. H. Fieldsteel, "Freeze-drying is an effective method 
for preserving infectious type C retroviruses," Journal of Virological 
Methods 1982, 5:165-171. 



78 

credibility. I must tell you as well that we got slides of 
infected cells from the French, and we weren't getting positive 
immunof luorescence assays regularly with their reagents nor our 
sera. That was why we developed our own IFA. So we couldn't be 
100 percent sure that our agent and their agent were the same. We 
therefore continued to keep ARV as a separate name. 



Press Conference on the Isolation of ARV. August 16. 1984 



Hughes: If you follow scientific etiquette, the press conference or the 
publicity should follow publication in a peer-reviewed journal. 

Levy: That's right, and we did have a press conference. My paper came 
out in Science, and there were a lot of calls. So I said to Marc 
Conant, "I think there probably should be a press conference, and 
I want you there." Because he had been so helpful to me. So they 
had one. 

Hughes: The university? 

Levy: The university public relations group organized the event. I 
remember, I used the blackboard, and [San Francisco Chronicle 
reporter] Randy Shilts covered it here. Because the virus had 
already been found, they didn't emphasize that this was an 
independent discovery but rather that the virus was in an area in 
California where there are many cases. The articles emphasized 
healthy people being infected. 

Hughes: Was that the emphasis the press chose to take -from your 
presentation? 

Levy: I'd have to read the article again. I remember being somewhat 

disappointed that they didn't pick up on the fact that we really 
had been among the first to find the virus . 

What makes it important is that we were a small group. When 
I first started work on isolating the virus, there were only four 
of us. Then later we had six or eight. Our paper has almost 
everything that Gallo's four papers had; we put it into one. We 
had better serology. We had almost 100 percent people with AIDS 
showing antibodies, once we had our immunof luorescent assay 
working . 



79 

Infecting Cell Lines 



Levy: So now after we got the virus out, we started to look at 

peripheral white blood cells using immunof luorescence, but they 
died off, and not a lot of them got infected. So as I had known 
from all my work in viruses before, I started to try to infect 
cell lines. I couldn't get any cell lines infected. 

Hughes: What were you using for cell lines? 

Levy: Oh, there were a lot of them around --MOLT4, CEM. They were tumor 
cells lines, T-cell lines, B-cell lines, macrophage cell lines. I 
couldn't get it to work until we tried HUT78 cells that I got 
sometime before this from Adi Gazdar who developed the cell line. 

Hughes: Was it easy to get HUT78? 

Levy: Adi Gazdar was a friend of mine. We had worked together at NIH. I 
didn't have the money to get it from ATCC [American Tissue Culture 
Collection]. It would have cost me $80, so I thought, Why don't 
we just get it from the source--Gazdar? In the long run it was 
better, because then I knew what I got. At least I knew this was 
HUT78. 

Hughes : What do you mean? 

Levy: If I got it from the American Tissue Culture Collection, it should 
be right. But I wasn't getting lines from them because of the 
cost. Instead of asking someone else, I chose to get the cells 
from the researcher who derived the line, so I did not think there 
could be any mix-up. 

Hughes: Was there any hesitation to give them to you? 

Levy: No. I wrote, Adi sent the cell line to me, and we called it 
HUT78 AG , for Adi Gazdar, so everyone knew the source. 

Hughes: Crewdson made quite a point of the fact that Gallo was using a 
subgroup of the cell line, H9. 1 What difference did that make? 

Levy: I'll tell you this story. Much of the work on AIDS, I was doing, 
in the lab myself. 

Hughes: You mean instead of-- 



'John Crewdson, "The great AIDS quest," Chicago Tribune, November 19, 
1989, section 5, p. 13. 



80 



Levy: Instead of a technician. I like being in the lab. But in those 
days, I had to do a lot of the work. So I went in the back room, 
and I inoculated our virus, ARV-2, which was the one that was 
growing really well in cell lines. Ends up this isolate is not 
our best grower, but it was the one that did best then. ARV-2 did 
not replicate well in most cell lines. Our ARV-1 strain didn't 
grow well in any cells, and so we froze it away. 

When I put ARV-2 in the HUT78 cells, it grew. So drawing 
from my days with the Henles, I quickly developed an 
immunofluorescent assay using these cells. We called it the E 
line since it was the fifth cell line I had tried in that 
experiment. 

Hughes: Why does the virus grow in one cell line rather than another? 

Levy: Well, that has now become a major area of research. The viral 

envelope has to interact with the cell surface to get inside the 
cell, and some cell lines have a cell surface that permits it to 
enter and some do not. So this virus grows well in HUT78. By the 
way, we had other viruses that did not go into HUT78 but enter 
other cells. That question has formed one of the major avenues of 
study in my laboratory. 

Because you're interested in how an investigator reaches 
decisions on research, let me repeat that I worked on murine 
viruses, xenotropic viruses. They grow in a variety of different 
cell lines, and these viruses can be distinguished by what cells 
they grow in. So it was a natural for me to think, ARV, what does 
it grow in? Therefore I tried lots of cell lines. I also asked 
whether we could get it to grow in a variety of different animal 
cells. I tried all sorts of animal cells as well as human cells. 



More on the Immunof luorescence Assay for HIV 



Levy: The assay is conducted as follows: you fix the cells on a slide 
with cold methane /acetone. Then you add the human serum in 
different dilutions, and the antiviral antibodies if present 
attach to the viral proteins associated with the cells. Then you 
use an antibody that detects human antibodies . This second 
antibody is fluoresceinated and therefore can be detected with a 
fluorescent microscope. If antibodies in the serum reacted 
nonspecif ically to human cells, every cell in the assay would 
stain. So specificity would be lost. 



81 

So I devised a simple approach: mix 50 percent infected 
cells with 50 percent uninfected cells, then perform the IFA. Any 
sera giving 50 percent or less staining and in a particular manner 
would be considered positive. With that technique, Larry 
Kaminsky, who was a dermatology fellow in my lab, did the 
immunofluorescent assays. To this day, every serum under analysis 
is given an LK number in continuing this process. I taught Larry 
as I was taught, and he worked out the pH conditions and the 
system needed for best results. We found out we could do the IFA 
in twenty minutes , making it later helpful for kidney transplant 
surgery. At first Larry did all the sera for San Francisco--for 
the blood bank, for everyone in the community. 

Then we taught the IFA to Judy Wilbur at the [San Francisco 
Health Department] city clinic, and she used it. We sent cells to 
Chip Sheppard at the state lab [State of California Department of 
Health Services], and he set up the assay over there. Evelyne 
Lennette received the cells and began doing the test at her 
company, Virolab in Berkeley. They did immunof luorescence assay 
[IFA], so then after awhile, we stopped doing it routinely for 
everybody. I couldn't afford it. So I'm very pleased that we 
were able to farm out this technology long before ELISAs were 
commercially available. 

Hughes: Over what period? 

Levy: That was from April of '84 until March of '85, when the commercial 
ELISA came out. Herb Perkins from the Irwin Memorial Blood Bank 
in the early days, for example, would call on me: "Jay, can you do 
a serum?" Many of my early publications, like with Herb on 
hemophilia, 1 with Marion Kuerper and the others, were IFA-based. 
Lots of work. 

Hughes: Were you doing this testing gratis? 

Levy: Oh, yes. But IFA wasn't sophisticated enough for other 

researchers, so many did not accept this approach for looking at 
anti-HIV antibodies. Yet you could use this assay in a developing 
country. Also, we didn't have an ELISA plate reader nor could we 
afford one. We also did not have immunoblot assays developed for 
extracting and placing proteins on gels, which is what Bob Gallo's 
group had done. These are techniques that required equipment that 
we did not have. In the end, many were saying you had to do 
immunoblot in order to really know the result on an antibody test. 



'H. A. Perkins, S. Samsen, J. Garner, et al., "Risk of AIDS for 
recipients of blood components from donors who subsequently developed 
AIDS," Blood 1987, 70:1604-1610. 



82 

We kept arguing for iiranunof luorescence, and I had to publish a 
couple of papers to prove it. 1 I wanted the developing countries 
to know that they could test for HIV in their own laboratories 
with just a slide containing fixed cells. 

Hughes: And IFA was picked up as the technique? 
Levy: No, IFA was considered too subjective. 
Hughes: They wanted ELISA? 

Levy: They wanted ELISA or immunoblot. A simple serologic assay did not 
seem to appeal to investigators studying what appeared to be a 
difficult agent to find. I found an unreasonably tremendous 
resistance to IFA. It was a cheap test, and anyone could do it. 

Hughes: What about sensitivity? 

Levy: Sensitivity was very good with IFA. The problem was, one could 
argue, and it's true, that you had to be fairly experienced to 
read it. You had to have practice in reading for a few days to be 
certain. Several individuals came to our lab to learn IFA. We 
actually published how you would detect a positive [reaction] by 
various distributions of the antigen, with the criteria that were 
needed; 2 it was not hard. 

Hughes: Describe exactly how you read the test. 

Levy: You put cells that have been reacted with serum and 

f luoresceinated anti-human antibodies under a fluorescent 
microscope. The laser beam picks up the anti-human antibodies 
that fluoresce. When you look inside the cell, you see 
fluorescence in a characteristic pattern. Moreover, we mixed 



'L. S. Kaminsky, T. McHugh, D. Stites, P. Volberding, G. Henle, W. 
Henle, J. A. Levy, "High prevalence of antibodies to AIDS-associated 
retroviruses (ARV) in acquired immune deficiency syndrome and related 
conditions and not in other disease states," Proceedings National Academy 
of Sciences (USA) 1985, 82:5535-5539. 

E. T. Lennette, S. Karpatkin, J. A. Levy, "Indirect immuno fluorescence 
assay for antibodies to the human immunodeficiency virus (HIV)," Journal of 
Clinical Microbiology 1987, 25:199-202. 

Z L. S. Kaminsky, T. McHugh, D. Stites, et al., "High prevalence of 
antibodies to AIDS-associated retroviruses (ARV) in acquired immune 
deficiency syndrome and related conditions and not in other disease 
states," Proceedings National Academy of Sciences 1985, 82:5535-5539. 



83 

positive infected cells with uninfected cells to rule out 
nonspecific staining. 

Hughes: So if you get one fluorescent cell, the assay is positive? 

Levy: No, on these assays you'd have to have 50 percent or a little 

less, depending on the level of antibodies present. At least 40 
percent had to be positive. Alternatively, if you had 80 percent 
positive, you had to do it again, since antibodies to normal cells 
must be involved. Or you need to absorb out the antibodies to 
human cells. The procedures were not difficult. 

One day, when I'm able to tell the story, all these 
barricades to getting issues resolved faster, because we were not 
given the attention, will be surprising. The focus was on the 
East Coast. 

Hughes: Now, was the focus on the East Coast because Gallo had the 

prestige and the money and the government behind him? Or was it 
because until recently West Coast medicine was in the shadow of 
what was going on on the East Coast? 

Levy: I think it was both. I think that if it had been anyone else 
competing with me on this topic, I still would have problems 
getting our message accepted, because this school was not a strong 
advocate on AIDS, never has been, and other schools would have 
picked up the momentum and gone with it. 



Changing Research Foci 



Hughes: From 1983 on you focussed exclusively on AIDS? 

Levy: I continued to do some work on the murine xenotropic viruses 
through "85. Then I combined that work with a study on using 
those animal viruses to mix with the human virus [HIV] to show 
that you could get HIV into animal cells if they carried the 
envelope coat of a different retrovirus. But the studies in the 
1980s were mainly aimed at AIDS. Kaposi's sarcoma at first had 
been the issue. Kaposi's is getting new focus now in my lab. 1 



'J. A. Ambroziak, D. J. Blackbourn, B. Herndier, et al., "Herpes-like 
sequences in HIV-infected and uninfected Kaposi's sarcoma patients," 
Science 1995, 268:582-583. 



84 

I had to give up work on endogenous human retroviruses that 
we were finding in placentas 1 ; there was no money, yet it's a 
fascinating area which unfortunately no one has picked up on yet. 
I hope one day I can go back to it. I had to give up all the work 
on xenotropic viruses: Why are they inherited in the animals? 
What do they do? What about the anti-xenotropic virus factor that 
I described? It's a lipoprotein that neutralizes the virus. I've 
had phone calls recently, "What's being done on it?" "Nothing." 
"Why?" "There's no one to fund it." Now there is practically no 
person outside of the NIH working on xenotropic viruses, to my 
knowledge. It is unbelievable for such an important field. We 
have money really only for human disease. 

In March 1984, when I came from that meeting on HTLV where 
Gallo gave me a hard time, I had lunch with the Henles, and I said 
to them, "You know, we have the AIDS virus, but I hate giving up 
xenotropic viruses. They said, "Don't think twice. Move to human 
systems. That's where you'll make your mark." 

Hughes: Were they thinking of funding too? 

Levy: Funding, respect, prominence. In retrospect, of course that was 
the answer, but I was still disdainful of people who jump into 
opportunities and don't continue in basic, fundamental work. I 
have really learned the realities, because it has changed 
everything in my career. My whole existence here at UCSF was down 
the tubes, so to speak, while I was working in the murine systems. 
The minute HIV and AIDS came and I began to work in that field, I 
was much more protected. I don't know if I still have the base, 
but I'm still respected for what we are trying to do. People meet 
me in the elevators and they say, "Jay, you're doing such good 
work now." And I say, "That would be fine if they'd leave the 
damn 'now 1 out." [laughter] Because really I am doing the same 
thing I did before. Everything I learned in the animal system, I 
moved to the human system, and since there were very few 
biologists doing it in the 1980s, we were able to advance the HIV 
field quite quickly and have many publications . 

Hughes: Is it working on human systems, or AIDS per se, that makes you 
acceptable? 

Levy: It's human systems and AIDS. I don't know if I worked on AIDS in 
cats, if I would get this acceptance. It's the human aspect, yes. 



'J. Nelson, J. Leong, J. A. Levy, "Normal human placentas contain 
virus-like RNA-directed DNA polymerase activity," Proceedings National 
Academy of Sciences (USA) 1978, 75:6263-6267. 



85 



I think you hit on something very interesting. If it were 
human arteriosclerosis caused by a virus, that would be fantastic, 
If it were human diabetes caused by a virus, that would also be 
better. But AIDS--we had a dean [Rudi Schmid] here who didn't 
want to mention the word; you had a head of medicine [Lloyd 
Hollingsworth "Holly" Smith] who didn't want to mention it. They 
thought it would reduce the number of residents and interns who 
came to work here. It was a financial and political issue. AIDS 
research was not a popular area but had to be worked on. So how 
do you get a base from which you can really influence policy? My 
laboratory until recently has not been the place people come and 
say, "What do you think? Where is AIDS research going?" We had 
many of the right answers, but we were never asked. 



Discovering the Importance of CDS Cells 



Hughes: One of the technical breakthroughs was the realization that, to 

keep the cultures going, you had to keep adding fresh white blood 
cells. Would you talk about technical breakthroughs? 

Levy: "Fresh cells" may be confusing. What you need is enough target 
cells for the virus to keep replicating. You also need to 
stimulate those cells so they're activated and thus susceptible to 
infection. 

Hughes: You mean, so that they're dividing? 

Levy: They're dividing. So you've got to take the white cells out and 
add a mitogen, like phytohemagglutinin, PHA, and then three days 
later, wash it out and add your virus. You also need to do that 
to activate the viruses inside an infected person's white cells to 
come out and grow. 

Hughes: These are all techniques that existed before AIDS? 

Levy: Those techniques were around. I have to say that Francoise Barre- 
Sinoussi in her article went through the technique for growing the 
virus in very good detail and most are still used today. 

Hughes: In 1983? 

Levy: Eighty- three. But what she didn't say, as I recall, was you had 
to keep adding in fresh normal white cells. In fact, because we 
are purists , when we were trying to isolate the virus , we never 
added in normal lymphocytes as fresh targets. We took the white 
cells from a patient, put them into culture, added PHA, and virus 



86 

came out or it didn't come out. By this method, we didn't isolate 
a lot of viruses. It wasn't until '86 that we figured out why. 
It was because the CDS cells that are in the blood sample as well, 
when activated by the PHA, work against the virus; they suppress 
the virus. 

## 

Levy: When we discovered this effect of CDS cells, I was as excited as 
I've ever been in HIV research. I think I was even more excited 
than finding the virus, because the virus came about by culturing. 
With CD8-cell function, we had to figure it out and then devise 
the experiments to prove it. 

Hughes: How did you happen to work that out? 

Levy: Because we couldn't get the virus out of the blood of so many 

people, many of them healthy. Why? Was the virus not there? I 
remembered work with the Henles on Epstein-Barr virus: I knew that 
it was the CDS cells which suppress the Epstein-Barr virus. So I 
said, "Let's take out the CDS cells." There was at that time a 
technique to remove CDS cells from a blood sample. You need 
monoclonal antibodies to the CDS molecule. You attach them on a 
plate; you add the blood sample to the plate; the CDS cells attach 
to the antibodies in the plate. Then you remove the non-adherent 
cells that lack CDS cells and put them in the culture. In one 
week, by using this procedure, the virus came out. Then we 
collected the CDS cells and added them back to the culture. The 
virus went away. We could repeat this process. The results were 
just dramatic. 

Chris Walker, my postdoc, made that observation with me and 
did beautiful work. 1 The finding was cited by Channel 5 as the 
most important science story of '86. We had TV people (Dave 
McElhatton) here in December 1986 to film the lab and give the 
report. It deserved it, and it still deserves it. We're still 
trying to figure out the mechanism. I think that's what really 
put us on the map in terms of discoveries in AIDS research. 



Collaborating with Chiron Corporation 



Levy: We also benefitted from the fact that our virus, ARV-2, was cloned 
very soon after its isolation. When I had the virus and I saw all 



'C. M. Walker, D. J. Moody, D. P. Stites, J. A. Levy, "CD8+ 
lymphocytes can control HIV infection in vitro by suppressing virus 
replication," Science 1986, 234:1563-1566. 



87 



the competition, I only had a small group, and I didn't have 
anyone who did molecular biology. I went down to see Bill Rutter 
at our university. 1 Now, there again, talk about my family of 
past contacts: Bill Rutter was in biochemistry, and his 
personality and my personality match very well. He's a very 
outgoing person, very bright, very accomplished, but likes fun 
like I like fun. We joke around a lot and I have great respect 
for him. 

So I called and later met Bill one day in his office, and I 
said, "We have this AIDS virus that we need to clone." He said, 
"Jay, we can do it in my lab [in the Department of Biochemistry 
and Biophysics, UCSF] , but you should really go and see my company 
[Chiron Corporation] since there we can do it faster." I got 
nervous; I said, "Company, you know, that's new for me." I had 
been told not to work with companies. Well, that's why Herb Boyer 
got burned, and I just was not ready to do it. 

Bill said, "Just go over and talk to the group." So I went 
over to Chiron, and I was overwhelmed by all the equipment, 
organization. I knew that if I wanted to be in this competition 
to clone and sequence HIV and find a solution for this problem, I 
needed the help of a company. Bill said to me, "We could clone 
this virus in two or three years in my lab at UCSF. We can do it 
in two months at my company." 

So we began working with Chiron. And there again the Gallo 
publication, his comments, and his manipulation of the media and 
the stories led us astray. He kept saying the AIDS virus was 
HTLV-III. It offends me so much the way he manipulated the 
interpretation of his EM [electron microscope] pictures, all his 
data, to make it sound like the virus he found was related to 
HTLV. It was a totally different family, totally different. Like 
apples and oranges. 

So when Chiron went to clone our virus, they said, "We'll 
use an HTLV probe to find the viral DNA." I said, "Don't! It's 
totally different. Do an acute infection and take the DNA from 
the acute infection." But for one month they did it using an HTLV 
probe, and then they came back and said, "Jay, you were right. 



'For more on Rutter and his contributions, see: William J. Rutter, 
The Department of Biochemistry and the Molecular Approach to Biomedicine at 
the University of California, San Francisco, volume 1, an oral history 
conducted in 1992 by Sally Smith Hughes, Ph.D., Regional Oral History 
Office, The Bancroft Library, University of California, Berkeley, 1998. 
Also available online at: http://www.lib.berkeley.edu/BANC/Biotech/ 



88 



It's not HTLV." We lost a month. But for that delay, we could 
have been ahead of the competition. As it was, we were the first 
but by only a few days [to clone and sequence the AIDS virus]. 



Cloning and Sequencing the Virus 



Hughes: Grmek mentions four groups that were cloning and sequencing the 
virus . * 

Levy: That is right. We worked with Paul Luciw and Dino Dina at Chiron 
and cloned and sequenced our prototype virus with their group. 
Luciw is now at Davis, but he was at Chiron then. It is perhaps 
interesting to note that when we described our virus, Murray 
Gardner asked if he could have it. He had gotten Gallo's virus, 
and he had gotten Montagnier's virus. Murray was one of those 
individuals that everyone trusted. He was really friendly, a 
communicative and cooperative person, so no one minded giving him 
the virus. Well, he set one of his students, Marty Bryant, to 
compare them. Now, this work was going on in '84. He presented 
the data at a meeting in Colorado. The results showed that HTLV- 
IIIB and LAV looked exactly alike in terms of restriction enzyme 
analyses of the viral genome, but ARV-2 was very different. 

Hughes: Did this set off alarms immediately? 

Levy: It didn't. Many thought, Oh, the group in California has 
something strange. 

Hughes : [ laughs ] Maverick . 

Levy: Yes, it's a maverick, exactly the word. 

In fact, I was back at NIH in November 1984, and Mai Martin 
and Janet Hartley asked me to give an informal talk on my 
research, and I did. At the end of the talk, Mai Martin said, 
"But Jay, I just came from a meeting in Colorado where Murray 
Gardner presented his data, and I think you'd better be very 



'The virus was cloned virtually simultaneously by groups at NIH and 
the Pasteur Institute. The nucleotide sequence was established, again 
almost simultaneously, by groups at the Pasteur Institute, NIH, UCSF- 
Chiron, and Genentech. For details, see: Mirko D. Grmek, History of AIDS: 
Emergence and Origin of a Modern Pandemic, Princeton, N.J.: Princeton 
University Press, 1990, pp. 74-75. 



89 

careful, because your virus is really a maverick. It's quite 
different from the Gallo virus and the Montagnier virus." 

I said, "Malcolm, we have two other virus isolates, and 
they're totally different from the first one I got." And that's 
when he went, "Oh, my God." Absolute quote: "Oh, my God." And he 
knew, and I knewbut I don't know if I realized the ramifications 
of that finding at the moment. When he challenged me with, "You 
have a maverick," and then I said, "But wait a second," to defend 
it, suddenly it all came through. From then on, Malcolm went on a 
campaign to show that what Gallo had was really the French virus , 
and Gallo was saying, "I never received the French virus," and all 
the lies continued. Malcolm is most courageous, because he's 
continued to provide the truth all the way up to the courts. 

Hughes: Is there anything to be said about the other cloning teams? There 
was the NIH-Harvard team, which of course was using HTLV-III; and 
then there was the group at the Pasteur with LAV, which included 
the Englishman, [Simon] Wain-Hobson. 

Levy: He did the molecular work with Montagnier. 

Hughes: I'm talking about the sequencing. 

Levy: Oh, sequencing. Okay, fine. 

Hughes: And then Paul Luciw-- 

Levy: At Chiron. 

Hughes: Right. And then what about Genentech? 

Levy: They took the Gallo virus. 

Hughes: What did these groups find? 

Levy: The results showed that IIIB and LAV were very similar in 

nucleotide sequence. But people wanted to know, couldn't that be 
by chance? 

Hughes: When this sequencing was going on, was everybody very aware that 
this was a real race, that there were four teams competing? 

Levy: Absolutely. I joined up with Chiron because they came to me, and 
they really wanted to work with me to develop the AIDS virus 
story. I said, "Look, if you want to work with me, I can't work 
under the conditions I have. I have nothing in this tiny little 
room at UCSF. Can you help me out? Can you give some money to 
the lab to renovate a room, and we can work better?" 



90 

"Absolutely," and they gave us some funds for a part-time 
technician, and we really got going. 

Genentech called and said, "Give us the virus and we'll 
clone it." I said, "Well, I would like you to help me out." They 
said, "Oh, we'll do this for free for you." So I said, "Thank you 
very much but no." To this day, there are people over there that 
don't forgive me for not giving them the virus. But they were not 
willing to help me with my lab. Chiron was and really helped us 
make progress. 

Hughes: I thought Genentech did work with ARV. 

Levy: No. Never. They may now, because Phil Herman is more active, and 
there are others there at Genentech who would like to use ARV-SF2. 

So we were in a race, and we got it cloned first. I can 
remember that Chiron wanted to announce it to the press, and I was 
very uncomfortable. Our [UCSF] public relations person, Michele 
Reichman, didn't approve of press conferences before publication. 
But I had no control: Chiron was going to do it if we joined them 
or not. So they did it; they made an announcement. 

Hughes: Now, this is just the cloning, not the sequencing. 

Levy: The cloning. However, that was a big step towards a vaccine. The 
virus has an RNA genome that makes a DNA copy of itself through 
its reverse transcriptase enzymes. This DNA integrates into the 
chromosome of the cell. That DNA is captured by selective probes 
for eventual cloning. By this time, I was deriving an infectious 
DNA copy of the virusone that gives rise to infectious virus 
once introduced into a cell. So when Chiron was probing with 
HTLV, they never found ARV because the AIDS virus differs from 
HTLV. What we did was take the early viral DNA products in the 
cytoplasm as the virus is replicating and pulled out the clone . 
We looked at its restriction mapping, and those results formed the 
first paper. 1 The data were important in showing the differences 
between ARV and HTLV-III/LAV. 

Hughes: So right away, you were getting a clue- 
Levy: That the restriction maps of IIIB and LAV as compared to ARV were 
different. But LAV and IIIB were exactly the same. In fact, each 
of them had a second virus variant in the analyzed preparation, a 
small amount of a related virus variant. Now, can you see how 



: P. A. Luciw, S. J. Potter, K. Steimer, et al., "Molecular cloning of 
AIDS-associated retrovirus," Nature 1984, 312:760-763. 



91 

crazy it would be to think that this finding is by chance? Gallo 
did say it was probably the same person, or a contactthe 
subjects giving IIIB and LAV both came from New York and could 
have known each other. I found these explanations highly 
unlikely. 

So there was a big race to clone the virus first, and Chiron 
made the announcement. I was somewhat accused of wanting 
publicity, but really it was Chiron that handled the press 
conference. Nothing was linked to the university. But truthfully 
it wasn't the right thing to do. A scientist should have a 
publication before a press announcement. And in fact, when we 
later called Science, they said, "No, we're not taking your paper 
because you already made a press release." But Nature took it. 
And then Gallo published in Science. He had two papers. I heard, 
Luc Montagnier's paper went to Nature, and it was held up because 
Gallo has all these connections at Nature, and they decided not to 
publish it. Quickly it went to Cell, 1 and Cell published it 
within a few days. 

Hughes: Is that the clone, or is that the sequence? 

Levy: Clone. So that got everybody's paper out about the same time. 

Hughes: And then you were racing to sequence? 

Levy: Then we were racing to sequence, and we got there at around the 
same time. We published it in Science, 2 and it's a beautiful 
papera really comprehensive article. 

Hughes: With no press announcement? 

Levy: No, that time, we published before any press announcement. 

Hughes: After the cloning, did people think that the vaccine was right 
around the corner? 

Levy: Yes. Around the corner. Many thought once you express the 

proteins, you've got the vaccine. They didn't know that all the 
viruses [HIV isolates] were different. We did, but I think we 
were still optimistic. 



'S. Wain-Hobson, P. Sonigo, 0. Danos, et al., "Nucleotide sequence of 
the AIDS virus, LAV," Cell 1985, 40:9-17. 

2 R. Sanchez-Pescador, M.D. Power, P.J. Barr, et al., "Nucleotide 
sequence and expression of an AIDS-associated retrovirus (ARV-2)," Science 
1985, 227:484-492. 



92 
Controversy over the Virtual Identity of HTLV-III and LAV 



Hughes: You and the others who were working on sequencing the virus almost 
immediately recognized the significance of having, for all intents 
and purposes, identical sequences for LAV and HTLV-III. But how 
long did it take the press and the scientific community to 
recognize the implications of this work? 

Levy: When the truth emerges, you'll find that it was known but made a 
cover-up by the government. 

Hughes: How? 

Levy: In the government, researchers were not allowed to call the AIDS 
virus anything but HTLV-IIIB. That was a directive from the 
government, and any connection to LAV was essentially hidden. 
Moreover, the French apparently were not totally convinced IIIB 
was LAV--here I don't understand the French. 

Hughes: But it's more than finding the virus. One of the things that was 
motivating this battle for credit was the tremendous monetary 
prize. 

Levy: Well, the U.S. government wanted it, I suppose for royalties from 
the patent. They're getting it. 

Hughes: Yes, but the Pasteur Institute needed it too. 

Levy: They're getting 50 percent. But the Pasteur Institute left the 
patent fight; they couldn't afford fighting the U.S. government. 
So they dropped it. They said, "Okay, we'll do 50-50." Now 
they're starting up the legal battle again. I can't understand 
it, and I will never be quite privy to it. Crewdson probably will 
be one day. Perhaps in his book. There are all sorts of stories 
that we can't approach here, because they're not documented. I 
can only talk from my viewpoint, from conversations with Gallo and 
things that I know from events back then. 

But this story was a real cover-up, and every bit of effort 
was made to hush up everyone. The most famous story was Murray 
Gardner's. After he proved in Colorado, through the work of Marty 
Bryant, that IIIB and LAV were identical, they decided to write a 
paper. He sent the manuscript to me, and I said it was okay. He 
sent it to Montagnier; he said it was okay. And Gallo squelched 
it. Gallo 's group said, "No, you can't publish it." 

In fact, he did more than that. The story that one day will 
be published after all these issues are discovered is that Peter 



93 

Fischinger went from the NCI to visit Murray Gardner about 
building a primate facility to increase the primate colony. And 
in that conversation, Peter Fischinger either said it directly or 
inferred, "If you want this facility, you'd better not publish 
your paper." 

Hughes: How do you know that? 

Levy: Because Murray Gardner told me that. I was furious and said, 

"Murray, you're being blackmailed." He said, "Jay, what can I do? 
I need the facility, and they have a lot of power, and I'll be 
left picking up the pieces." Which is true. Marty Bryant, who is 
now talking openly about it, called me and asked me, could I do 
something to convince Murray otherwise. I couldn't. And Marty 
Bryant left research. He is now a pediatrician. So that's one of 
the worst stories from this history. I can assure you that the 
lawyers are trying to get the documentation but it will be 
difficult to get the real letters, et cetera. 

Hughes: Pasteur's lawyers? 

Levy: No, the U.S. government investigating the case, because Gallo has 
appealed his misdemeanor charge, and now the OSI [Office of 
Scientific Integrity, NIH] is trying to really get him, to show 
what a dishonest person he is. They needed all the correspondence 
from me and Murray but I cannot find copies of all this. 
Unfortunately, I didn't even have a copy of my 1984 letter to Bob 
Gallo asking for his rabbit antibody, but John Crewdson had it. 

Hughes: Because he got it from Gallo? 

Levy: Yes. Freedom of Information Act. So he's faxed me--now I have a 
copy in my file. Amazing. I'm very disappointed that I do not 
have the documents to reveal these important events in history. 



Mikula Popovic's Use of Pooled AIDS Virus 



Hughes: Crewdson also makes the point that Popovic used pooled virus in 
his attempts to isolate the virus. 1 Would you comment? 

Levy: That is the worst technique, and when I read it, I didn't believe 
it. 



'John Crewdson. "The great AIDS quest," p. 11. 



94 

Hughes: When you read it at the time? 

Levy: I read it at the time in Science. I said, "Who would ever do 
that?" 

Hughes: Why did he? 

Levy: Because he thought that the viruses were all defective, and they 
would help one another, and then he would get out a real 
infectious virus. It is a technique used by a person who's not a 
well-trained virologist. Now, Mai Martin just told me at the 
Berlin meeting [Ninth International Conference on AIDS, 1990] he 
doesn't even think Popovic ever used a pool. There's no record in 
any of his notebooks. All of a sudden, out comes this virus, and 
it's IIIB. 

Hughes: You mean LAV? 

Levy: LAV, yes. Well, they called it HTLV-III. 

Hughes: Yes. But it's one and the same virus. Crewdson claims that 

there's no possible way of tracing the genealogy of these viruses 
that were supposedly being grown at the same time as LAV. 1 

Levy: Yes, that's right. None at all. They don't have them frozen away 
and the notebooks are incomplete . 

Hughes: What? 

Levy: They never kept the records. 

Hughes: But what about records? 

Levy: Many records disappeared. There were no records of the cell 
cultures from which the viruses came. Now, some of this is 
understandable. We just cleaned out my freezer. I'm a little 
more sensitive now to saving samples, but in the old days, I would 
have thrown out a lot of that stuff. Why do I need to keep the 
first isolate of ARV? I have it now in culture anyway. So it's 
admirable the NIH was able to go back to the freezer and find the 
original IIIB strain. Only at NIH where they've got lots of money 
and freezers could you do this. And who wants to clean them out? 
I think that's probably a good explanation for the story. But 
they had no records of these other virus isolates. The most 
recent paper in Nature where they said they took all the earliest 



Crewdson. "The great AIDS quest," p. 11, 



95 

ones and compared them, they found exactly the same results. The 
virus was LAV. 

I think what's also so fascinating is, even the French virus 
was a contaminant. 

Hughes: So we'll never know? 

Levy: What do you mean? 

Hughes: We'll never know what Gallo was growing? 

Levy: Yes. If they were ever growing it. My point is, they were never 
growing anything. They said they had RF in culture at the end of 
'83. They didn't; it appeared in '84. They got it in '83, but 
they never had it growing, as far as I can tell. 

Hughes: What's RF? 

Levy: It's a Haitian isolate. My feeling is that they never had 

anything growing; they couldn't get anything to grow. They got 
LAV; it grew; they got it into HUT78 so they had an assay system 
for the virus. 



Controversy over the Cell Line. HUT7 8 



Levy: Now, we didn't talk about HUT78. That's a very important point in 
this history. It's probably the only one, like getting Al Capone 
on income tax, that they may get Gallo on. Because Popovic wrote 
that he went into his incubator and took out a T cell leukemia 
line and subcloned it. I read the paper; I thought that it was a 
line that he had established and was growing. It ends up being 
HUT78, but they didn't say that. They gave it a new name, H9. 

Hughes: Implying that it was a new cell line? 

Levy: I think so. A new cell line, absolutely. They tried to deny 

that, in fact. Popovic says, "I wasn't sure what line I had when 
I opened the incubator; we had so many lines." Is that an 
argument of a good scientist? 

Hughes: Why was he trying to cover up the cell line identity? 

Levy: Because again, he was following his boss. I think that they knew 
all along it was HUT78. HUT78 is easily available at ATCC, so 
anyone who wanted to work with HIV could get it there. Instead, 



96 

these scientists had to write to Bob Gallo, and what he did was 
create an incredible collaboration with everyone around the world. 
From what I gather--! never got anythingyou had to ask his 
permission to publish, and his name was on many of the papers. It 
was a way of maintaining control. 

Hughes: Is there any difference between H9 and HUT78? 

Levy: None! They did chromosome checks and cell surface markers. 

They're exactly the same. One wonders if Popovic even cloned the 
cells. But he probably did. 



Scientific Controversy and AIDS Research 



Hughes: Well, what implications does this episode have for AIDS research 
and for science as a whole? 

Levy: Well, I'll tell you it has turned lots of people away from AIDS 
research. To me, it reflects the Reagan years, where dishonesty 
reigned, and it just dribbled down to science. My only hope is 
that Clinton is going to clean things up. Although Harold Varmus 
and I have our differences, I think Harold's going to NIH as 
director will bring integrity back to the institution. He won't 
put up with these shenanigans. I think Gallo is worried, although 
he's at NCI, which is a little independent from NIH. The incident 
has been very destructive, terribly destructive for science. 

Hughes: Well, it's been destructive for science as a whole, wouldn't you 

say, because this is one of a number of instances where the public 
perception is that scientists can't be trusted. 

Levy: That's exactly right, and Gallo should have been disciplined long 
ago. Hopefully Gallo will have his day in court this month. The 
lawyer from OSI asked me to testify against Gallo. I just 
couldn't do that. 

Hughes: Why? 

Levy: Because I don't have anything concrete from letters or other 

documents. I have conversations; I have hearsay. It's better yet 
to get the Marty Bryants and the Murray Gardners to testify. And 
it's very uncomfortable to testify against a fellow scientist. 
It's very dif ficult--it 's scary. I have little money now; I have 
no ongoing grants, and it is very political there at NIH. I mean, 
if they wanted to help me out, they could help me out. They're 
not helping me out with financial problems. The system is very 



97 



bad, in terms of protection. If you really want to be an honest 
person and do the right thing, you better have tremendous 
security--f inancial and political. 



Giving the Virus an Official Name 



Hughes: Dr. Levy, as you well know, you were on a subcommittee of the 
International Committee on the Taxonomy of Viruses, which was 
empowered to name the AIDS virus. Why was it considered necessary 
to convene a subcommittee to name this virus? Isn't that a little 
out of the ordinary? Normally, the discoverer names the virus. 

Levy: Exactly right. But since the discoverer was being challenged by 

another "discoverer," the issue was not settled. Luc Montagnier's 
group had called it LAV; Gallo was calling it HTLV-IIIB; and we of 
course were calling it ARV. I would not have been uncomfortable 
calling it LAV; I didn't like the term, but I agree, the first 
person to get there should name it. If Gallo wasn't at NIH, he 
would never have gotten away with this, but he did. So U.S. 
researchers were saying, "We've got to call it IIIB." And since 
that was so confusing, and most people were uncertain as to what 
to call it, they decided they'd better form a committee and at 
least get one universal name for the virus. 

Each of us put in our own suggestions for names. It was 
quite clear that if any of the three major discoverers put in a 
name, it would never make it. I personally liked human 
immunodeficiency virus, but I didn't put it in. Of course, I put 
ARV in, as well as others. 

Hughes: Why didn't you suggest HIV? 

Levy: Because if they said, "Jay Levy wants HIV," I can assure you that 
Bob Gallo and Luc Montagnier would have said, "We're not voting 
for it." It had to be a neutral person. I know Bob Gallo would 
have said that; I don't know about Luc. When we came up with HIV, 
which Harold Varmus handled as committee chair, I congratulated 
Harold. He did a terrific job. It would have been very tough to 
bring us all together in the same room. These are pretty high- 
powered, opinionated people. He did it strictly by fax and 
phones. 

Hughes: The committee never met? 



98 

Levy: We never met. Harold had the prestige and the respect to get 
people like Gallo to at least listen. Even in the end, when 
everything was done, Gallo and Essex refused to sign. 

Hughes: Well, I understand this process went on for quite some time. What 
actually occurred? 

Levy: First we were asked to turn in names. We wanted every name 

possible. And then we all voted, and we narrowed it down. We 
each gave reasons why we liked or we didn't like a suggestion. We 
narrowed it down to, I don't know, a handful, and then we voted, 
and HIV won. 

Hughes: Why? 

Levy: Because it was the best name of all of them. There was human 

retrovirus, HRV; there was human lentivirus. We knew it had to 
have an H--that we all agreed on--and it should have only three 
letters. 

Hughes: Why would it have to have an H? 

Levy: For human, in case there were other AIDS viruses that came along, 
and of course we knew there were. The committee didn't want to 
call it human retrovirus, because there are other retroviruses. 
Now, there were lots of complaints about HIV, because many people 
said, "Maybe they don't have immune deficiency." But we quickly 
said--I was one of the ones--"Polio virus is polio virus, but not 
everybody who is infected with the virus gets polio." So HIV is 
the best that you can do. 

Hughes: Why didn't Essex and Gallo endorse HIV? 

Levy: Because they wanted it to be HTLV-IIIB. 

Hughes: Harold Varmus has written a paper on this subject. 

Levy: On naming it? 

Hughes: Yes. Let me quote Harold Varmus. He said, "Some perceive, 
wrongly in my view, that our final recommendation," which of 
course was to name the virus HIV, "will form a verdict upon 
contested issues of priority of discovery, issues that could 
influence patent rights, the awarding of major prizes, patriotic 



99 

sentiments, and financial gain." 1 Was this background on your mind 
as you were choosing a name for the virus? 

Levy: No, that never came into my mind. But then again, I wasn't in the 
running for a patent, although we have a patent on our virus. We 
were not in the running for the big patent with Montagnier and 
Gallo. But obviously neither Gallo nor Montagnier was going to 
allow IIIB or LAV to be accepted as official names for the virus. 



Patenting the Virus 

Hughes: You can patent a virus? 

Levy: This was a surprise. Yes, you can patent a virus, but you should 
patent the virus for its use in some kind of diagnostic test or 
approach. So what the French did is they patented the virus as 
grown in peripheral white cells. Gallo took the same virus and put 
it into the H9 cell line, which of course is HUT78, and he said, 
"Well, I not only discovered the virus," which now we know is the 
French virus, "but I showed that it can be used in this diagnostic 
test for antiviral antibodies." And then Adi Gazdar said, "Yes, 
but you took my cell line, HUT78." So Gallo had to give Adi Gazdar 
some financial compensation. I don't know the details but it was 
interesting. 

Hughes: So you can patent a virus to be used for a specific purpose. 

Levy: Yes, for a purpose. 

Hughes: Was there precedent for this? 

Levy: I think it originated with the AIDS problem. Now, it's routine. 
Any time they find a new virus, they rush to patent it. With all 
due respects, Jonas Salk said, "To patent polio is like patenting 
the sun." 2 

Hughes: Thank you very much, Dr. Levy. 
Transcribed and Final Typed by Shannon Page 



'Harold Varmus, "Naming the AIDS virus," In: E. Juengst and B. Koenig, 
eds., The Meaning of AIDS, New York: Praeger, 1989, p. 3. 

2 Salk made the comment in response to a question by Edward R. Murrow, 
who asked on national television who owned the patent on Salk's polio 
vaccine. Salk replied: "Well, the people I would say. There is no patent. 
Could you patent the sun?" (Jane S. Smith, Patenting the Sun: Polio and 
the Salk Vaccine. New York: William Morrow and Company, 1990, p. 338.) 



100 



TAPE GUIDE--Jay A. Levy 



Interview 1: February 16, 1993 

Tape 1, Side A 1 

Tape 1, Side B 13 

Tape 2, Side A 24 

Tape 2, Side B 35 

Interview 2: February 22, 1993 

Tape 3, Side A 37 

Tape 3, Side B 48 

Tape 4, Side A 51 

Tape 4, Side B 62 

Interview 3: July 25, 1993 

Tape 5, Side A 64 

Tape 5, Side B 75 

Tape 6, Side A 86 

Tape 6, Side B 98 



APPENDICES 101 

A. UCSF News Release "UC-San Francisco Studies Confirm French 

Finding of Retrovirus in AIDS and Demonstrate a Retrovirus 
Could be Passed Through Blood Clotting Factor," May 8, 1984 101 

B. Letter to Jay A. Levy from UC Office of the President, 

Patent, Trademark, and Copyright Office, June 27, 1984 103 

C. "Virus Outpaces AIDS Here, Study Finds," San Francisco 

Examiner, July 1, 1984 105 

D. "HIV Survivors Who Have Beaten Disease," San Francisco 

Chronicle, August 9, 1994 107 

E. "Jay Levy Still Forging Ahead Despite Years of Being Ignored 

by Peers," UCSF Newsbreak, February 25 -March 10, 1995 108 

F. "Proven Connection- -HIV Causes AIDS," San Francisco 

Chronicle, May 30, 2000 110 

G. Curriculum vitae, Jay A. Levy 112 



University 


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101 . APPENDIX A 

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San Francisco 


532 Parnassus Avenue San Francisco, CA 94143 (415) 666-255: 






Michela Reichman, Assistant Chancellor 

Source: Andy Evangelista (415) 666-2557 EMBARGOED FOR RELEASE; 

7:00 AM (PDT) , WEDNESDAY, MAY 9 

UC-SAN FRANCISCO STUDIES CONFIRM FRENCH FINDING OF RETROVIRUS IN AIDS 

AND DEMONSTRATE A RETROVIRUS COULD BE PASSED THROUGH BLOOD CLOTTING FACTOR 

TORONTO A UC-San Francisco virologist today reported results of two studies 
that add further support to the theory that a retrovirus plays a major role in 
acquired immune deficiency syndrome. 

A study by Jay Levy, MD, UCSF associate professor of medicine and an 
investigator in the Cancer Research Institute, confirms findings by French 
scientists that a retrovirus lymphadenopathy associated virus (LAV) could 
be the primary cause of AIDS. So far, Levy has found evidence of LAV or a 
LAV-like agent in blood cells of 28 of 50 AIDS patients in San Francisco. In 
three of the 28, Levy's laboratory has direct proof, of the similarity to LAV. 

The study was reported here today at a joint meeting of the American 
Society of Clinical Oncology and the American Association for Cancer Research. 

Last year, researchers (F. Barre-Sinoussi, L. Montagnier, J.C. Chermann) at 
the Pasteur Institute in Paris discovered LAV in blood of AIDS and pre-AIDS 
patients in France. The suspected virus grows preferentially in certain 
lymphocytes (white blood cells) , which become damaged or diminished in AIDS 
patients. The loss of these cells appears to be responsible for their inability 
to fight off opportunistic infections and cancer. Levy's research group found 

retroviral enzymes and proteins in white blood cells, as well as antibodies to 

**- 
LAV, which indicate infection, in over 50 percent of the patients studied. 

Evidence of the virus was not detected in any of 21 healthy controls. For the 
study, Levy used reagents -supplied by the Pasteur Institute researchers to 
compare his isolates with theirs. Electron micrographs also have confirmed the 
similarities, Levy reported. 

The relationship of the UCSF LAV-like agent and LAV to the HTLV-III 
retrovirus, recently described by Robert Gallo of the National Cancer Institute, 
is not yet known, says Levy. Recent reports, however, indicate strong 

(more) 
messengered and transmitted: 5/8/84 03:06:48 



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J 



on Ketro virus in HJ.U5 fage 2 

102 



/.iniil arities between LAV and HTLV-IH. Although they are major steps in AIDS 
' r esearch, Levy cautioned that these new findings do not yet establish absolute 
p[00 f that either virus or a similar one is -the -cause of AIDS. He is conducting 
experiments, infecting animals with the UCSF isolates, in an attempt to 
determine whether or not they are responsible for AIDS. 

In a separate presentation at the ASCO and AACR meetings, Levy today 
reported results showing retroviruses can survive procedures previously used to 
produce the clotting factor (Factor VIII) used by hemophiliacs. Levy, working 
with researchers from Cutter Laboratories in Berkeley (Milton M. Mozen, PhD, and 
George Mitra, PhD), tested the stability of a mouse retrovirus, resembling LAV, 
through the clotting factor production process. The process did not 
substantially inactivate the retrovirus, Levy reported. 

This is counter to previous beliefs that a retrovirus could not survive 
such a process, and the study possibly explains why some 30 hemophiliacs in the 
United States have developed AIDS. The factor, used by hemophiliacs to prevent 
uncontrollable bleeding, is usually prepared from blood contributed by thousands 
of donors. The study by Levy and his coworkers did indicate that the heating 
procedure used now by Cutter eliminates the retrovirus effectively. 

The process is now being used by .maufacturers of Factor VIII to further 
minimize the chances of hemophiliacs contracting AIDS, says Levy. 

Taken together, Levy's studies indicating presence of LAV or a LAV-like 
agent in the blood of AIDS patients in San Francisco and demonstration that a 
retrovirus can be transmitted in blood clotting factors ~ lend further support 
to the theory that a retrovirus is involved in AIDS. 

Levy's research is supported by grants from the state of California and the 
National Institutes of Health. His UCSF research team includes Susan Kramer, 
PhD, Lyndon Oshiro, PhD, Anthony Hoffman, Jill Landis and Joni Shimabukoro. 



03:06:48 



103 APPENDIX B 

. kr^ A> p.(j A-P- ^rjL ' '>V 
UNIVERSITY OF CALIFORNIA SYSTEMWIDE ADMINISTRATION 



. LOS ANCELES . BIVERS . DE . SAN D1ECO . 5AN . rRANC , sco ^ BAnUA . SANTA 




Patent, Trademark and Copyright Office 

Office of the President 

2490 Channing Way BERKELEY, CALIFORNIA 9.720 

(415) 642-5000 



June 21, 1984 



Professor Jay A. Levy 
Cancer Research Institute 
Department of Medicine 
1282 Medical Science Building 
University of California 
SAN FRANCISCO CAMPUS 94143 

Dear Professor Levy: 

Re: ISOLATION OF A RETROVIRUS FROM A PATIENT WITH ACQUIRED 
IMMUNE DEFICIENCY SYNDROME 
NIH Grant Number 34980 . 

STATE OF CALIFORNIA Contract Number 83-00060 
UC Case: 84-11 8-1 - 

Thank you for disclosing your invention pursuant to University 
policy. 

Your disclosure will be reviewed to determine patentability, 
patent obligations to parties outside the University, and whether 
the University will undertake formal patent action. 

We will keep you advised relative to our evaluation and may ask 
you for additional information. Normally, about ninety days are 
required for this procedure. 

In the interim, please let us know if you intend to publish or 
present a paper or need to disclose this invention in any other 
manner to others outside the University (other than as noted in 
the Record of Invention) . Such a disclosure could result in a 
loss of patent rights in most foreign countries, to the extent 
that foreign rights are still available. It is our intent to act 
as promptly as necessary in patent matters, such as not to 
intefere with your desire to publish research results promptly 
through the usual academic channels. 

i 

Rights to file patent applications abroad have been most probably 
lost due to your presentation in Toronto, Canada. I would 




104 



Professor Jay A. Levy 
June 27, 1984 
Page 2 



appreciate information as to the exact date of this presentation, 

If you have any questions concerning these procedures, please do 
not hesitate to call me at 8-582-5000 (ATSS) or 415-642-5000. 



Sincerely, 



Valentin Fikovsky 
Patent Manager 



cc: Professor Paul A. Volberding <J=<I3 
L. Mardie Petrakis, Contract and Grant 

Office, UCSF 
Roger G. Ditzel, Director 

Patent, Trademark, and Copyright Office 



105 



APPENDIX C 





here, study finds 



By Richard F. Harris 
Examiner science writer 

Exposure to the virus suspected of causing 
AIDS is far more widespread among gay men 
in San Francisco than the disease itself, accord 
ing to results of experimental blood tests. 

A survey of blood products from gay San 
Francisco men, tested by the federal Centers 
for Disease Control in Atlanta, documents the 
rapid spread of the suspected AIDS virus in 
The City. 

A positive test result does not mean the 
person will become ill, but the consequences 
are uncertain. 

Samples collected in a hepatitis study in 



potentially exposed to the virus before the 
results are understood? 

The question is agonizing for homosexuals 
who would like to know whether they have 
been exposed, even though the test doesn't 
reveal whether they are contagious and does 
not predict whether they will develop the dis 
ease. 

It Is also a worry for health officials, who 
fear widespread testing will lead gay men to 
abandon healthy changes in lifestyle. Health 
experts say those habits are still the most im 
portant protection against AIDS, even among 
people who may harbor the virus. 

Part of the problem is that the so-called 



1978 show 1 percent of this sexually active 
population had been exposed to the AIDS vi 
rus. By 1982, 24 percent of that group had been 
exposed, according to Dr. Harold Jaffe, co-di 
rector of the CDC's AIDS Task Force. 

More recent samples reportedly show 50 
percent of that population had been exposed to 
the virus, according to widely circulating re 
ports about the CDC research. Jaffe, however, 
declined to confirm the last figure. 

Because the ability to detect the suspect 
AIDS virus has proceeded much faster than an 
interpretation of that test, the findings present 
a tough dilemma: Should the test be made 
widely available to homosexuals and others 



San Francisco Examiner 
July 1, 1984 



AIDS tests do not detect the disease, but rather 
determine whether individuals have at any 
time come In contact with the virus. 

People exposed to the virus build disease- 
fighting antibodies, which linger in the blood 
stream and can be detected years after initial 
contact by the new test 

Dr. Jay Levy, a virologist at UC-San Francis 
co who has conducted his own tests of more 
than 300 blood samples from gays in The City, 
would say only that his findings show the virus 
is "prevalent" among gay men who have been 
sexually active. 

The precise figures from his study and that 
done by CDC are not Important, he said, be 



cause neither represents a cross-section of San 
Francisco's gay community. 

The federal study is of a group of men at 
high risk for hepatitis, which is spread like. 
AIDS through exchange of body fluids, and 
Levy's studies are of men who consider them-, 
selves at risk for the disease. 

Both studies support an expectation among 
health officials that exposure rates to the virus, 
will vastly overshadow the 550-plus cases diag 
nosed to date in The City. 

Levy's laboratory is far too small to conduct'. " 
exposure tests except in specific research pro]-" 
ects, but a test could be mass-produced by the 



106 



Big increase in AIDS virus exposure 



From Page Al 

end of the year by any of five biotech 
nology firms now working to develop 
one. 

There is as yet no absolute scientif 
ic proof that the suspected virus 
causes the often fatal immune system 
disorders of the acquired immune de 
ficiency syndrome, although many 
AIDS researchers believe the virus, 
discovered last year in France, is at 
the root of the problem. 

The chief suspect is called lym- 
phadenopathy associated virus, hu 
man T-cell leukemia virus or AIDS-as- 
sociated retrovirus, depending on the 
laboratory where it was isolated. 

Although scientists expect the 
three suspects to be one and the same 
virus, that has yet to be proven. 

Like people once exposed to the 
hepatitis B virus, many of the men 
who show signs of exposure to the 
AIDS virus appear to be in good 
health. 

The vast majority of people carry 
ing hepatitis antibodies live a health 
ful life without ever being sickened by 
the virus. 

So far, AIDS has apparently fol 
lowed the hepatitis pattern: A minori 
ty of people exposed to the virus get 
the full-blown disease; some get only a 
milder form of infection called lym- 
phadenopathy; and some have so far 
shown no signs of illness. 

The epidemic is too young for sci 
entists to know whether that pattern 
will hold. 



Until that question, among many 
others, is resolved, prominent AIDS 
researchers suggest the test for AIDS 
: should be confined to research labs 
and blood banks, rather than made 
available for general testing. 

"I'm not sure I want to be tested," 
said Dr. Paul Volberding, who as head 
of the AIDS clinic at San Francisco 
.General Hospital may have been ex 
posed to blood from AIDS patients or 
other disease materials. 

No health worker has contracted 
the disease from his or her work, he 
said, but there is no telling how people 
might interpret a positive exposure 
test. 

'Does it mean (exposed people) are 
not insurable? Will they lose their 
jobs? Are they going to get AIDS? 
There are a lot of important issues I 
don't think have been very well 
thought out," Volberding said. 

Noting that 10 AIDS patients died 
last week at S.F. General, Volberding 
said, "People dont know how horrible 
this disease is." 

Until more is known about inter 
preting the test, AIDS researchers are 
concerned it will spur unwarranted 
fear about the results. 

The question is compounded by 
the fact that so many people are likely 
to be identified as potential AIDS vic 
tims by the antibody test. 

Health officials are also concerned 
that some at-risk men will conclude 
from the test results that the disease 
has already done its maximum dam 



age. That could lead some people ,tc 
abandon the low-risk lifestyles thai 
have made remarkable inroad; 
among gay men. 

Ironically, as far as scientists can 
tell, those healthful habits are even 
more critical for men who have been 
exposed to the virus. 

If virus is lying dormant in those 
people, a strong immune system 
would be more likely to keep it at bay, 
Volberding said. 

"Not only is it important to avoid 
exposure to other (sexually transmit 
ted) agents, but to keep your head in 
good shape and find ways of coping 
with (disease-linked) emotions such as 
depression," said Rob Roy Woodman, 
a psychologist with the city-funded 
AIDS Health Project 

Until its significance is known, the 
test itself could provoke depression, 
Volberding said. 

"We don't want a test like that to 
become routinely available until some 
of these questions are answered," said 
Dr. James Chin, a leading AIDS re 
searcher in the state's Office of Health 
Services. 

Despite these considerable draw 
backs for individuals, scientists note 
the test will be an indispensable tool 
for research and a long-sought meth 
od of assuring that blood bank 
supplies are free of AIDS. 

Otherwise, Chin said, "The whdle 
medical, legal and ethical ramifica 
tions have to be worked out I don't 
think we have any good answers to 
them right now." 



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107 

By David Perlman 
Chronicle Science Editor 

Yokohama 

Hundreds of healthy men and 
women whose immune systems re 
main undamaged years after they 
were infected by the AIDS virus 
may offer promising clues to new 
treatments and vaccines to combat 
the epidemic, one of America's 
outstanding young AIDS research 
ers reported here today. 

Dr. David Ho of New York 
City's Aaron Diamond AIDS Re 
search Center is studying a small 
contingent of volunteers known 
among themselves as "long-term 
survivors" to learn why they seem 
to resist every attack by the virus 
es that invaded their bodies, and 
he has found significant keys to 
the puzzle. 

More than 500 of the survivors 
are being followed by AIDS spe 
cialists at the San Francisco Health 
Department, but Ho is concentrat 
ing on a group of 10 nine men 
and one woman who volunteer 
ed to be research subjects hi New 
York. All have been infected for at 
least a dozen years, all are totally 
free of disease symptoms, and 
none shows any decrease in the 



APPENDIX D 

functioning CD-4 cells of their im 
mune systems. 

CD-8Cil 

In addition, all continue to 
show healthy numbers of CD-8 
cells, which many scientists con 
sider to be extremely important in 

The subjects 
continue to show 
healthy numbers of 
CD-8 cells 



protecting immunity to the ravag 
es of HTV, the AIDS virus. 

The CD-8 cells apparently de 
cline in number as HIV-infected 
people begin to show signs of 
AIDS. 

-Scientist after scientist at this 
10th International Conference on 
AIDS has called for more research 
into the unknown factors trigger 
ed by the CD-8 cells whose impor 
tance was first recognized years 
ago by Dr. Jay Levy of the Univer 
sity of California at San Francisco. 

"We have no clue at all as to 
what factor in the CD-8 cells is 



working to suppress the virus," Ho 
said. "It remains an unanswered 
question." 

One answer, however, may lie 
in the basic nature of Levy's pro 
tective CD-8 cells, Ho suggested. 
They may belong to a cell class 
called cytotoxic T lymphocytes, or 
CTLs, which are known to destroy 
all kinds of cells that are infected 
by viruses. 

Volunteer Group 

In the volunteer group Ho is 
studying, seven of the long-term 
survivors are gay, two are intrave 
nous drug users and one is a het 
erosexual woman. None appears to 
be linked by any unique genetic 
pattern, he said, and neither Ho 
nor his colleagues have been able 
to discover a "unique lifestyle" 
that makes them different from 
others who typically progress to 
disease after HIV infection. 

In most of the group, Ho said, 
even the most meticulous analysis 
has failed to find any trace of virus 



now, while in the others the virus 
count is at least a thousand times 
lower than in infected men and 
women who have already been hit 
by one or more of the AIDS diseas 
es. 

All members of the group that 
Ho is studying have mounted a 
strong antibody response that can 
neutralize the virus, Ho reported, 
and the evidence suggests that 
when the survivors were first in-" 
fected the viruses stopped repro 
ducing after only a few days. 

"We know these are pretty 
wimpy viruses," Ho said, but Just . 
how their host humans have weak 
ened them to the point of impo- 
. tence remains a mystery, he said. 

Whatever characteristics ac 
count for their survival, the find 
ings should provide valuable 
guideposts and research targets 
"to lead us toward new vaccines or 
therapeutics," Ho said. "And that 
may at least provide a ray of hope 
to patients." 



SF Chronicle 
August 9, 1994 



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108 

By ALLEN J. BALDERSON 

Jay Levy is one of UCSF's many AIDS he 
roes. He was one of the first researchers in 
the world to identify the mysterious HIV virus 
as the cause of AIDS more than a decade 
ago. 

But his studies on long-term survivors of 
the disease, and how CDS cells may play an 
important role, have basically been ignored 
for years by much of the research community. 
Yet, he has forged ahead, never wavering 
from his commitment to his original findings. 

Now, though, many of these same re 
searchers are rediscovering Levy's seminal 
work and in a rash of new journal articles, 




giving the UCSF researcher some long over 
due acclaim. 

To understand Levy's research, a few ba 
sics on HIV infection are in order. This diaboli 
cal virus mutates each time it multiplies, and 
is thus able to escape the immune system's 
ability to destroy it. HIV can infect as many as 
1 00 billion cells in the body, without seem 
ingly affecting a person's health. HIV's main 
targets are CD4 lymphocytes, a group of 
white blood cells that help the immune sys 
tem function. The number of CD4 cells in the 
blood has been an important parameter for 
researchers and clinicians alike in measuring 
the immune system's function. In people not 
infected with HIV, CD4s measure anywhere 
from 600 to 1200 cells/ul. When CD4 cell 
levels drop below 500, there is concern that 
the disease may be advancing. 

CDS lymphocytes, another component of 
the immune system, are present in uninfected 
people at about half the number of CD4 cells. 
In many diseases, these cells are respon 
sible for attacking and killing virus-infected 
cells or cancer cells. Levy's work indicates 



APPENDIX E 



that some CDS cells, in very low numc jr s. 
can block HIV replication in CD4 cells withe 
killing the CD4 cells. This novel antiviral activ 
ity can be observed in healthy infected people, 
especially in those living with HIV for many 
years. 

These observations, first made by Levy in 
1986, led to the discovery of a substance 
secreted by CDSs now known as the CD8+ 
cell antiviral factor or CAP. This protein is a 
cellular factor or "cytokine" unlike any of the 
previous cellular products identified. Levy's 
lab now is undertaking a more complete study 
of this protein. His group recently noted that 
certain cellular factors produced by other 
immune cells can affect the ability of the CDS 
cells in HIV-infected people to suppress virus 
replication. These findings could explain why 
there is a loss in the antiviral activity of CDS 
cells over time, even before the reduction in 
CD4 cells. "It may be that the cytokines pro 
duced by CD4 cells are decreased sufficiently 
to compromise CDS cell function," explains 
Levy. 'The virus no longer is held in check by 
the CDS cells and then advancement to AIDS 
takes place." 

People with HIV who have lived longerthan 
10 years with a normal CD4 count (over 500 
cells/ul) have several characteristics associ 
ated with their strong CDS antiviral response. 
These long-term survivors have limited 
amounts of virus in their blood, the virus is not 
very virulent, and it does not infect a wide 
variety of cell types. The CDS cells appear to 
be responsible for these features because 
they can limit the replication and mutation in 
HIV over time, says Levy. Strong CDS activa 
tion seems to keep the HIV from wreaking 
havoc on a person's system. 

HIV patients and physicians should know 
that while a blood test can show a CDS cell 
count, it will not indicate the number of cells 
producing cell antiviral factoror CAR "You 
need to have laboratory experiments exam 
ine the function of the CDS cells how well 
they will suppress virus replication in the CD4 
lymphocyte," says Levy. In one study, Levy's 
group found that if the virus is readily recov 
ered from cultured white cells, then the CDS 
cells are not functioning effectively. 'This is a 
very quick method of determining whether or 
not one's immune system is losing its ability to 
control HIV," says Levy. 

To develop a marker for diagnosis and 
clinical follow-up, CAP needs to be identified, 
according to Levy. "We then can make an 
antibody that can be used to detect this CDS 
factor in the blood and on the surface of cells. 
Then we can count the cells that are produc 
ing this protein and look at changes in this 
important antiviral response over time." 

"Quite frankly, I'd rather see a cellular im 
mune activity that could kill the virus-infected 
cells, but it's apparent that the major factor 



109 



Immune Pathogenesis 



inhibitory 
event 



inhibitory 
event 




* Productive 
Infection 



Source: "HIV and the Pathogenesis of AIDS" 

observed in healthy HIV-infected people and 
long-term survivors is this anti-HIV suppress 
ing response," says Levy. 'This CDS cell activ 
ity can keep the virus from replicating and 
allows the body to maintain a healthy state. We 
surmise that if the virus is unable to replicate, 



"This CDS cell activity can 
keep the virus from replicat 
ing and allows the body to 
maintain a healthy state. " 

AIDS researcher Jay Levy 



eventually the infected cells will die as a nor 
mal matter of course. The number of infected 
cells in the body will be reduced, as we previ 
ously observed in infected chimpanzees." 

At present, there are no practical ways to 
stimulate CDS antiviral activity. Nevertheless, 
learning how long-term survivors maintain 



AIDS as a result. The persistent HIV infection 
and disease progression in baboons will en 
able Levy and his colleagues to study new 
therapies and vaccines. Baboons, which have 
immune systems similar to humans, also are 
substantially cheaperthan other animal mod 
els such as Rhesus monkeys or chimpan 
zees. Ababoon costs around $1 ,800 (up from 
$500 just a few months ago); the price tag on 
a Rhesus monkey is $2,500 and jumps to 
$30,000 for a chimpanzee. 

While Levy is gratified that his research 
finally is gaining attention, he must continue 
to wage his bureaucratic funding battles be 
cause he says research money is going else 
where and not into basic science. 'There is 
not enough attention being paid to research 
that can find an effective treatment for AIDS," 
he says. "And they [people in charge of fund 
ing] just don't see the ramification AIDS re 
search has to other disciplines, for example 
cancer." 

Meanwhile, AIDS continues its relentless 
march into our lives, making it today the 
number one killer of Americans between the 



110 



APPENDIX F 



Proven Connection 
HIV Causes AIDS 

Differences between U.S. and African 
epidemics don't disprove cause of both 



By Jay Levy, Nancy Padian 
and Jeff Sheehy 

THE VIEW PUBLISHED in Open Fo 
rum last week during South African 
President Thado Mbeki's visit to San 
Francisco gives the impression that the 
usociation between HIV and AIDS is still 
questionable. The contrary is true. 

The overwhelming evidence indicates 
that HIV causes AIDS. 

The HIV deniers have pointed to Presi 
dent Mbeki's recognition that HIV in Afri 
ca has been transmitted predominately by 
heterosexual contact, as opposed to the 
United States and other developed coun 
tries where HIV has been transmitted pre 
dominately by homosexual contact. The 
belief has been stated that this discrepancy 
somehow proves that HIV does not cause 
AIDS. 

It is important not to confuse the epide 
miology of HFV transmission in the United . 
States with what is occurring in Africa. In 
this county, the studies used to determine 
the odds of transmitting HIV in a single act 
pf unprotected vaginal sex between an in 
jected man and an uninfected woman, 
"hich stand at about 1,000 to 1, excluded 
isk factors known to increase HIV trans- 
nission. These low odds do not hold in the 
:resence of other well-established risk fac- 
:ors, prominent in Africa, such as other 
sexually transmitted diseases, which can 
ncrease the risk. Thus warnings, based on 
cience about heterosexual transmission 
hat lead people to change their behaviors 
o save their own lives and the lives of 
>thers, have been a critical component of 
>ur prevention strategies. 

Indeed, successful HIV prevention pro- 
irams have actually been responsible for 
naintaining low infection rates among 
teterosexuals in this country. 

Notwithstanding this country's success 



in limiting heterosexual transmission of 
HIV, there are many factors that could 
account for the widespread heterosexual 
epidemic in Africa that differ from what we 
have observed here. As is the casei with 
virtually all illnesses and infections, pat 
terns of disease distribution and transmis 
sion differ depending on location. 

Some of these factors are biological, and 
some are behavioral and social. Biologi 
cal factors include the high prevalence of 
other sexually transmitted diseases, which 
facilitate transmission, and the high rates 
of bacterial vaginosis among women, 
known to increase susceptibility. Also, in 
Africa a predominant virus (clade C) may 
be more easily transmitted through muco- 
sal contact. Further, the presence of many 
tropical diseases, as well as nutritional and ' 
other factors among people in developing , 
countries, may compromise their general 
immune competence and thus increase 
susceptibility to HIV infectioa 

Behavioral and social factors that could 
facilitate the heterosexual spread of HIV 
in Africa include a greater power imbal 
ance between genders that makes it much 
more difficult for women to avoid sexual 
contact with an infected husband or to 
negotiate condom use. Importantly, there 
is less access to health care, which greatly 
contributes to high rates of sexually trans 
mitted diseases and other health problems 
that might increase susceptibility to HIV. 

Finally, far fewer resources have been 
available for successful prevention pro 
grams when such resources are urgently 
needed in Africa and the developing world 
to fight this disease. 

There is an abundance of evidence prov 
ing that HIV causes AIDS. A fact sheet 
(found at http://hivinsite.ucsf.edu/) pre 
pared by the Office of Communications 
and Public Liaison at the National Institute 



San Francisco Chronicle 
May 30, 2000 



of Allergy and Infectious Diseases clearly 
shows the link: 

Koch's postulates, developed in the late 
19th century, are the most cited criteria 
used over the years to prove the connec 
tion between disease-causing agents and 
disease. These tenets have served as the 
litmus test for determining the cause of any 
epidemic disease. 

To restate: 

1. Epidemiological association: The sus 
pected cause must be strongly associated 

with the disease. 

2. Isolation: The suspected pathogen 
can be isolated and propagated out 
side the host. 

3. Transmission pathogenesis: Transfer 
of the suspected pathogen to an uninfected 
host,- man or animal, produces the disease 
in that host. 



Ill 




k 

MARGARET SCOTT / Special to The Chronicle 

With regard to postulate 1, numerous 
studies from around the world show that 
virtually all AIDS patients carry antibodies 
that indicate HIV infection. 

With regard to postulate 2, modern lab 
oratory techniques have allowed the isola 
tion of HIV in virtually all AIDS patients, as 
well as in almost all HIV-positive individu 
als with both early- and late-stage disease. 
In addition, the polymerase chain reaction 
procedure and other sophisticated molecu 
lar techniques have enabled researchers to 
document the presence of HIV genes in 
virtually all patients with AIDS, as well as in 
individuals in earlier stages of HIV disease. 

HIV infection always precedes AIDS. 
Postulate 3 has been fulfilled in tragic inci 
dents such as those involving three labora 
tory workers with no other risk factors who 
have developed AIDS or severe immune 



deficiency after accidental exposure to 
concentrated, pure HIV in the laboratory. 
In all three cases, HIV was isolated from 
the infected individual, sequenced and 
shown to be identical to the infectious 
virus from the laboratory. 

In additipn, through June 1999, the 
Centers for Disease Control received re 
ports of 55 health care workers in the 
United States with documented, occupa- 
tionally acquired HIV infection, of whom 
25 have developed AIDS in the absence of 
other risk factors. The development of 
AIDS following infection with HIV also 
has been repeatedly observed in pediatric 
and adult blood-transfusion cases, in moth 
er-to-child transmission, and in studies of 
hemophilia, injection-drug use and sexual 
transmission in which antibodies to HIV 
can be documented using serial blood sam 
ples. Indeed, young children free of any 
risk factors that might be associated with 
immune disorders (e.g., illicit drug use, 
malnutrition, therapy for other diseases) 
have developed AIDS. HIV was the only 
infectious agent associated with their dis 
ease. 

We know that HIV causes AIDS. We 
know how HIV is transmitted. We know 
that advising people to avoid contact with 
HIV is the best way to avoid infection. We 
can only hope that the public is aware that 
encouraging even one person to stop prac 
ticing safe sex, to believe that HIV is no 
longer something to be feared, can have 
tragic consequences. 

The reality underlying this divisive con 
troversy is that so much remains to be 
done. In several communities here in the 
United States, HIV is spreading. In Africa 
and in much of the developing world, the 
spread of the disease is catastrophic. If left 
unchallenged, HIV will continue to infect 
and sicken the populations of the world. 
Instead of continuing to question the over 
whelming evidence that HIV causes AIDS, 
let us join together to fight this infectious 
agent before it can create even more devas 
tating damage in the world. 

Dr. Jay Levy is professor of medicine at 
UCSF, and director of the Laboratory for 
Tumor and AIDS Vims Research. Dr. Nan 
cy Padian is professor of obstetrics, gynecol- 
ogy, and reproductive science at UCSF, 
and director of international research at 
UCSF'sAlDS Research Institute. JeffShee- 
hy is the communications deputy director 
for UCSF's AIDS Research Institute. 



Jay A. Levy, M.D. 



112 



APPENDIX G 



Date and Place of Birth: 



Present Address: 



Home: 
Marital Status: 

Education and Degrees: 
1960 
1961 
1965 



Present Positions: 



Awards & Honors: 



CURRICULUM VITAE 

November 21, 1938; Wilmington, Delaware 

Cancer Research Institute, University of California, 
School of Medicine, San Francisco, CA 94143-1270 

1111 Lake Street, San Francisco, CA 941 18 
Married 



B.A. - Wesleyan University, Middletown, CT 
Research Fellow, Universite de Paris, Paris, France 
M.D. - Columbia University, College of Physicians and 
Surgeons, New York, NY 

Professor, Department of Medicine; 

Research Associate, Cancer Research Institute; 

Director, Laboratory for Tumor and AIDS Virus Research 

University of California, School of Medicine, San Francisco, CA 

Phi Beta Kappa, Sigma Xi, Wesleyan Memorial Award, 1959-60 
Fulbright and French Government Awards, 1960-61 
Research Career Development Award, 1972-77 
American Cancer Society-Eleanor Roosevelt International 

Cancer Fellowship, 1978-79 
Safani Lectureship on Leukemia, Dartmouth-Hitchcock Medical 

School, 1979 

ICRETT Fellowship, 1982 

Wallace P. Rowe Memorial Lectureship, Lerici, Italy, 1984 
Murray Thelin Award, National Hemophilia Foundation, 1986 
B. Frank Polk Memorial Lectureship, School of Hygiene and 

Public Health, Johns Hopkins University, Baltimore, 1986 
Patricia R. Woodard Lectureship, 1987 
American Medical Association Distinguished Lecturer, 

Chicago, 1987 
Nathalie Schmidt Memorial Lectureship, Northern 

California/ American Society of Microbiology, 1987 
Certificate of Appreciation, American Cancer Society National 

Board of Directors, 1987 
Miles- Yale Lectureship, Yale University, 1988 
Harry M. Rose Memorial Lectureship, Columbia University, 

College of Physicians and Surgeons, 1988 
Maxwell L. Rosten Memorial Lectureship, University of 

California, Irvine, 1989 
Distinguished Visiting Lecturer, San Francisco State 

University, 1990 



Jay A. Levy,M.D. 113 



Distinguished Lecturer, Creighton University, 1991 
Distinguished Lecturer, Washington State University, 1991 
Maurice R. Hilleman Lecture, Children's Hospital, 

Philadelphia, 1993 
Courage Award, Chronic Fatigue Immune Dysfunction 

Syndrome Foundation, 1993 
The Miles, Inc. Distinguished Lectureship, Washington State 

University, 1993 
Fellow, American Association for the Advancement of Science, 

1993 
University Lecturer, The University of Texas, Southwestern 

Medical Center, 1993 

Divisional Lecturer, American Society of Microbiology, 1994 
Award of Distinction, American Foundation for AIDS Research 

(AmFAR), 1994 
Henry T. Finch Jr. Lecturer, Regional HIV AIDS Consortium, 

Charlotte, NC, 1995 

Armine T. Wilson Lecturer, Delaware Medical Society, 1995 
Distinguished Alumnus Award, Wesleyan University, 1995 
Fellow, Molecular Medicine Society, 1995 
Fellow, Infectious Diseases Society of America, 1996 
Fessinger-Springer Memorial Lecturer, University of Texas at 

El Paso, TX, 1996 
Doctor of Science Honorary Degree, Wesleyan University, 

Middletown, CT, 1996 
Distinguished Speaker, Biology Department and the Center for 

Genetics and Molecular Medicine Seminar Series, University of 

Louisville, Louisville, KY 
Distinguished Lecturer, Distinguished Lecture Series, University 

of Kentucky, Lexington, KY, 1996 
Distinguished Lecturer, Distinguished Lecture Series, Montefiore 

Medical Center, Albert Einstein College of Medicine, Bronx, 

NY, 1996 
Special Recognition Award for Outstanding Leadership as Chair 

of the Finance Committee, American Association for Cancer 

Research, 1997 
One of the Ten Most Influential People of the Bay Area, San 

Francisco Sunday Chronicle Examiner, 1998 
Wellcome Visiting Professorship Award, University of Puerto 

Rico, 1999 
George Sarlo Award for Mentorship in AIDS, AIDS Research 

Institute, UCSF, 1999 
Heroes in Medicine Award, International Association of 

Physicians in AIDS Care, 2000 
Leon G. Smith Infectious Disease Institute Hall of Fame, St. 

Michael's Medical Center, Newark, NJ, 2000. 



Editor (1988-2000); 

Editor in Chief (2000-): AIDS 



Jay A. Levy, M.D. 
Editorial Boards: 



Committees: 



114 



Cancer Research 
Virology 

Journal of Clinical Immunology 
Clinical and Diagnostic Laboratory Immunology 
Molecular Aspects of Medicine, -2001 
AIDS Research and Human Retroviruses 
AIDS Abstracts 

International Journal of Oncology 
Microbiologica 
AIDS '91 Summary 
AIDS '92 Summary 
AIDS Information 
AIDS Patient Care and STDs 
International Journal of Oncology 

Cell and Developmental Biology Study Section, 

American Cancer Society, 1983-87 
International Advisory Committee, International Conference on 

AIDS, 1986-1996 
Scientific Program Committee, International Conference on 

AIDS, 1987, 1990, 1992 
Chair, Scientific Program Committee, 6th International 

Conference on AIDS, San Francisco, 1990 
Program Committee, American Association for 

Cancer Research, 1983-84; 1986-87 
Scientific Advisory Board, American Association for 

Cancer Research, 1984-87 
Long-Range Planning Committee, American Association for 

Cancer Research, 1987-90, 1990-93 
Board of Directors, American Association for 

Cancer Research, 1988-91 
Special Conferences Committee, American Association for 

Cancer Research, 1989-92 
Chair, Local Committee for Annual Meeting, American 

Association for Cancer Research, 1989 
Local Committee for Annual Meeting, American Association for 

Cancer Research, 1 994 
Minority Issues Committee, American Association for Cancer 

Research, 1990-93; 1996-2000 
Clowes Award Committee, American Association for Cancer 

Research, 1992 
Representative, Physicians for Human Rights, American 

Association for Cancer Research, 1992- 
Legislative Committee, American Association for Cancer 

Research, 1992- 
Chair, By-Laws Committee, American Association for 

Cancer Research, 1992-93 



Jay A. Levy,M.D. 115 

Chair, Finance Committee, American Association for Cancer 

Research, 1993-96 
Scientific Advisory Board, American Foundation for 

AIDS Research, 1986- 
Chair, Science Policy Committee, American Foundation for AIDS 

Research, 1994- 
Executive Committee, American Foundation for AIDS Research, 

1994- 
Board of Directors, American Foundation for AIDS 

Research, 1993- 
Executive Board, American Committee for the 

Weizmann Institute of Science, 1987- 
Board of Trustees, Wesleyan University, Middletown, CT, 1988- 

91 

Advisory Board, International Alliance for Haiti, 1989- 
Chair, Basic Science Section, 2nd Annual Conference on 

"Neurological and Neuropsychological Complications of 

AIDS Infections," Monterey, CA, 1990 
Chair, Basic Science Section, 3rd Annual Conference on 

"Neurological and Neuropsychological Complications of 

AIDS Infections," Padua, Italy, 1991 
Co-chair, Basic Science Section, 4th Annual Conference on 

"Neuroscience of HIV Infection: Basic and Clinical Frontiers," 

Vienna, Austria, 1993 
Advisory Board, Chronic Fatigue Immune Dysfunction Syndrome 

(CFIDS) Foundation, 1990-1996 
Advisory Board, International AIDS Society, 1993-1996 
Scientific Advisory Board, Oregon Regional Primate Research 

Center, 1994-96 
Scientific Committee, 5th Annual Conference on "Neuroscience 

of HIV Infection: Basic and Clinical Frontiers," Vancouver, 

B.C., 1994 
Scientific Committee, 6th Annual Conference on "Neuroscience 

of HTV Infection: Basic and Clinical Frontiers," Paris, 1996 
Friend, Xth International Congress of Virology, Jerusalem, Israel, 

1996 

International Scientific Committee, XI International Conference 

on AIDS, Vancouver, B.C., 1996 
Program Committee, Annual Meeting of the American 

Association for Cancer Research, 1996 
Membership Development Committee, American Association for 

Cancer Research, 1996-99 
Program Committee, Annual Meeting of the American 

Association for Cancer Research, 1997 

Mayor Willie Brown's AIDS Scientific Advisory Council, 1997- 
Intemational Scientific Advisory Board, Rhone-Poulenc-Rorer, 

1997 
Scientific Advisory Committee, Brown University/Tufts 

University Center for AIDS Research, 1997- 



Jay A. Levy, M.D. 116 



International Review Committee, 12th World AIDS Conference, 

Geneva, Switzerland, 1998 
American Foundation for AIDS Research, Opportunity Fund 

Committee, New York, NY, 1998- 
Board of Directors, People to People Ethiopian/ American AIDS 

Association, 1999- 
Agence Nationale de Recherches sur le Sida, Government of 

France, Scientific Advisory Board, 1999- 
Chair, Local Arrangements Committee, 91 st AACR Annual 

Meeting, 1999-2000 
Chair, Molecular Biology Subcommittee: Cancer Genetics ffl: 

Human and Retroviral Oncogenes- Structure and Function/Viral 

Oncogenesis, 91 st AACR Annual Meeting, 1999-2000 
International Scientific Review Committee, XIH International 

AIDS Conference, 2000 
Advisory Committee, United Religious Initiative Foundation, 

2000- 
Organizing Committee, 3 rd International Symposium on 

Neuro Virology, 2000 
Scientific Advisory Board, NIH HIV Vaccine Design and 

Development Team, Chiron Corp., 2001 
International Scientific Board, 10 th Conference on Neuroscience 

of HIV Infection, 2001 
Scientific Review Committee, 1 st LAS Conference on HIV 

Pathogenesis and Treatment, 2001 
Scientific Advisory Committee, Deutsches 

Krebsforschungszentrum, Heidelberg Germany, 2001 



Committees - UCSF: Committee for Human Research, 1 974-77 

Vice Chairman, Committee for Human Research, 1976-77 

Representative to Academic Senate, Dept. of Medicine, 1980-81 

Student Research Committee, 1987-94 

Chancellor's AIDS Coordinating Council, 1989-95 

Executive Committee, Center for AIDS Research, 1988- 

ALDS Research Council, 1988-1990 

Organizer, AIDS Research Workshop, 1985-90 

Faculty, Graduate Group in Oral Biology, 1989- 

Chair, Track A Basic Science Committee, 6th International AIDS 

Conference, 1990 

Faculty, Center for AIDS Prevention Studies, 1990- 
Faculty, Fogarty International Fellowship Program, 1990- 
Promotion Committee, Department of Medicine, 1990- 
Ad Hoc Committee on Aerosol Transmission of HFV Infection, 

1991 

Ad Hoc Committee on HIV and Health Care Providers, 1991 
United Way Faculty Representative, Cancer Research Institute, 

1991 
Faculty, Molecular Medicine, 1993- 



Jay A. Levy, M.D. 



Memberships: 



Patents: 



117 

Biosafety Committee, 1993-1998 

Minority Affairs Committee, American Association for Cancer 

Research, 1996-2000 

Chancellor's Advisory Board on AIDS, 1996-97 
Dean's Task Force on AIDS Program Planning, 1996 
UCSF AIDS Research Institute, Executive Committee, 1996- 
UCSF AIDS Research Institute, Steering Committee, 1997- 
Medical Network Group for UCSF Medical Students, 1997- 
Preceptor, Course IDS 131/132 Foundations of Patient Care, 

1997- 
UCSF Chancellor's Advisory Board on AIDS and Emerging 

Infections, 1997- 

Chair, ARI TAG for HIV vaccines, 1997- 
Organizer, HIV Vaccine Workshop, 1 997 
Organizer, Anti-Bacteria Vaccine Workshop, 1998 
General Clinical Research Center (GCRC) Advisory Committee, 

1998- 
UCSF California AIDS Research Center, Advisory Committee, ex 

officio, 1999- 

Scientific Advisory Group, Institute for Global Health, 2000 - 
HIV Basic Science Executive Steering Committee, 2000 - 

American Association for the Advancement of Science 

American Association for Immunologists 

American Association for Cancer Research 

American Society for Clinical Investigation 

American Society for Microbiology 

American Society for Tropical Medicine and Hygiene 

American Society for Virology 

Association of American Physicians 

Association of IUCC Fellows 

International AIDS Society 

International Union Against Cancer 

Western Association of Physicians 

Western Society for Clinical Research 

Infectious Diseases Society of America 

HIV Medical Association of the Infectious Diseases Society of 

America 

"Purifed AIDS-associated virus ARV-2" (Patent No. 4,716,102) 
"HFV-2 strains capable of infecting humans and non-human 
primates, and infected non-human primates with immune system 
disease" (Patent No. 5,543,131) 
"CD8+ cell antiviral factor" (Patent No. 5,565,549) 
"Hybridization assays for detecting the presence of an AIDS- 
associated virus" (Patent No. 5,736,328) 



Training and Experience: 



Jay A. Levy, M.D. 
1959-1960 



1960-1961 



1961-1965 



Summer 1962 



Summer 1963 



Summer 1964 



1965-1966 



1966-1967 



1967-1970 



May 1970 



118 

Teaching Assistant in Biology, Wesleyan University, Middletown, 
Connecticut. Biochemical research conducted on fungi in the 
laboratory of Dr. V. Cochrane. 

Fulbright and French Government Fellowships. Laboratoire de 
Biologie Animal, Universite de Paris, Paris, France. Under the 
direction of Professor Th. Lender and Professor E. Wolff. Studies 
on regeneration of planaria. 

College of Physicians and Surgeons, Columbia University. 
Research conducted with Drs. H. Rose and H. Rosenkranz on 
lysogenic bacteria, and Dr. B.C. Curnen on viruses in Burkitt's 
lymphoma. 

USPHS Summer Fellowship, Jerusalem, Israel; Work at the 
Kiryat Hayovel Health Clinic, Department of Public Health and 
Social Medicine, Hebrew University. Under Professor S- Kark. 

Lederle Medical Fellowship, Karolinska Institute!, Stockholm, 
Sweden. Conducted research with Professors E. and G. Bertani 
on lysogenic bacteria. 

Louisiana State University Medical Fellowship. Makerere 
University College, Kampala, Uganda. Training in tropical 
medicine under the direction of Dr. Lawrence (England) and Dr. 
D.J. Jelliffe (USA). Research conducted on viral etiology of 
Burkitt's lymphoma, in collaboration with Drs. T.M. Bell and 
A. Haddow, East African Virus Research Institute, Entebbe, 
Uganda. 

Intern in Medicine, Hospital of the University of Pennsylvania. 
Under Dr. J.B. Wyngaarden. Research conducted in the 
laboratory of Drs. Werner and Gertrude Henle, Philadelphia, on 
Epstein-Barr virus (EBV) in Burkitt's lymphoma. 

First-year Resident in Medicine, Hospital of the University of 
Pennsylvania. Under Dr. J.B. Wyngaarden. Research on EBV 
continued in the laboratories of Drs. Henle and Dr. Robert 
Austrian. Research on human lymphocytes conducted in Dr. 
Vittorio Defendi's laboratory, Wistar Institute, Philadelphia, 
Pennsylvania. 

Staff Associate, National Cancer Institute, National Institutes of 
Health, Bethesda, Maryland. Studies of DNA and RNA 
oncogenic viruses in the laboratory of Drs. Robert J. Huebner, 
Wallace P. Rowe and Janet W. Hartley. 

Collaborated with Dr. Alfred Prince, New York Blood Center and 
Dr. George Kafuko, Director of the East African Virus Research 



Jay A. Levy, M.D. 119 

Institute, Entebbe, Uganda. Search for EBV and infectious 
hepatitis virus in wild chimpanzees in forests of Uganda. 

1970-1971 Second-year Resident in Medicine, University of California, 

School of Medicine, San Francisco, California. Under Dr. L.H. 
Smith, Jr. Research conducted on epithelial cell transformation 
with Dr. T. Crocker in the Cancer Research Institute (Director, 
David A. Wood, M.D.). 

1971-1972 Visiting Scientist CNRS, INSERM. NATO Fellowships, Paris, 

France. (1) Studies on human cell transformation by murine RNA 
tumor viruses were conducted in the laboratory of Dr. M. Boiron, 
Hopital St. Louis, Paris. (2) Work on infection of mammalian 
cells with DNA from RNA virus-transformed rodent cells was 
performed in collaboration with Drs. M. Hill and J. Hillova, 
Villejuif. (3) Further characterization of the anti-viral inhibitor 
associated with NZB cells was done in collaboration with Drs. C. 
Jasmin and J.-C. Chermann in the laboratory of Dr. G. Mathe, 
Villejuif. 

1972-1977 Assistant Clinical Professor, Department of Medicine; Research 

Associate, Cancer Research Institute, University of California, 
School of Medicine, San Francisco, CA. Established laboratory 
for the study of endogenous type C viruses. 

1978-1982 Associate Professor in Residence, Department of Medicine; 

Research Associate, Cancer Research Institute, University of 
California, School of Medicine, San Francisco, CA. 

1978-1979 Eleanor Roosevelt Fellowship. Visiting Scientist. 7/1/78-1/1/79, 

with Dr. Nechama Haran-Ghera, Department of Chemical 
Immunology, Weizmann Institute of Science, Rehovot, Israel. 
Research on T-cell differentiation and radiation-induced tumors. 
1/1/79-8/1/79, with Professor Fran?ois Jacob, Institut Pasteur, 
Paris, France. Studies on type C virus interaction with murine 
embryonal carcinoma cells. 

1982 (April) ICRETT (International Cancer Technology Transfer) Fellowship. 

Visiting Scientist, Weizmann Institute of Science, Rehovot, Israel. 
With Professor Nechama Haran-Ghera. Research on dual-tropic 
type C viruses in mouse T-cell leukemias. 

1982-1985 Associate Professor in Residence, Departments of Medicine, 

Microbiology and Immunology; Research Associate, Cancer 
Research Institute, University of California, School of Medicine, 
San Francisco, CA. 



Jay A. Levy, M.D. 120 

1985-1996 Professor in Residence, Department of Medicine, Research 

Associate, Cancer Research Institute, University of California, 
School of Medicine, San Francisco, CA. 

1996-present Professor in Residence, Department of Medicine, Division of 

Hematology/Oncology; Research Associate, Cancer Research 
Institute, University of California, School of Medicine, San 
Francisco, CA. 



Jay A. Levy, M.D. 121 

PUBLICATIONS 

Original Articles 

1. Cochrane VW, Berry SJ, Simon FG, Cochrane JC, Collins CB, Levy JA, Holmes PK. 
Spore germination and carbon metabolism in Fusarium solani. HI. Carbohydrate 
respiration in relation to germination. Plant Physiol 38: 533-541, 1963. 

2. Bertani LE, Levy JA. Conversion of lysogenic Escherichia coli by nonmultip lying, 
superinfecting Bacteriophage P2. Virology 22: 634-640, 1964. 

3. Rosenkranz HS, Levy JA. Hydroxyurea: A specific inhibitor of deoxyribonucleic acid 
synthesis. Biochim Biophys Acta 96: 181-183, 1965. 

4. Rosenkranz HS, Garro AJ, Levy JA, Carr HS. Studies with hydroxyurea. I. The 
reversible inhibition of bacterial DNA synthesis and the effect of hydroxyurea on the 
bactericidal action of streptomycin. Biochim Biophys Acta 114: 501-515, 1966. 

5. Levy JA, Henle G. Indirect immuno fluorescence tests with sera from African children 
and cultured Burkitt's lymphoma cells. J Bacteriol 92: 275-276, 1966. 

6. Levy JA, Tanabe E, Curnen EC. Occurrence of reovirus antibodies in healthy African 
children and in children with Burkitt's lymphoma. Cancer 21: 53-57, 1968. 

7. Levy JA, Huebner RJ, Kern J, Gilden RV. High titre T antigen with minimal amounts of 
structural antigen in adenovirus-infected cells treated with hydroxyurea. Nature 217: 
744.745, 1968. 

8. Levy JA, Virolainen M, Defendi V. Human lymphoblastoid lines from lymph node and 
spleen. Cancer 22: 517-524, 1968. 

9. Levy JA, Henle G, Henle W, Zajac BA. Effect of reovirus type 3 on cultured Burkitt's 
lymphoma tumor cells. Nature 220: 607-608, 1968. 

10. Levy JA, Huebner RJ. Isolation of murine leukemia virus from a mouse lymphoma 
(273/L) associated with reovirus type 3 infection. Nature 225: 949-950, 1970. 

1 1 . Parkman R, Levy JA, Ting RC. Murine sarcoma virus: the question of defectiveness. 
Science 168: 387-389, 1970. 

12. Levy JA, Pincus T. Demonstration of biological activity of a murine leukemia virus in 
New Zealand Black mice. Science 170: 326-327, 1970. 

13. Levy JA, Buell DN, Creech C, Hirshaut Y, Silverberg H. Further characterization of the 
WI-L1 and WI-L2 lymphoblastoid lines. J Natl Cancer List 46: 647-654, 1971. 

14. Levy JA. Demonstration of differences in murine sarcoma virus foci formed in mouse 
and rat cells under a soft agar overlay. J Natl Cancer Inst 46: 1001-1007, 1971. 



Jay A. Levy.M.D. 122 

15. Levy JA, Rowe WP. Lack of requirement of murine leukemia virus for early steps in 
infection of mouse embryo cells by murine sarcoma virus. Virology 45: 844-847, 1971. 

16. Levy JA, Levy SB, Hirshaut Y, Kafuko G, Prince A. Presence of EBV antibodies in sera 
from wild chimpanzees. Nature 233: 599-560, 1971. 

17. Yuspa SH, Morgan DL, Levy JA. In vitro cultivation of a chemically induced epidermal 
carcinoma: Establishment of three cell lines and isolation of murine leukemia virus. J 
Natl Cancer Inst 50: 1561-1570, 1973. 

18. Levy JA, Hartley JW, Rowe WP, Huebner RJ. Studies of FBJ osteosarcoma virus in 
tissue culture. I. Biologic characteristics of the C-type viruses. J Natl Cancer Inst 51: 
525-539, 1973. 

19. Levy JA, Chermann J-C, Jasmin C, Raynaud M. Mise en evidence d'une substance a 
effet antiviral dans le milieu culture de cellules de souris NSB. C.R. Acad Sc Paris 277: 
1421-1423, 1973. 

20. Levy JA. Xenotropic viruses: Murine leukemia viruses associated with NTH Swiss, 
NZB, and other mouse strains. Science 182: 1151-1153, 1973. 

2 1 . Levy JA. Autoimmunity and neoplasia. The possible role of C-type viruses. Am J Clin 
Pathol 62: 258-280, 1974. 

22. Levy JA, Kazan PM, Varmus HE. The importance of DNA size for successful 
transfection of chicken embryo fibroblasts. Virology 61: 297-302, 1974. 

23. Arnstein P, Levy JA, Oshiro LS, Price PJ, Suk W, Lennette EH. Recovery of murine 
xenotropic type-C virus from C57L mice. J Natl Cancer Inst 53: 1787-1972, 1974. 

24. Levy JA. Host range of murine xenotropic virus: replication in avian cells. Nature 253: 
140-142, 1975. 

25. Levy JA, Hartley JW, Rowe WP, Huebner RJ. Studies of FBJ osteosarcoma virus in 
tissue culture, n. Autoinhibition of focus formation. J Natl Cancer Inst 54: 615-619, 
1975. 

26. Levy JA, Kazan P, Vamier O, Kleiman H. Murine xenotropic type C viruses. 
I. Distribution and further characterization of the virus in NZB mice. J Virol 16: 844- 
853, 1975. 

27. Levy JA, Ihle JN, Oleszko O, Barnes RD. Virus-specific neutralization by a soluble non- 
immunoglobulin factor found naturally in normal mouse sera. Proc Natl Acad Sci (USA) 
72: 5071-5075, 1975. 

28. Levy JA, Levy SB, Levinson W. Inactivation of murine RNA tumor viruses by isatin 
beta-thiosemicarbazone, its derivatives and analogs. Virology 74: 426-431, 1976. 



Jay A. Levy, M.D. 123 

29. Levy JA, Weiss RM, Dirksen ER, Rosen MR. Possible communication between murine 
macrophages oriented in linear chains in tissue culture. Exper Cell Res 103: 375-385, 
1976. 

30. Levy JA, Datta S, Schwartz RS. Recovery of xenotropic virus but not ecotropic virus 
during graft-versus-host reaction in mice. Clin Irnmunol Immunopathol 7: 262-279, 
1977. 

3 1 . Leong JC, Kane JP, Oleszko O, Levy JA. Antigen-specific, non-immunoglobulin factor 
that neutralizes xenotropic virus is associated with mouse serum lipoproteins. Proc Natl 
Acad Sci (USA) 74: 276-280, 1977. 

32. Levy JA. Murine xenotropic type C viruses. EL Phenotypic mixing with mouse and rat 
ecotropic C-type viruses. Virology 77: 797-810, 1977. 

33. Levy JA. Murine xenotropic type C viruses. IE. Phenotypic mixing with avian leukosis 
and sarcoma viruses. Virology 77: 811-825, 1977. 

34. Oshiro LS, Levy JA, Riggs JL, Lennette EH. Distinction between envelope antigens in 
murine xenotropic and ecotropic type C viruses by immunoelectron microscopy. J Gen 
Virol35:317-323, 1977. 

35. Hahn BH, Mehta J, Knotts LL, Huebner RH, Ihle JN, Levy JA. The effect of altered 
lymphocyte function on the immunologic disorders of NZB/NZW mice. H Response to 
anti-thymocyte globulin. Clin Immunol Immunopathol 8: 225-237, 1977. 

36. Gardner MB, Ihle JN, Pillarisetty RJ, Talal N, DuBois EL, Levy JA. Type C virus 
expression and host response in diet-cured NZB/W mice. Nature 268: 341-344, 1977. 

37. Dirksen ER, Levy JA. Virus-like particles in placentas from normal individuals and 
patients with systemic lupus erythematosus. J Natl Cancer Inst 59: 1 187-1 192, 1977. 

38. Levy JA, Kazan PL, Reilly CA Jr, Finkel MP. FBJ osteosarcoma virus in tissue culture, 
m. Isolation and characterization of non-virus-producing FBJ-transformed cells. J Virol 
26: 11-15, 1978. 

39. Avery RJ, Levy JA. Relationship of endogenous virus production to spontaneous 
transformation of cultured cells. J Gen Virol 39: 427-435, 1978. 

40. Nelson J, Leong J, Levy JA. Normal human placentas contain virus-like RNA-directed 
DNA polymerase activity. Proc Natl Acad Sci (USA) 75: 6263-6267, 1978. 

41. Levy JA, Rutledge F, Dimpfl J, Silagi S. Recovery of three distinct biologically active 
type C viruses from cloned C57B1/6 melanoma cells. J Gen Virol 43; 283-288, 1979. 

42. Avery RJ, Levy JA. The effect of ethidium bromide on C type virus production and 
induction. Virology 95: 277-284, 1979. 



Jay A. Levy, M.D. 124 

43. Levy JA, Joyner J, Nayar KT, Kouri RE. Genetics of xenotropic virus expression in 
mice. I. Evidence for a single locus regulating spontaneous production of infectious virus 
in crosses involving NZB/BINJ and 129/J strains of mice. J Virol 30: 754-758, 1979. 

44. Varnier O, Levy JA. Differential effect of dexamethasone on replication of ecotropic and 
xenotropic mouse type C viruses. Virology 96: 604-614, 1979. 

45. Kane JP, Hardman DA, Dimpfl JC, Levy JA. Apolipoprotein is responsible for 
neutralization of xenotropic type C virus by mouse serum. Proc Natl Acad Sci (USA) 76: 
5957-5961, 1979. 

46. Nayar KT, Levy JA, Kouri RE. Xenotropic virus expression and susceptibility to 
3-methylcholanthrene-induced cancer. Cancer Res 40: 64-67, 1980. 

47. Levy JA, Joyner J, Borenfreund E. Mouse sperm can horizontally transmit type C 
viruses. J Gen Virol 51: 439-443, 1980. 

48. Levy JA, Barrett SG, Leong JC, Dirksen ER. Transformation of macrophages from NZB 
hybrid mice by simian virus 40. J Reticul Soc 29(1): 35-46, 1981. 

49. Nelson JA, Levy JA, Leong JC. Human placentas contain a specific inhibitor of RNA- 
directed DNA polymerase. Proc Natl Acad Sci (USA) 78: 1670-1674, 1981. 

50. Fischbach M, Volberding P, Talal N, Levy J. Genetic analysis of induction of anti- 
polyadenylic acid antibodies and xenotropic C type viruses. Clin Exp Immunol 44: 615- 
619,1981. 

5 1 . Levy JA, Bin Ibrahim A, Shirai T, Ohta K, Nagasawa R, Yoshida H, Estes J, Gardner M. 
Dietary fat affects immune response, production of antiviral factors, and immune 
complex disease in NZB/NZW mice. Proc Natl Acad Sci (USA) 79: 1974-1978, 1982. 

52. Levy JA, Dimpfl J, Hardman D, Kane P. Transfer of mouse anti-xenotropic virus 
neutralizing factor to human lipoproteins. J Virol 42: 365-371, 1982. 

53. Levy JA, Arnstein P, Dirksen ER, Siperstein M, Wiley M. Differentiated mouse 
epithelial cell line with hepatocyte characteristics. Differentiation 22: 12-18, 1982. 

54. Levy JA, Oleszko O, Dimpfl J, Lau D, Rigdon RH, Jones J, Avery R. Murine xenotropic 
type C viruses. TV. Replication and pathogenesis in ducks. J Gen Virol 61: 65-74, 1982. 

55. Levy JA, Jakob H, Paulin D, Kelly F, Chermann J-C, Jacob F. Productive infection of 
embryonal carcinoma cells with ecotropic mouse type C viruses and subsequent arrest of 
differentiation. Virology 120: 157-170, 1982. 

56. Levy JA, Fieldsteel AH. Freeze-drying is an effective method for preserving infectious 
type C retroviruses. J Virol Methods 5: 165-171, 1982. 



Jay A. Levy, M.D. 125 

57. Ibrahim AB, Stobo JD, Levy JA. Unusual characteristics of peritoneal macrophages from 
aged autoimmune-prone mice. Cell Immunol 72: 28-39, 1982. 

58. Levy JA, Sumner PE, Hooser LE. Rapid tissue culture method for detection of 
mycoplasma hyorihinis. J Gen Microbiol 128: 2817-2820, 1982. 

59. Vamier OE, Repetto CM, Raffanti SP, Alama A, Levy JA. Host range differences among 
xenotropic type C retroviruses isolated from mouse kidney cell cultures. J Gen Virol 64: 
425-428, 1983. 

60. Putman DL, Nayar KT, O'Neill B, Premkumar-Reddy E, Levy JA, Kouri RE. Genetics of 
xenotropic virus expression in mice. II. Expression of major virus structural proteins in 
crosses involving NZB/B1NJ, SWR/J and 129/J strains of mice. Proc Exp Biol Med 173: 
217-221, 1983. 

61. Varnier OE, Hoffman AD, Nex0 BA, Levy JA. Murine xenotropic type C viruses. 
V. Biologic and structural differences among three cloned retroviruses isolated from 
kidney cells from one NZB mouse. Virology 132: 79-84, 1984. 

62. Marx PA, Maul DH, Osborn KG, Lerce NW, Moody P, Lowenstine LJ, Hendrickson RV, 
Arthur LO, Gilden RV, Gravell M, London WT, Sever JL, Levy JA, Munn RJ, Gardner 
MB. Simian AIDS: Isolation of a typeD retrovirus and transmission of the disease. 
Science 223: 1083-1086,1984. 

63. Leong JC, Wood SO, Lyford AO, Levy JA. Purification of a specific inhibitor of reverse 
transcriptase from human placenta. Int J Cancer 33: 435-439, 1984. 

64. Levy JA, Lee HM, Kawahata RT, Spitler LE. Purification of monoclonal antibodies from 
mouse ascites eliminates contaminating infectious mouse type C viruses and nucleic 
acids. Clin Exp Immunol 56: 114-120, 1984. 

65. Levy JA. Confirmation of the successful cultivation of Treponema pallidum in tissue 
culture. Microbiologica 7: 367-370, 1984. 

66. Hays EF, Levy JA. Differences in lymphomagenic properties of AKR mouse 
retroviruses. Virology 138: 49, 1984. 

67. Leong JC, Nelson JA, Levy JA. Optimal conditions for detection of reverse transcriptase 
activity in human placentas. Biochem Biophys Acta 782: 441-445, 1984. 

68. Levy JA, Hoffman AD, Kramer SM, Landis JA, Shimabukuro JM, Oshiro LS. Isolation 
of lymphocytopathic retroviruses from San Francisco patients with AIDS. Science 225: 
840-842, 1984. 

69. Levy JA, Mitra G, Mozen MM. Recovery and inactivation of infectious retroviruses 
added to factor VJJI concentrates. Lancet ii: 722-723, 1984. 



Jay A. Levy, M.D. 126 

70. Luciw PA, Potter SJ, Steimer K, Dina D, Levy JA. Molecular cloning of AIDS- 
associated retrovirus. Nature 312: 760-763, 1984. 

71. Hill AB, May W, Kaminsky L, Levy JA, Penny R, Cooper DA. Acquired immune 
deficiency syndrome and related conditions in a Sydney hospital. Med J Aust 141: 573- 
578, 1984. ' 

72. Cooper DA, Gold J, May W, Kaminsky L, Penny R, Levy JA. Contact tracing in the 
acquired immune deficiency sydnrome: Evidence for transmission of virus and disease 
by an asymptomatic carrier. Med J Aust 141: 579-582, 1984. 

73. Levy JA, Tobler LH, McHugh TM, Casavant CH, Stites DP. Long-term cultivation of 
T cell subsets from patients with acquired immune deficiency syndrome. Clin Immunol 
Immunopathol 35: 328-336, 1985. 

74. Sanchez-Pescador R, Power MD, Barr PJ, Steimer KS, Stempien MM, Brown-Shimer 
SL, Gee WW, Renard A, Randolph A, Levy JA, Dina D, Luciw PA. Nucleotide sequence 
and expression of an AJDS-associated retrovirus (ARV-2). Science 227: 484-492, 1985. 

75. Drew WL, Mills J, Levy JA, Dylewski J, Casavant C, Ammann AJ, Brodie H, Merigan T. 
Cytomegalovirus infection and abnormal T lymphocyte subset ratios in homosexual men. 
Ann Intern Med 103: 61-63, 1985. 

76. Ammann AJ, Kaminsky L, Cowan M, Levy JA. Antibodies to AJDS-associated 
retrovirus distinguish between pediatric primary and acquired immunodeficiency 
diseases. J Am Med Assoc 253: 3116-3118, 1985. 

77. Levy JA, Mitra GA, Wong MF, Mozen MM. Inactivation by wet and dry heat of AJDS- 
associated retroviruses during during factor VHI purification from plasma. Lancet i: 
1456-1457, 1985. 

78. Levy JA, Kaminsky LS, Morrow WJW, Steimer K, Luciw P, Dina D, Hoxie J, Oshiro L. 
Infection by the retrovirus associated with the acquired immunodeficiency syndrome. 
Ann Intern Med 103: 694-699, 1985. 

79. Morrow WJW, Ohashi Y, Hall J, Pribrow J, Hirose S, Shira T, Levy JA. Dietary fat and 
immune function. I. Antibody response, lymphocyte and accessory cell function in (NZB 
x NZW)F, mice. J Immunol 135: 3857-3863, 1985. 

80. Yumura W, Hartori S, Morrow WJW, Mayes DC, Levy JA, Shirai T. Dietary fat and 
immune function. H Effects on immune complex nephritis in (NZB x NZW)Fj mice. J 
Immunol 135: 3864-3868, 1985. 

81. Kaminsky LS, McHugh T, Stites D, Volberding P, Henle G, Henle W, Levy JA. High 
prevalence of antibodies to AIDS-associated retroviruses (ARV) in acquired immune 
deficiency syndrome and related conditions and not in other disease states. Proc Natl 
Acad Sci (USA) 82: 5535-5539, 1985. 



Jay A. Levy, M.D. 127 

82. Levy JA, Shimabukuro J. Recovery of AIDS-associated retroviruses from patients with 
AIDS or AIDS-related conditions, and from clinically healthy individuals. J Infect Dis 
152: 734-738, 1985. 

83. Hoffman AD, Banapour B, Levy JA. Characterization of the AIDS-associated retro virus 
reverse transcriptase and optimal conditions for its detection in virions. Virology 147: 
326-335, 1985. 

84. Hoxie JA, Haggarty BS, Rackowski JL, Pilsbury N, Levy JA. Persistent noncytopathic 
infection of human lymphocytes with AIDS-associated retrovirus (ARV). Science 229: 
1400-1402, 1985. 

85. Ollero M, Leal M, Wichman L, Lissen E, Levy J. Antibodies to the AIDS-associated 
retrovirus in hemophiliacs and other individuals from Southern Spain: Lack of 
correlation with lymphocyte sub-population. AIDS Res 1: 439-445, 1985. 

86. Levy JA, Hollander H, Shimabukuro J, Mills J, Kaminsky L. Isolation of AIDS- 
associated retroviruses from cerebrospinal fluid and brain of patients with neurological 
symptoms. Lancet ii: 586-588, 1985. 

87. Levy JA, Shimabukuro J, McHugh T, Casavant C, Stites D, Oshiro L. AIDS-associated 
retroviruses (ARV) can productively infect other cells besides human T helper cells. 
Virology 147: 441-448, 1985. 

88. Coleman DL, Luce JM, Wilber JC, Ferrer JJ, Stephens BG, Margetten W, Wagar EA, 
Hadley WK, Pifer LL, Moss AR, Dodek PM, Levy JA, Murray JF. Antibody to the 
retrovirus associated with the acquired. immunodeficiency syndrome (AIDS). Presence in 
presumably healthy San Franciscans who died unexpectedly. Arch Intern Med 146: 713- 
716, 1986. 

89. Ragni MV, Tegtmeier GE, Kaminsky LS, Levy JA, Lewis JH, Spero JA, Bontempo FA, 
Handwerk-Leber C, Bayer WL, Zimmerman DH, Britz JA. AIDS retrovirus antibodies in 
hemophiliacs treated with factor VUI or factor IX concentrates, cyroprecipitates, or fresh- 
frozen plasma: Prevalence, seroconversion rate, and clinical correlation. Blood 67: 592- 
595, 1986. 

90. Steimer KS, Puma JP, Power MD, Powers MA, George-Nascimento C, Stephans JC, 
Levy JA, Sanchez-Pescador R, Luciw PA, Barr PJ, Hallewell RH. Differential antibody 
responses of individuals infected with AIDS-associated retroviruses surveyed using the 
viral core antigen p25s a expressed in bacteria. Virology 150: 283-290, 1986. 

91. Wofsy CB, Cohen JB, Hauer LB, Padian NS, Michaelis BA, Evans LA, Levy JA. 
Isolation of the AIDS-associated retrovirus from genital secretions from women with 
antibodies to the virus. Lancet i: 527-529, 1986. 

92. Levy JA, Cheng-Mayer C, Dina D, Luciw PA. AIDS retrovirus (ARV-2) clone replicates 
in transfected human and animal fibroblasts. Science 232: 998-1001, 1986. 



Jay A. Levy, M.D. 128 

93. Banapour B, Sernatinger J, Levy JA. The AIDS-associated retrovirus is not sensitive to 
lysis or inactivation by human serum. Virology 152: 268-271, 1986. 

94. Ammann A, Levy JA. Laboratory investigation of pediatric acquired immunodeficiency 
syndrome. Clin Immunol Immunopathol 40: 122-127, 1986. 

95. Mitra G, Wong MF, Mozen MM, McDougal JS, Levy JA. Elimination of infectious 
retroviruses during preparation of immunoglobulins. Transfusion 26: 394-397, 1986. 

96. Ulstrup JC, Skaug K, Brunn JN, Peterson G, Frolond S, Levy JA. Immunofluorescenstest 
i diagnostikken av AJDS-assosiert virusinfeksjon I Norge. Tidssrk Nor Laegeforen nr. 5, 
106: 387-389, 1986. 

97. Morrow WJW, Wharton M, Strieker RB, Levy JA. Circulating immune complexes in 
patients with Acquired Immune Deficiency Syndrome contain the AJDS-associated 
retrovirus. Clin Immunol Immunopathol 40: 515-524, 1986. 

98. Levy JA, Pan L-Z, Beth-Giraldo B, Kaminsky L, Henle G, Henle W, Giraldo G. Absence 
of antibodies to the human immunodeficiency virus in sera from Africa prior to 1975. 
Proc Natl Acad Sci (USA) 83: 7935-7937, 1986. 

99. Morrow WJW, Homsy J, Swanson CA, Ohashi Y, Estes J, Levy JA. Dietary fat 
influences the expression of autoimmune disease in MRL/lpr/lpr mice. Immunology 59: 
439-443, 1986. 

100. Walker CM, Moody DJ, Stites DP, Levy JA. CD8+ lymphocytes can control HIV 
infection in vitro by suppressing virus replication. Science 234: 1563-1566, 1986. 

101. McHugh TM, Stites DP, Casavant CH, Carlson JR, Yee J, McVay PA, Busch MP, Levy 
JA. Evaluation of the indirect immunofluorescence assay as a confirmatory test for 
detecting antibodies to the human immunodeficiency virus. Diag Immunol 4: 233-240, 
1986. 

102. Winkelstein W, Jr, Lyman DM, Padian N, Grant R, Samuel M, Wiley JA, Anderson RE, 
Lang W, Riggs J, Levy JA. Sexual practices and risk of infection by the human 
immunodeficiency virus: The San Francisco Men's Health Study. J Am Med Assoc 257: 
321-325, 1987. 

103. Lang W, Anderson RE, Perkins H, Grant RM, Lyman D, Winkelstein W, Jr, Royce R, 
Levy JA. Clinical, immunologic, and serologic findings in men at risk for acquired 
immunodeficiency syndrome: The San Francisco Men's Health Study. J Am Med Assoc 
257: 326-330, 1987. 

104. Lennette ET, Karpatkin S, Levy JA. Indirect immunofluorescence assay for antibodies to 
the human immunodeficiency virus (HIV). J Clin Microbiol 25: 199-202, 1987. 



Jay A. Levy, M.D. 129 

105. Koenig RE, Pittaluga J, Bogart M, Castro M, Nunez F, Vilorio I, Delvillar I, Calzada M, 
Levy JA. Prevalence of antibodies to the human immunodeficiency virus in the 
Dominican Republic. J Am Med Assoc 257: 631-634, 1987. 

106. Greenspan D, Greenspan JS, Hearst NG, Pan L-Z, Conant MA, Abrams DI, Hollander H, 
Levy JA. Relation of oral hairy leukoplakia to infection with HIV and the risk of 
developing AIDS. J Infect Dis 155: 475-481, 1987. 

107. Pan L-Z, Cheng-Mayer C, Levy JA. Patterns of antibody response in individuals infected 
with the human immunodeficiency virus. J Infect Dis 155: 626-632, 1987. 

108. Hollander H, Levy JA. Neurologic abnormalities and recovery of human 
immunodeficiency virus from cerebrospinal fluid. Ann Intern Med 106: 692-695, 1987. 

109. Winkelstein W, Wiley JA, Lang W, Levy JA. The San Francisco Men's Health Study. 
HI. Reduction in human immunodeficiency virus transmission among 
homosexual/bisexual men. Am J Public Health 77: 685-688, 1987. 

110. Luciw PA, Cheng-Mayer C, Levy JA. Mutational analysis of the human 
immunodeficiency virus (HIV): the orf-B region down-regulates virus replication. Proc 
Natl Acad Sci (USA) 84: 1434-1438, 1987. 

111. Kaplan LD, Wolfe PR, Volberding PA, Feorino PA, Levy JA, Abrams DI, Kiprov D, 
Wong R, Kaufman L, Gottlieb MS. Lack of response to suramin in patients with AIDS 
and AJDS-related complex. Am J Med Assoc 82: 615-620, 1987. 

1 12. Cheng-Mayer C, Rutka JT, Rosenblum ML, McHugh T, Stites DP, Levy JA. The human 
immunodeficiency virus (HIV) can productively infect cultured human glial cells. Proc 
Natl Acad Sci (USA) 84: 3526-3530, 1987. 

113. Evans LA, 'McHugh TM, Stites DP, Levy JA. Differential ability of human 
immunodeficiency virus isolates to productively infect human cells. J Immunol 138: 
3415-3418, 1987. 

114. Haran-Ghera N, Peled A, Leef F, Hoffman AD, Levy JA. Enhanced AKR 
leukemogenesis by the dual tropic viruses: I. The time and site of origin of potential 
leukemic cells. Leukemia 1(5): 442-449, 1987. 

115. Peled A, Hoffman AD, Levy JA, Haran-Ghera N. Enhanced AKR leukemogenesis by the 
dual tropic viruses: U. Effect on cell-mediated immune responses. Leukemia 1(5): 450- 
456, 1987. 

1 16. Strieker RB, McHugh TM, Moody DJ, Morrow WJW, Stites DP, Shuman MA, Levy JA. 
An AJDS-related cytotoxic autoantibody reacts with a specific antigen on stimulated 
CD4+T cells. Nature 327: 710-713, 1987. 

117. Hoffman AD, Levy JA: Mouse xenotropic viruses can inhibit cell transformation. 
Virology 160: 60-65, 1987. 



Jay A. Levy, M.D. 130 

118. Morrow WJW, Wharton M, Lau D, Levy JA: Small animals are not susceptible to HIV 
infection. J Gen Virol 68: 2253-2257, 1987. 

119. 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 acquired immunodeficiency syndrome (AIDS) and AIDS-related 
conditions. J Infect Dis 156: 1-8, 1987. 

120. Perkins HA, Samsen S, Garner J, Echenberg D, Allen JR, Cowan M, Levy JA: Risk of 
AIDS for recipients of blood components from donors who subsequently developed 
AIDS. Blood 70: 1604-1610, 1987. 

121. Eichberg JW, Zarling JM, Alter HJ, Levy JA, Berman PW, Gregory T, Lasky LA, 
McClure J, Cobb KE, Moran PA, Kennedy RC, Chang TC, Dreesman GR: Tcell 
responses to human immunodeficiency virus (HIV) and its recombinant antigens in HFV- 
infected chimpanzees. J Virol 61: 3804-3808, 1987. 

122. Homsy J, Thomson-Honnebier GA, Cheng-Mayer C, Levy JA: Detection of human 
immunodeficiency virus (HIV) in serum and body fluids by sequential competition 
ELISA. J Virol Meth 19: 43-56, 1988. 

123. Nelson JA, Wiley CA, Reynolds-Kohler C, Reese CE, Margaretten W, Levy JA: Human 
immunodeficiency virus detected in bowel epithelium from patients with gastrointestinal 
symptoms. Lancet i: 259-262, 1988. 

124. Evans LA, Homsy JM, Morrow WJW, Gaston I, Sooy CD, Levy JA: Human monoclonal 
antibody directed against gag gene products of the human immunodeficiency virus. J 
Immunol 140: 941-943, 1988. ' 

125. Cheng-Mayer C, Homsy J, Evans LA, Levy JA: Identification of HIV subtypes with 
distinct patterns of sensitivity to serum neutralization. Proc Natl Acad Sci 85: 2815- 
2819, 1988. 

126. Dean NC, Golden JA, Evans L, Warnock ML, Addison TE, Hopewell PC, Levy JA: 
Human immunodeficiency virus recovery from bronchoalveolar lavage fluid in patients 
with AIDS. Chest 93: 1176-1179, 1988. 

127. Cheng-Mayer C, Seto D, Tateno M, Levy JA: Biologic features of HIV that correlate 
with virulence in the host. Science 240: 80-82, 1988. 

128. Evans LA, Moreau J, Odehouri K, Legg H, Barboza A, Cheng-Mayer C, Levy JA. 
Characterization of a noncytopathic HIV-2 strain with unusual effects on CD4 
expression. Science 240: 1522-1525, 1988. 

129. Homsy J, Tateno M, Levy JA. Antibody-dependent enhancement of HIV infection. 
Lancet 1: 1285-1286, 1988. 



Jay A. Levy, M.D. 131 

130. Jacobson MA, Crowe S, Levy JA, Aweeka F, Gambertoglio J, McManus N, Mills J. 
Effect of foscamet therapy on infection with HIV in patients with ADDS. J Infect Dis 
158: 862-865, 1988. 

131. Tateno M, Levy JA. MT-4 plaque formation can distinguish cytopathic subtypes of the 
human immunodeficiency virus (HIV). Virology 167: 299-301, 1988. 

132. Walker CM, Steimer KS, Rosenthal KL, Levy JA. Identification of HIV envelope type- 
specific T helper cells in an HIV-infected individual. J Clin Invest 82: 2172-2175, 1988. 

133. Castro BA, Weiss CD, Wiviott LD, Levy JA. Optimal conditions for recovery of the 
human immunodeficiency virus from peripheral blood mononuclear cells. J Clin 
Microbiol 26: 2371-2376, 1988. 

134. Cowan MJ, Walker C, Culver K, Weintrub PS, Wara DW, Levy JA. Maternally 
transmitted human immunodeficiency virus (HIV) infection in children. ADDS 2(6): 437- 
441, 1988. 

135. Winkelstein W, Wiley JA, Padian NS, Samuel M, Shiboski S, Ascher MS, Levy JA. The 
San Francisco Men's Health Study: Continued decline in HIV seroconversion rates 
among homosexual/bisexual men. Am J Public Health 78: 1472-1474, 1988. 

136. Evans LA, Moreau J, Odehouri K, Seto D, Thomson-Honnebier G, Legg H, Barboza A, 
Cheng-Mayer C, Levy JA. Simultaneous isolation of HIV- 1 and HFV-2 from an AIDS 
patient. Lancet 2: 1389-1391, 1988. 

137. Sematinger J, Hoffman A, Hardman D, Kane JP, Levy JA. Neutralization of mouse 
xenotropic virus by lipoproteins involve binding to the virion. J Gen Virol 69: 2657- 
2661, 1988. 

138. Michaelis B, Levy JA. HIV replication can be blocked by recombinant human interferon 
beta. AIDS 3: 27-3 1,1989. 

139. Krowka JF, Stites DP, Jain S, Steimer KS, George-Nascimento C, Gyenes A, Barr PJ, 
Hollander H, Moss AR, Homsy JM, Levy JA, Abrams DI. Lymphocyte proliferative 
responses to human immunodeficiency virus antigens in vitro. J Clin Invest 83: 1198- 
1203, 1989. 

140. Morrow WJW, Homsy J, Eichberg JW, Krowka J, Pan L-Z, Gaston I, Legg H, Lerche N, 
Thomas J, Levy JA. Long-term observation of baboons, rheusus monkeys, and 
chimpanzees inoculated with HIV and given periodic immunosuppressive treatment. 
AIDS Res Hum Retrovir 5: 233-245, 1989. 

141. Greenspan D, Greenspan JS, DeSouza YG, Levy JA, Unger AM. Oral hairy leukoplakia 
in an HIV -negative renal transplant recipient. Oral Pathol 18: 32-34, 1989. 



Jay A. Levy, M.D. 132 

142. Walker CM, Levy JA. A diffusible lymphokine produced by CD8 + T lymphocytes 
suppresses HFV replication. Immunology 66: 628-630, 1989. 

143. Walker CM, Moody DJ, Stites DP, Levy JA. CD8+ T lymphocyte control of HIV 
replication in cultured CD4+ cells varies among infected individuals. Cell Immunol 119: 
470-475, 1989. 

144. Tateno M, Gonzalez-Scarano F, Levy JA. The human immunodeficiency virus can infect 
CD4-negative human fibroblastoid cells. Proc Natl Acad Sci (USA) 86: 4287-4290, 
1989. 

145. Levy JA, Margaretten W, Nelson J. Detection of HIV in enterochromaffin cells in the 
rectal mucosa of an AIDS patient. Am J Gastroenterol 84: 787-789, 1989. 

146. Edwards JR, Ulrich PP, Weintraub PS, Cowan MJ, Levy JA, Wara DW, Vyas GN. 
Polymerase chain reaction compared to concurrent viral cultures of rapid identification of 
human immunodeficiency virus infection among high-risk infants and children. J Pediatr 
115: 200-203, 1989. 

147. Swanson CA, Levy JA, Morrow WJW. Effect of low dietary lipid on the development of 
Sjogren's syndrome and haematological abnormalities in (NZB x NZW)pi mice. Ann 
Rheum Dis 48: 765-770, 1989. 

148. Homsy J, Meyer M, Tateno M, Clarkson S, Levy JA. The F c and not the CD4 receptor 
mediates antibody enhancement of HIV infection in human cells. Science 244: 1357- 
1360, 1989. 

149. Castro BA, Eichberg JW, Lerche NW, Levy JA. HIV from experimentally infected 
chimpanzees: Isolation and characterization. J MedPrimatol 18: 337-342, 1989. 

150. Evans LA, Thomson-Honnebier G, Steimer K, Paoletti E, Perkus M, Hollander H, Levy 
JA. Antibody-dependent cellular cytotoxicity is directed against both the gp!20 and gp41 
envelope proteins of the human immunodeficiency virus. AIDS 3: 273-276, 1989. 

151. Edwards JR, Ulrich PP, Weintrub PS, Cowan MJ, Levy JA, Wara DW, Vyas GN. 
Polymerase chain reaction compared with concurrent viral cultures for rapid identification 
of human immunodeficiency virus infection among high-risk infants and children. J 
Pediatr 115: 200-203, 1989. 

152. Cheng-Mayer C, Weiss C, Seto D, Levy JA. Isolates of human immunodeficiency virus 
type 1 from the brain may constitute a special group of the AIDS virus. Proc Natl Acad 
Sci (USA) 80: 8575-8579, 1989. 

153. Cheng-Mayer C, lanello P, Shaw K, Luciw PA, Levy JA. Differential effects of nefon 
HIV replication: Implications for viral pathogenesis in the host. Science 246: 1629- 
1632, 1989. 



Jay A. Levy, M.D. 133 

154. Schoidt M, Greenspan D, Levy JA, Nelson JA, Chemoff D, Hollander H, Greenspan JS. 
Does HIV cause salivary gland disease? AIDS 3: 819-822, 1989. 

155. Yong W, Wyman S, Levy JA. Optimal conditions for synthesizing complementary DNA 
in the HIV endogenous reverse transcriptase reaction. AIDS 4: 199-206, 1990. 

156. Homsy J, Meyer M, Levy JA. Serum enhancement of human immunodeficiency virus 
(HIV) correlates with disease in HIV-infected individuals. J Virol 64: 1437-1440, 1990. 

157. Levy JA, Ferro F, Greenspan D, Lennette ET. Frequent isolation of HHV-6 from saliva 
and high seroprevalence to the virus in the population. Lancet 335: 1047-1050, 1990. 

158. Castro BA, Barnett SW, Evans LA, Moreau J, Odehouri K, Levy JA. Biologic 
heterogeneity of human immunodeficiency virus type 2 (HFV-2) strains. Virology 178: 
527-534, 1990. 

159. Tang S, Levy JA. Parameters involved in the cell fusion induced by HP/. AIDS 4: 409- 
414, 1990. 

160. York-Higgins D, Cheng-Mayer C, Bauer D, Levy JA, Dina D. Human 
immunodeficiency virus type 1. Cellular host range, replication, and cytopathicity are 
linked to the envelope region of the viral genome. J Virol 64: 4016-4020, 1990. 

161. Wiviott LD, Walker CM, Levy JA. CD8+ lymphocytes suppress HIV production by 
autologous CD4+ cells without eliminating the infected cells from culture. Cellular 
Immunol 128: 628-634, 1990. 

162. Levy JA, Ferro F, Lennette ET, Oshiro L, Poulin L. Characterization of a new strain of 
HHV-6 (HHV-6sp) recovered from the saliva of an HIV-infected individual. Virology 
178: 113-121,1990. 

163. Cheng-Mayer C, Quiroga M, Tung JW, Dina D, Levy JA. Viral determinants of HIV- 1 
T cell/macrophage tropism, cytopathicity, and CD4 antigen modulation. J Virol 64: 
4390-4398, 1990. 

164. Canivet M, Hoffman AD, Hardy D, Sernatinger J, Levy JA. Replication of HFV-1 in a 
wide variety of animal cells following phenotypic mixing with murine retroviruses. 
Virology 178: 543-551, 1990. 

165. Levy JA, Landay A, Lennette ET. HHV-6 inhibits HFV-1 replication in cell culture. J 
Clin Microbiol 28: 2362-2364, 1990. 

166. Liu Z-Q, Wood C, Levy JA, Cheng-Mayer C. The viral envelope gene is involved in 
macrophagic tropism of an HFV-1 strain isolated from the brain. J Virol 64: 6143-6153, 
1990. 



Jay A. Levy, M.D. 134 

167. Castro BA, Walker CM, Eichberg JW, Levy JA. Suppression of human 
immunodeficiency virus replication by CD8+ cells from infected and uninfected 
chimpanzees. Cell Immunol 132: 245-255, 1991. 

168. Martin NL, Levy JA, Legg HS, Weintrub PS, Cowan MJ, Wara DW. Detection of HIV- 1 
in infants by an anti-HIV IgA assay using recombinant proteins. J Peds 118: 354-358, 
1991. 

169. Shioda T, Levy JA, Cheng-Mayer C. Macrophage and T-cell-line tropisms of HIV-1 are 
determined by specific regions of the envelope gp!20 gene. Nature 349: 167-169, 1991. 

170. Mackewicz CE, Ortega HW, Levy JA. CD8+ cell anti-HIV activity correlates with the 
clinical state of the infected individual. J Clin Invest 87: 1462-1466, 1991. 

171. Cheng-Mayer C, Seto D, Levy JA. Altered host range of HIV-1 after passage through 
various human cell types. Virology 181: 288-294, 1991. 

172. Allen S, Vandeperre P, Serufilira A, Lapage P, Carael 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. 

173. Brown M, Reed S, Levy JA, Busch M, McKerrow JH. Detection of HIV-1 in Entamoeba 
histolytica without evidence of transmission to human cells. AIDS 5: 93-96, 1991. 

174. Tang S, Levy JA. Inactivation of HIV-1 by trypsin and its use in demonstrating specific 
virus infection of cells. J Virol Meth 33: 39-46, 1991. 

175. Bamett SW, Barboza A, Wilcox CM, Forsmark CE, Levy JA. Characterization of human 
immunodeficiency virus type 1 strains recovered from the bowel of infected individuals. 
Virology 182: 802-809, 1991. 

176. Weiss CD, Levy JA, White JM. Oligomeric organization of gp!20 on infectious human 
immunodeficiency virus type 1 particles. J Virol 64: 5674-5677, 1991. 

177. Rowley A, Castro B, Levy J, Sullivan J, Koup R, Fresco R, Shulman S. Failure to 
confirm the presence of a retrovirus in cultured lymphocytes from patients with Kawasaki 
syndrome. Ped Res 29: 417-419, 1991. 

178. Castro BA, Nepomuceno M, Lerche NW, Eichberg JW, Levy JA. Persistent infection of 
baboon and rhesus monkeys with different strains of HIV-2. Virology 184: 219-226, 
1991. 

179. Pan L-Z, Sheppard HW, Winkelstein W, Levy JA. Lack of HIV detection in persistently 
seronegative homosexual men with high or medium risk for infection. J Infect Dis, 
164:962-964,1991. 



Jay A. Levy, M.D. 135 

180. Poulin L, Evans LA, Tang S, Barboza A, Legg H, Littman D, Levy JA. Several CD4 
domains can play a role in HIV infection of cells. J Virol 65: 4893-4901, 1991. 

181. Weintrub PS, Ulrich PP, Edwards JR, Souther F, Levy JA, Cowan MJ, Vyas GN. Use of 
polymerase chain reaction for the early detection of HIV infection in the infants of HFV- 
seropositive women. AIDS 5: 881-884, 1991. 

182. Landay AL, Jessop C, Lennette ET, Levy JA. Chronic fatigue syndrome: A clincial 
condition associated with immune activation. Lancet, 338: 707-712, 1991. 

183. Walker CM, Thomson-Honnebier GA, Hsueh FC, Erickson AL, Pan L-Z, Levy JA. 
CD8+ T cells from HIV-1 infected individuals inhibit acute infection by human and 
primate immunodeficiency viruses. Cell Immunol 137:420-428, 1991. 

184. Walker CM, Erickson AL, Hsueh FC, Levy JA. Inhibition of HIV replication in acutely 
infected CD4+ cells by CD8+ cells involves a non-cytotoxic mechanism. J Virol, 65: 
5921-5927, 1991. 

185. Le Guem M, Levy JA. Human immunodeficiency virus (HIV) type 1 can superinfect 
HIV-2-infected cells: pseudotype virions produced with expanded cellular host range. 
Proc Natl Acad Sci (USA), 89:363-367, 1991. 

186. Cheng-Mayer C, Shioda T, Levy JA. Host range, replicative, and cytopathic properties of 
human immunodeficiency virus type 1 are determined by very few amino acid changes in 
tat and gp!20. J Virol, 65: 6931-6941, 1991. 

187. Koenig RE, Tolentino M, Taveras L, Ferro F, Zomoso C, Ferreiras J, Mates G, Oquist C, 
Capellan M, Amoros C, Gaton F, Lavandera M, de Castro L, Connelly M, Levy JA. 
Prevalence of HTLV infection in the Dominican Republic: association with neurological 
disease. AIDS Res and Human Retroviruses, 8:221-226, 1992. 

188. Tang SB, Poulin L, Levy JA. Lack of human immunodeficiency virus tupe 1 (HFV-1) 
replication and accumulation of viral DNA in HIV-1 -infected T cells blocked in cell 
replication. J Gen Virol 73:933-939, 1992. 

189. Shioda T, Levy JA, Cheng-Mayer C. Small amino acid changes in the V3 hypervariable 
region of gp!20 can affect the T-cell-line and macrophage tropism of human 
immunodeficiency virus type 1. Proc Natl Acad Sci 89:9434-9438, 1992. 

190. Poulin L, Levy JA. The HTV-1 we/" gene product is associated with phosphorylation of a 
46 kD cellular protein. AIDS, 6:787-791, 1992. 

191. Castro BA, Homsy J, Lennette E, Murthy KK, Eichberg JW, Levy JA. HTV-1 expression 
in chimpanzees can be activated by CD8+ cell depletion or CMV infection. Clin 
Immunol and Immunopathol, 65:227-233, 1992. 



Jay A. Levy, M.D. 136 

192. Barboza A, Castro BA, Whalen M, Moore CCD, Parkin JS, Miller WI, Gonzalez-Scarano 
F, Levy JA. Infection of cultured human adrenal cells by different strains of HIV. AIDS 
6:1437-1444, 1992. 

193. Barnett SW, Quiroga M, Werner A, Dina D, Levy JA. Distinguishing features of an 
infectious molecular clone of the highly divergent and noncytopathic human 
immunodeficiency virus type 2 UC1 strain. J Virol 67:1006-1014, 1993. 

194. Pan, LZ, Werner A, Levy JA. Detection of plasma viremia in HIV-infected individuals at 
all clinical stages. J Clin Micro 31:283-288, 1993. 

195. Mosier DE, Gulizia RJ, Maclssac PD, Torbett BE, Levy JA. Noncytopathic macrophage- 
tropic HIV isolates rapidly deplete CD4+ T cells in human-PBL-SCID mice. Science, 
260: 689-692, 1993. 

196. Werner A, Levy JA. Human immunodeficiency virus type 1 envelope gp!20 is cleaved 
after incubation with recombinant soluble CD4. J Virol 67:2566-2574, 1993. 

197. LeGuem M, Shioda T, Levy JA, Cheng-Mayer C. Single amino acid change in Tat 
determines the different rates of replication of two sequential HIV-1 isolates. Virology 
195:441-447, 1993. 

198. Landay AL, Mackewicz C, Levy JA. An activated CD8+ T cell phenotype correlates with 
anti-HFV activity and asymptomatic clinical status. Clin Immunol Immunopathol, 69:106- 
116, 1993. 

199. Kliks SC, Shioda T, Haigwood NL, Levy JA. V3 variability can influence the ability of 
an antibody to neutralize or enhance infection by diverse strains of human 
immunodeficiency virus type 1. ProcNatl Acad Sci 90:11518-11522, 1993. 

200. Mackewicz CE, Ortega H, Levy JA. The anti-HIV activity 'in CD8+ cell culture fluids is 
not associated with other known cytokines. Cell Immunol 153:329-343, 1994. 

201. Eaton AM, Ugen KE, Weiner DB, Wildes T, Levy JA. An anti-gp41 human monoclonal 
antibody which enhances HIV-1 infection in the absence of complement. AIDS Res and 
Hum Retrovir 10:13-18, 1994. 

202. Sawai ET, Baur A, Struble H, Peterlin BM, Levy JA, Cheng-Mayer C. Human 
immunodeficiency virus type 1 Nef associates with a cellular serine kinase in T 
lymphocytes. Proc Natl Acad Sci 91:1539-1543, 1994. 

203. Dumitrescu O, Kalish M, Kliks SC, Bandea CI, Levy JA. Characterization of HIV-1 
strains isolated from children in Romania: identification of a new envelope subtype. J 
Infect Dis 169:281-288, 1994. 

204. Koito A., Harrowe G, Levy JA, Cheng-Mayer C. Functional role of the V1/V2 region of 
human immunodeficiency virus type 1 envelope glycoprotein gp!20 in infection of 
primary macrophages and soluble CD4 neutralization. J Virol 68:2253-2259, 1994. 



Jay A. Levy, M.D. 137 

204. Ichimura H, Kliks SC, Visrutaratna S, Ou CY, Kalish ML, Levy JA. Biologic, serologic, 
and genetic characterization of HIV- 1 Subgroup E isolates from Northern Thailand. AIDS 
Res Hum Retrovir 10:263-269, 1994. 

205. Hemdier BG, Werner A, Amstein P, Abbey NW, Demartis F, Cohen RL, Shuman MA, 
Levy JA. Characterization of a human Kaposi's sarcoma cell line that induces angiogenic 
tumors in animals. AIDS 8:575-581, 1994. 

206. Pan LZ, Levy JA. Inhibition of HIV replication by trichosanthin in peripheral blood 
mononuclear cells. Curr Ther Res 55:718-727, 1994. 

207. Kliks SC, Wara DW, Landers DV, Levy JA. Features of the human immunodeficiency 
virus (HF/-1) that could influence maternal-child transmission. J Am Med Assoc 
272:467-474, 1994. 

208. Mackewicz CE, Landay A, Hollander H, Levy JA. Effect of zidovudine therapy on CD8+ 
T cell anti-HIV activity. Clin Immunol Immunopathol, 73:80-87, 1994. 

209. Barnett SW, Murthy KM, Herndier BG, Levy JA. An AJJDS-like condition is induced in 
baboons by HIV-2. Science 266:642-646, 1994. 

210. Poulin L, Fauchon M, Darveau A, Levy JA. Inhibition of protein synthesis by HF/-1 Nef 
gene product. J Gen Virol, 75:2977-2984, 1994. 

211. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A, and the 
International Chronic Fatigue Syndrome Study Group (Levy JA). The chronic fatigue 
syndrome: a comprehensive approach to its definition and study. Ann Int Med 121:953- 
959, 1994. 

212. Mackewicz CE, Yang LC, Lifson JD, Levy JA. Noncytolytic CD8+ cell anti-HIV 
responses and neutralizing antibody titers in primary HIV infection. Lancet 344:1671- 
1673, 1994. 

213. Hsueh FW, Walker CM, Blackbourn DJ, Levy JA. Suppression of HIV replication by 
CD8+ cell clones derived from HIV-infected and uninfected individuals. Cell Immunol 
159:271-279, 1994. 

214. Mackewicz CE, Blackbourn DJ, Levy JA. CD8+ T cells suppress human 
immunodeficiency virus replication by inhibiting viral transcription. Proc Natl Acad Sci 
(US A), 92:2308-23 12, 1995. 

215. Ambroziak JA, Blackbourn DJ, Hemdier B, Glogau RG, Gullett JH, McDonald AR, 
Lennette ET, Levy JA. Herpes-like sequences in HIV-infected and uninfected Kaposi's 
sarcoma patients. Science 268:582-583, 1995. 



Jay A. Levy, M.D. 138 

216. Luciw AP, Pratt-Lowe E, Shaw KES, Levy JA, Cheng-Mayer C. Acute infection of 
rhesus macaques with T-cell line-tropic and macrophage-tropic clones of simian/human 
immunodeficiency viruses (SHIV). Proc Natl Acad Sci 92:7490-7494, 1995. 

217. Sawai ET, Baur AS, Peterlin BM, Levy JA, Cheng-Mayer C. A conserved domain and 
membrane targeting of Nef from HIV and SFV are required for association with a cellular 
serine kinase activity. J Biol Chem 270:15307-15314, 1995. 

218. Allan JS, Ray P, Brossard S, Whitehead E, Hubbard G, Butler T, Brasky K, Luciw P, 
Cheng-Mayer C, Levy JA, Steimer K, Li J, Sodroski J, Garcia-Moll M. Infection of 
baboons with simian/human immunodeficiency viruses. J AIDS and Hum Retrovir 9:429- 
441, 1995. 

219. Tang S, Patterson B, Levy JA. Highly purified quiescent human peripheral blood CD4+ T 
cells are infectible by human immunodeficiency virus but do not release virus after 
activation. J Virol 69:5659-5665, 1995. 

220. Ichimura H, Levy JA. Polymerase substrate depletion: a novel strategy for inhibiting the 
replication of the human immunodeficiency virus. Virology 211:554-560, 1995. 

221. El-Amad Z, Murthy KK, Higgins K, Cobb EK, Haigwood NL, Levy JA, Steimer KS. 
Resistance of chimpanzees immunized with recombinant gp!20sF2 to challenge by HIV- 
1SF2- AIDS 9:1313-1322, 1995. 

222. Barker E, Mackewicz CE, Levy JA. Effects of TH! and Tjj2 cytokines on CD8+ cell anti- 
HP/ response: implications for long-term survival. Proc Natl Acad Sci (USA), 92:1 1 135- 
11139, 1995. 

223. Levy JA, Ramachandran B, Barker E, Guthrie J, Elbeik T. Plasma viral load, CD4+ cell 
counts, and HIV- 1 production by cells. Science 271: 670-671, 1996. 

224. Miller G, Rigsby MO, Heston L, Grogan E, Sun R, Metroka C, Levy JA, Gao SJ, Chang 
Y, Moore P. Antibodies to butyrate-inducible antigens of Kaposi's sarcoma-associated 
herpesvirus in patients with HF/-1 infection. New Engl J Med 334:1292-1297, 1996. 

225. Gulizia RJ, Levy JA, Mosier DE. The envelope gp!20 gene of human immunodeficiency 
virus type 1 determines the rate of CD4-positive T-cell depletion in SCID mice engrafted 
with human peripheral blood leukocytes. J Virol 70:4184-4187, 1996. 

226. Barnett SW, Legg HS, Sun Y, Klinger J, Blackbourn DJ, Locher CP, Levy JA. Molecular 
cloning of the human immunodeficiency virus subtype 2 strain HrV-2uc2- Virology 
222:257-4187, 1996. 

227. Voss TG, Fermin CD, Levy JA, Vigh S, Choi B, Garry RF. Alteration of intracellular 
potassium and sodium concentrations correlates with induction of cytopathic effects by 
human immunodeficiency virus. J Virol 70:5447-5454, 1996. 



Jay A. Levy,M.D. 139 

228. Murthy KK, Cobb EK, El-Amad Z, Ortega H, Hsueh FC, Satterfield W, Lee DR, Kalish 
ML, Haigwood NL, Kennedy RC, Steimer KS, Schultz A, Levy JA. Titration of a vaccine 
stock preparation of HIV-lsF2 in cultured lymphocytes and in chimpanzees. AIDS Res 
Human Retroviruses 12:1341-1348, 1996. 

229. Lennette ET, Blackboum DJ, Levy JA. Antibodies to human herpesvirus type 8 in the 
general population and in Kaposi's sarcoma patients. Lancet 348: 858-861, 1996. 

230. Blackboum DJ, Mackewicz CE, Barker E, Hunt TK, Herndier B, Haase AT, Levy JA. 
Suppression of HIV replication by lymphoid tissue CD8+ cells correlates with the clinical 
state of HlV-infected individuals. Proc Natl Acad Sci (USA) 93: 13125-13130, 1996. 

231. Hartley CA, Gilbert MJ, Brigido L, Elbeik T, Levy JA, Crowe SM, Mills J. Human 
immunodeficiency virus grown in CD4-expressing cells is associated with CD4. J Gen 
Virol 77: 2015-2023, 1996. 

232. Mackewicz CE, Levy JA, Cruikshank WW, Komfeld H, Center DM. Role of IL-16 in 
HIV replication. Nature 383:488-489, 1996. 

233. Mackewicz CE, Barker E, Levy JA. Role of P-chemokines in suppressing HIV 
replication. Science 274: 1393-1394, 1996. 

234. Barker E, Bossart KN, Locher CP, Patterson BK, Levy JA. CD8+ cells from 
asymptomatic HIV-infected individuals suppress superinfection of their peripheral blood 
mononuclear cells. J Gen Virol 77:2953-2962, 1996. 

235. Mackewicz CE, Orque R, Jung J, Levy JA. Derivation of Herpesvirus saimiri- 
transformed CD8+ T cell lines with noncytotoxic anti-HIV activity. Clin Immuno 
Immunopathol 82:274-281, 1997. 

236. Blackboum DJ, Ambroziak J, Lennette E, Adams M, Ramachahdran B, Levy JA. 
Infectious human herpesvirus 8 in a healthy North American blood donor. Lancet 
349:609-611,1997. 

237. Blackboum DJ, Locher CP, Ramachandran B, Bamett SW, Murthy KK, Carey KD, 
Brasky KM, Levy JA. Control of HIV replication in cultured baboon CD4+ cells by 
baboon CD8+ cells. AIDS 11:737-746, 1997. 

238. Gulizia RJ, Collman RG, Levy JA, Trono D, Mosier DE. Deletion of nef slows but does 
not prevent CD4-positive T-cell depletion in human immunodeficiency virus type 1- 
infected human-PBL-SCID mice. J Virol 71:4161-4164, 1997. 

239. Levy JA, Mackewicz C, Barker E. The CD8+ cell antiviral factor. J AIDS Res Human 
Retroviruses 15: S23-S26, 1997. 

240. Mackewicz CE, Barker E, Greco G, Reyes-Teran G, Levy JA. Do P-chemokines have 
clinical relevance in HIV infection? J Clin Invest 100:921-930, 1997. 



Jay A. Levy, M.D. 140 

241. Locher CP, DJ Blackbourn, KK Murthy, SW Bamett, KM Brasky, KD Carey, JA Levy. 
Super-infection with human immunodeficiency virus type 2 can reactivate virus 
production in baboons but is contained by a CDS T cell antiviral response. J Infect Dis 
176:948-959, 1997. 

242. Barker E, Bossart KN, Fujimura SH, Levy JA. CD28-costimulation increases CD8+ cell 
suppression of HIV replication. J Immunol 159:5123-5131, 1997. 

243. Blackbourn DJ, Lennette ET, Ambroziak J, Mourich DV, Levy JA. Human herpesvirus 8 
detection in nasal secretions and saliva. J Infect Dis 177: 213-216, 1998. 

244. Levy JA, Hsueh F, Blackbourn DJ, Wara D, Weintrub PS. CD8+ cell noncytotoxic 
antiviral activity in HIV-infected and uninfected children. J Infect Dis 177: 470-472, 
1998. 

245. Locher CP, Blackbourn DJ, Herndier BG, Reyes-Teran G, Bamett SW, Murthy KK, Levy 
JA. Transient virus infection and pathogenesis of a new HIV type 2 isolate, UC12, in 
baboons. AIDS Res Hum Retrovir 14:79-82, 1998. 

246. Barker E, Bossart KN, Levy JA. Primary CD8+ cells from HIV-infected individuals can 
suppress productive infection of macrophages independent of p-chemokines. Proc Natl 
AcadSci 95: 1725-1 729, 1998. 

247. Locher CP, Bamett SW, Hemdier BG, Blackbourn DJ, Reyes-Teran G, Murthy KK, 
Brasky KM, Hubbard GB, Reinhart TA, Haase AT, Levy JA. Human immunodeficiency 
virus-2 infection in baboons is an animal model for human immunodeficiency virus 
pathogenesis in humans. Arch Path Lab Med 122:523-533, 1998. 

248. Rezza B, Lennette E, Giuliani M, Pezzotti P, Caprilli F, Monini P, Butto S, Lodi G, Di 
Carlo A, Levy JA, Ensoli B. Prevalence and determinants of anti-lytic and anti-latent 
antibodies to human herpesvirus-8 among Italian individuals at risk of sexually and 
parenterally transmitted infections. Int J Cancer 77:361-365. 1998. 

249. Barker E, Mackewicz C, Reyes-Teran G, Sato A, Stranford S, Fujimura SH, 
Christopherson C, Chang, SY, Levy, JA. Virological and immunological features of long- 
term human immunodeficiency virus-infected individuals who have remained 
asymptomatic compared with those who have progressed to Acquired Immunodeficiency 
Syndrome. Blood 92: 3105-3114, 1998. 

250. Renne R, Blackbourn D., Whitby D, Levy JA, Ganem D. Limited transmission of 
Kaposi's sarcoma-associated herpesvirus in cultured cells. J Vir 72:5182-5188, 1998. 

25 1 . Greco G, Barker E, Levy, JA. Differences in HIV replication in CD4+ cell lymphocytes 
are not related to P chemokine production. ADDS Res Hum Retrovir 14:1407-1411, 1998. 

252. Barker E, Bossart KN, Levy JA. Differential effects of CD28 costimulation on HIV 
production by CD4+ cells. J Immunol 161: 6223-6227, 1998. 



Jay A. Levy, M.D. 

253. Mackewicz CE, Garovoy MR, Levy JA. HLA compatibility requirements for CD8+ cell - 
T-cell-mediated suppression of human immunodeficiency virus replication. J Virol 72: 
10165-10170, 1998. 

254. Blackbourn DJ, Osmond D, Levy JA, Lennette ET. Increased human herpesvirus-8 
seroprevalence in young homosexual men who have multiple sexual contacts with 
different partners. J Infect Dis 179:237-9, 1999. 

255. Greco G, Fujimura SH, Mourich DV, Levy, JA. Differential effects of HIV isolates on (3 
chemokine and interferon-y production and on cell proliferation. J Virol 73:1528-1534, 
1999. 

256. Stranford SA, Skurnick J, Louria D, Osmond D, Chang S, Sninsky J, Ferrari G, Weinhold 
K, Lindquist C, Levy JA. Lack of infection in HFV-exposed individuals is associated with 
a strong CD8+ cell noncytotoxic anti-HIV response. Proc Natl Acad Sci (USA) 96:1030- 
1035, 1999. 

257. Locher CP, Blackbourn DF, Levy JA. Suppression of human immunodeficiency virus 
type 1 replication by a soluble factor produced by CD8+ lymphocytes from HIV-2- 
infected baboons. Immunology Letters, 66:151-157, 1999. 

258. Greco G, Mackewicz C, Levy JA. Sensitivity of human immunodeficiency virus infection 
to various a, p and y chemokines. J Gen Virol 80:2369-2373, 1999. 

259. Barker E, Brossard K, Fujimura SH, Levy, JA. The role of CD80 and CD86 in enhancing 
CD8+ cell suppression of HIV replication. Cell Immuno. 196:95-103, 1999. 

260. Mourich DV, Lee S, Reyes-Teran G, Mackewicz CE, Levy JA. Lack of differences in nef 
alleles among HIV-infected asymptomatic long-term survivors and those who progressed 
to disease. AIDS Res Hum Retrovir. 15:1573-1575, 1999. 

261. Locher CP, Grant RM, Collisson EA, Reyes-Teran G, Elbeik T, Kahn JO, .Levy JA. 
Antibody and cellular immune responses in breakthrough infection subjects after HTV-1 
glycoprotein 120 vaccination. AIDS Res Hum Retrovir. 15:1685-1689, 1999. 

262. Mackewicz CE, Lieberman J, Froelich D, Levy JA. HIV virions and HIV infection in 
Vitro are unaffected by human granzymes A and B. AIDS Res Hum Retrovir. 16:367- 
372, 2000. 

263. Mackewicz CE, Patterson BK, Lee SA, Levy, JA. CD8+ cell non-cytotoxic anti-human 
immunodeficiency virus response inhibits expression of viral RNA but not reverse 
transcription or provirus integration. J Gen Virol 81:1261-1264, 2000. 

264. Blackbourn DJ, Lennette E, Klencke B, Moses A, Chandran B, Weinstein M, Glogau RG, 
Witte MH, Way DL, Kutzkey T, Herndier B, Levy, JA. The restricted cellular host range 
ofHHV-8. AIDS 14:1123-1133, 2000. 

265. Kliks S, Contag CH, Corliss H, Learn G, Rodrigo A, Wara D, Mullins JI, Levy JA. 
Genetic analysis of viral variants selected in maternal transmission of human 
immunodeficiency virus to newboms. AIDS Res Hum Retrovir 16:1223-1233, 2000. 



Jay A. Levy, M.D. 142 

266. Schito AM, Vittinghoff E, Hecht FM, Elkins MK, Kahn JO, Levy JA, Oksenberg JR. 
Longitudinal analysis of T cell receptor gene usage by CD8+ T cells in primary HIV 
infection in patients receiving highly active antiretroviral therapy. Blood 97:214-220, 
2001. 

267. Stranford SA, Ong JC, Martinez-Marino B, Busch M, Hecht FM, Kahn J, Levy JA. 
Reduction in CD8+ cell noncytotoxic anti-HIV activity in subjects receiving HAART 
therapy during primary infection. Proc Natl Acad Sci (USA). 98:597-602, 2001. 

268. Altfeld M, Rosenberg ES, Shankarappa R, Mukherjee JS, Hecht F, Eldridge RL, Addo 
MM, Poon SH, Phillips MN, Robbins GK, Kahn JO, Brander, C, Goulder PJ, Levy JA, 
Mullins JI, Walker BD. Cellular immune responses and viral diversity in individuals 
treated during acute and early fflV-1 infection. J Exp Med. 193:169-180, 2001. 

269. Ghanekar SA, Stranford SA, Ong JC, Walker JM, Maino VC, Levy JA. Decrease in HIV- 
1 specific CD4+ T cell proliferation in long term HIV- 1 -infected individuals undergoing 
antiretroviral therapy. AIDS, in press, 2001. 

270. Soumelis VS, Scott I, Gheyas F, Bouhour D, Cozon G, Cotte L, Huang L, Levy J, Liu J-J. 
Decrease in natural interferon-alpha producing cells is associated with disease 
progression in HIV-infected subjects. Blood. In print. 



Jay A. Levy, M.D. 143 

Reviews, Book Chapters and Letters 

1. Levy JA, Rowe WP. Problems faced and techniques developed in RNA tumor virus 
research. In: Atypical Virus Infections: Possible Relevance to Animal Models and 
Rheumatic Disease. (Christian CL, Phillips PE, Williams RC, Jr., eds). Arthritis 
Foundation Conference Series No. 15, The Arthritis Foundation, New York, pp 119-125, 
1971. 

2. Levy J A. Cats and cancer. J Am Med Assoc 229: 1654-1655, 1974. 

3. Levy JA. Type C virus inhibitor associated with cells cultivated from New Zealand Black 
mice. Persp Virol 9: 207-214, 1975. 

4. Levy JA. Xenotropic C-type viruses and autoimmune disease. J Rheumatol 2: 135-148, 
1975. 

5. Levy JA. Endogenous C-type viruses: Double agents in natural life processes. 
Biomedicine 24: 84-93, 1976. 

6. Levy JA. Type C RNA viruses and autoimmune disease. In: Autoimmunity: Genetic, 
Immunologic, Virologic and Clinical Aspects. (Talal N, ed), Academic Press, New York, 
pp 403-453, 1977. 

7. Levy JA. Endogenous C-type viruses in normal development, autoimmunity and cancer. 
Microbiology 46: 559-563, 1977. 

8. Levy JA. Endogenous C-type viruses in normal and "abnormal" cell development. 
Cancer Res 37: 2957-2968, 1977. 

9. Levy JA. Xenotropic type C viruses. In: Current Topics in Microbiology and' 
Immunology. Springer- Verlag, Heidelberg, 79: 111-213,1978. 

10. Levy JA. Phenotypic mixing among type C viruses: Mechanism for virus spread, 
somatic function, and oncogenesis. In: Viruses and Environment (Kurstak E, 
Maramorosch K, eds), Academic Press, pp 429-449, 1978. 

1 1 . Levy JA. Viral, anti-viral, cellular and nutritional factors associated with autoimmunity 
in mice. In: Immunoregulation and Autoimmunity (Krakauer R, Cathcartt MK, eds), 
Elsevier/North Holland, New York, pp 1 17-128, 1980. 

12. Levy JA. Are type-C viruses transforming agents? Biomedicine 34(1): 4-8, 1981. 

13. Levy JA, Volberding P, Oppermann H, Leong J. Retroviruses and differentiation. In: 
Expression of Differentiated Functions in Cancer Cells (Revoltella RF et al., eds), Raven 
Press, New York, pp 451-469, 1982. 



Jay A. Levy, M.D. 144 

14. Levy JA. Nutrition and the immune system. In: Basic and Clinical Immunology, 4th 
Edition (Fudenberg HH, Stites DP, Stobo J, Wells JV, eds), Lange Medical Publications, 
Los Altos, CA, pp 293-311, 1982. 

15. Levy JA, Ziegler JL. Acquired immune deficiency syndrome (AIDS) is an opportunistic 
infection and Kaposi's sarcoma results from secondary immune stimulation. Lancet ii: 
78-81, 1983. 

16. Levy JA. Mouse plasmacytoma cells produce infectious type C viruses. Lancet ii: 522, 
1983. 

17. Levy JA, Morrow WJW. Dietary regulation of the autoimmune process in murine lupus. 
Immunol Today 4: 249-250, 1983. 

18. Morrow WJW, Levy JA. Dietary fat and autoimmune disease. Arthritis Rheum 26: 
1532, 1983. 

19. Conte JE, Jr, Ammann AJ, Dritz SK, Volberding P, Follansbee SM, Perkins HA, Levy 
JA. The acquired immune deficiency syndrome (AIDS) - A multidisciplinary enigma - 
Medical Staff Conference, University of California, San Francisco. West J Med 140: 66- 
81, 1984. 

20. Levy JA. Peer review: The continual need for reassessment. Cancer Invest 2: 311-320, 
1984. 

21. Levy JA. Nutrition and the immune system. In: Basic and Clinical Immunology, 5th 
Edition (Stites DP, Stobo J, Fudenberg HH, Wells JV, eds), Lange Medical Publications, 
Los Altos, CA, pp 293-301, 1984. 

22. Levy JA. Xenotropic C-type viruses and autoimmune disease. J Rheumatol 11: 574-575, 
1984. 

23. Ziegler JL, Levy JA. The acquired immunodeficiency syndrome (AIDS) and cancer. 
Adv Viral Oncol 5: 239-255, 1985. 

24. Levy JA, Anderson RE. Prevalence of antibodies to AJDS-associated retrovirus in single 
men in San Francisco. Lancet i: 217, 1985. 

25. Koerper MA, Kaminsky LS, Levy JA. Differential prevalence of antibodies to AIDS- 
associated retrovirus in hemophiliacs treated with factor VIIJ concentrates versus 
cyroprecipitates: Recovery of infectious virus. Lancet i: 275, 1985. 

26. Morrow WJW, Levy JA. The viral etiology of ADDS. Clin Immunol Newsletter 6: 113- 
128, 1985. 

27. Homsy J, Morrow WJW, Levy JA. Life span of MRL/lpr/lpr mice. Immunol Today 6: 
120, 1985. 



Jay A. Levy, M.D. 145 

28. Kiprov DD, Anderson RE, Morand PR, Simpson DM, Chermann JC, Levy JA, Moss AR. 
Antilymphocyte antibodies and seropositivity for retroviruses in groups at high risk for 
AIDS. N Engl J Med 312: 1517, 1985. 

29. Levy JA. We Must Wage an All-Out Attack on AIDS. The Los Angeles Times, 
Commentary, September 23, 1985, p 5. 

30. Kaplan J, Sarnaik S, Levy JA. Transfusion-induced immunologic abnormalities not 
related to AIDS virus. N Engl J Med 313: 1227, 1985. 

31. Levy JA. Changing dogmas in retrovirology. In: Retroviruses and Human Pathology, 
(Gallo RC, Stehelin D, Vamier OE, eds), The Humana Press, pp 35-65, 1985. 

32. Staben C, Shimabukuro J, Stephans JC, Barr PJ, Sabin B, Parkes D, Luciw PA, Steimer 
KS, Levy JA, Dina D. The nature and significance of sequence variation among 
independent AIDS retro virus isolates. In: Vaccine '86, Cold Spring Harbor Laboratory, 
pp 345-350, 1986. 

33. Lyman D, Winkelstein W, Ascher M, Levy JA. The minimal risk of transmission of 
AIDS-associated retrovirus infection by oral-genital contact. J Am Med Assoc 255: 
1703, 1986. 

34. Conant M, Hardy D, Sernatinger J, Spicer D, Levy JA. Condoms prevent transmission of 
the AIDS-associated retrovirus. J Am Med Assoc 255: 1706, 1986. 

35. Winkelstein W, Wiley JA, Padian N, Levy JA. Potential for transmission of AIDS- 
associated retrovirus from bisexual men in San Francisco to their female sexual contacts. 
J Am Med Assoc 255: 901, 1986. 

36. Koenig RE, Gautier T, Levy JA. Unusual intrafamilial transmission of human 
immunodeficiency virus. Lancet ii: 627, 1986. 

37. Homsy J, Morrow WJW, Levy JA. Nutrition and autoimmunity: A review. Clin Exp 
Immunol 65: 473-488, 1986. 

38. LevyJA. The multi faceted retrovirus. Cancer Res 46: 5457-5468, 1986. 

39. Coffin J, Haase A, Levy JA, Montagnier L, Oroszlan S, Teich N, Temin H, Toyoshima K, 
Varmus H, Vogt P, Weiss R. Human immunodeficiency viruses [Letter]. Science 232: 
697, 1986. 

40. Stephans JC, Lee DJ, Miller EJ, Van Nest GA, Levy JA, George-Nascimento C, Parkes 
D, Barr PJ, Staben C, Dina D, Luciw P, Steimer KS. Specificities of monoclonal 
antibodies generated against genetically engineered envelope gene product of the AIDS 
retrovirus. In: Viruses and Human Cancer (Gallo RC, et al, eds). UCLA Symposia on 
Molecular and Cellular Biology, Vol. 43, Alan R. Liss, Inc., New York, 1987, pp 29-41. 



Jay A. Levy, M.D. 146 

41. Levy J A. Human retrovirus infection. In: Internal Medicine, Second Edition (Stein JH, 
ed), Little, Brown and Company, Boston, pp 1614-1617, 1987. 

42. Levy JA, Evans L, Cheng-Mayer C, Pan L-Z, Lane A, Staben C, Dina D, Wiley C, Nelson 
J. Biologic and molecular properties of the ADDS-associated retrovirus that affect 
antiviral therapy. Ann Inst Pasteur 138: 101-1 11, 1987. 

43. Levy JA, Evans L, Pan L-Z, Tateno M, Reed MF, Walker C, Homsy J, Cheng-Mayer C. 
Biologic heterogeneity of HIV and host immune response during HIV infection. In: 
Vaccines 1987, (Ginsberg H, Lemer R, Chanock R, eds), pp. 168-173, 1987. 

44. Levy JA. Indirect immunofluorescence assay for detection of anti-HFV antibodies. J Am 
MedAssoc257: 1176,1987. 

45. Michaelis B, Levy JA. Recovery of human immunodeficiency virus from serum. J Am 
Med Assoc 257: 1327, 1987. 

46. Koenig RE, Brache LG, Levy JA. HIV in the Dominican Republic. J Am Med Assoc 
258: 47, 1987. 

47. Winkelstein W Jr, Samuel M, Padian NS, Wiley JA, Lang W, Levy JA: On HIV 
transmission in homosexual/bisexual men: Response. Am J Public Health 77: 1552- 
1553, 1987. 

48. Levy JA. The human immunodeficiency virus and its role in ADDS. In: Viral Hepatitis 
and Acquired Immunodeficiency Syndrome (Villarejos, VM, ed). Louisiana State 
University- ICMRT, 1987, pp 17-24. 

49. Levy JA: The biology of the human immunodeficiency virus and its role in neurological 
disease. In: AIDS and the Nervous System (Rosenblum ML, et al, eds). pp 327-345, 
1988. 

50. Levy JA, Evans LA, Tateno M, Walker C, Homsy J, Cheng-Mayer C: Biologic, serologic 
and molecular differences among human immunodeficiency viruses (HIV). In: Human 
Retroviruses, Cancer and AIDS: Approaches to Prevention and Therapy (Bolognesi D, 
etal.,ed), pp. 91-100, 1988. 

5 1 . Cheng-Mayer C, Levy JA: Distinct biologic and serological properties of HIV from the 
brain. AnnNeurol, 23: s58-s61, 1988. 

52. Levy JA: The transmission of AIDS: The case of the infected cell. J Am Med Assoc 
259: 3037-3038, 1988. 

53. Levy JA: The human immunodeficiency virus and its pathogenesis. In: Medical 
Management of AIDS (Sande M, Volberding P, eds). Infect Dis Clin North Am 2: 285- 
297, 1988. 



Jay A. Levy, M.D. 147 

54. Levy JA. The human immunodeficiency virus and its pathogenic properties. In: 
Prevention of AIDS in Children, Adolescents, and Heterosexual Adults: An 
Interdisciplinary Approach (Schinazi RF, Nahmias AJ, eds). New York: Elsevier 
Science Publishing Company, Inc., 1988, pp 117-125. 

55. Homsy J, Cheng-Mayer C, Evans LA, Tateno M, Levy JA: Identification of human 
immunodeficiency virus antigenic subtypes with relevance to AIDS vaccines: A 
prototype study. In: Vaccines 1988 (Ginsberg H, Brown F, Lerner R, Chanock RM, eds). 
New York: Cold Spring Harbor Laboratory, pp 365-371, 1988. 

56. Cheng-Mayer C, Tateno M, Seto D, Levy JA: Distinguishing features of neurotropic 
human immunodeficiency viruses. In: Vaccines 1988 (Ginsberg H, Brown F, Lemer RA, 
Chanock RM, eds). New York: Cold Spring Harbor Laboratory, pp 259-263, 1988. 

57. Levy JA. The mysteries of HIV: Challenges for therapy and prevention. Nature 333: 
519-522, 1988. 

58. Levy JA: Retroviridae: Human immunodeficiency viruses. In: Laboratory Diagnosis of 
Infectious Diseases. Vol. II. Viral, Rickettsial and Chlamydial Diseases (Lennette EH, 
Halonen P, Murphy FA, eds). New York: Springer-Verlag, 1988, p 677-691. 

59. Levy JA. Human immunodeficiency virus: Pathogenesis of infection and the possibility 
of its control. Immunologiya (U.S.S.R.) 4: 14-20, 1988. 

60. Levy JA. Can an AIDS vaccine be developed? 1 Transfusion Med Rev 2: 264-271, 1988. 

61. Levy JA, Greenspan D. HIV in saliva. Lancet 2: 1248, 1988. 

62. Castro BA, Cheng-Mayer C, Evans LA, Levy JA. HIV heterogeneity and viral 
pathogenesis. AIDS 88 2: s!7-s27, 1988. 

63. Weiss RA, Levy JA. Virology overview. AIDS 88 2: 1-2, 1988. 

64. Levy JA. HIV and the transmission of AIDS (Response). J Am Med Assoc 260: 3587, 
1988. 

65. LevyJA: The human immunodeficiency viruses (HIV): Detection and pathogenesis. In: 
AIDS: Pathogenesis and Treatment. (Levy JA, ed). New York: Marcel Dekker, Inc., 
pp. 159-229, 1989. 

66. Hoxie JA, Levy JA. Mechanism of CD4+ cell killing by the human immunodeficiency 
virus. In: Concepts in Viral Pathogenesis III (Oldstone MBA, ed). New York: 
Springer-Verlag, 1989, pp. 215-224. 

67. Levy JA. Human immunodeficiency viruses and the pathogenesis of AIDS. J Am Med 
Assoc 261: 2997-3006, 1989. 



Jay A. Levy, M.D. 148 

68. Pan L-Z, Royce R, Winkelstein W, Levy JA. Human immunodeficiency virus type 1: 
Infection in homosexual men who remain seronegative for prolonged periods. N Engl J 
Med321: 1680,1989. 

69. Levy JA. Pathogenesis of human immunodeficiency virus infection. Ann NY Acad Sci 
567: 58-68, 1989. 

70. Eichberg J, Levy JA, Alter HJ. Primates as models to understand cofactors in AIDS. In: 
Cofactors in Human Immunodeficiency Virus-1 Infection and AIDS (Watson R, ed). 
CRC Press, 1989, p 223-229. 

71. Levy JA, Cheng-Mayer C, Evans LA, Walker CM, Homsy J, Castro BA. HIV and the 
pathogenesis of AIDS. In: News and Views on Research and Control: AIDS 89-90 
(de-The G, ed). Paris: McGraw-Hill, 1989. 

72. Evans LA, Levy JA. Characteristics of HIV infection and pathogenesis. Biochim 
Biophys Acta 989: 237-254, 1989. 

73. Levy JA. Human retro virus infections. In: Internal Medicine, Third Edition (Stein JH, 
ed). Boston: Little, Brown and Company, 1990, pp. 1411-1414. 

74. Levy JA, Cheng-Mayer C, Tateno M, Evans L, Homsy J. The biologic heterogeneity of 
HIV and the pathogenesis of AIDS. In: UCLA Symposia. Human Retroviruses. 
(Groopman JE, Chen ISY, Essex M, Weiss RA, eds.) New York: Wiley-Liss, 1990, 
pp. 191-205. 

75. Wiviott LD, Levy JA. HIV and features of its infection. In: HIV Infection and Disease. 
Monographs for Physicians and Other Health Care Workers. (Rapoza N, ed). Chicago: 
American Medical Association, 1989, p 57-70. 

76. Cheng-Mayer C, Levy JA. Human immunodeficiency virus infection of the CNS: 
Characterization of "neurotropic" strains. Curr Top Microbiol Immunol 160: 145-156, 
1990. 

77. Levy JA. Changing concepts in HIV infection: Challenges for the 1990's. AIDS 4: 1051- 
1058, 1990. 

78. Levy JA. The pathogenesis of HIV infection. Hosp Pract. 41-48, November 15, 1990. 

79. Levy JA. AIDS Care & International Journal of STD and AIDS. Journal Reviews. 
Lancet 336: 991, 1990. 

80. Levy JA. Features of HIV and the host response that influence progression to disease. In: 
Medical Management of AIDS , Second Edition (Sande M, Volberding P, eds). Infect Dis 
Clin North Am, pp 23-37, 1990. 



Jay A. Levy, M.D. 149 

81. Levy JA. Viral and cellular factors influencing HIV tropism. In: Mechanisms and 
Specificity of HIV Entry into Host Cells , Volume 300 (Duzgiines N, ed). Plenum Press, 
New York. pp. 1-17, 1991. 

82. Bamett SW, Levy JA. Human immunodeficiency viruses. In: Manual of Clinical 
Microbiology, 5th Edition. (Balows A, ed). ASM, Washington, DC, 1991, pp 1011- 
1023. 

83. Weiss CD, Levy JA. The acquired immunodeficiency syndrome (Virology). In: 
Encyclopedia of Human Biology (Dulbecco R et al., eds). San Diego: Academic Press, 
Inc., 1991, vol. l,pp 11-23. 

84. Levy JA. HTV research and ne/alleles. (Letter) Science 253:366, 1991 . 

85. Levy JA, Mackewicz C, Walker CM. Primary fflV-1 Infection. (Letter) N Engl J Med 
325:734, 1991. 

86. Levy JA. Conversations with Samuel Beckett. The American Scholar, 61:124-132, 1991. 

87. Levy JA. Viral and immunologic factors in HIV infection. In: Medical Management of 
AIDS , Third Edition (Sande M, Volberding P, eds). W.B. Saunders Company, 
Philadelphia, pp 18-32, 1992. 

88. Berger J, Levy JA. The human immunodeficiency virus, type 1 : The virus and its role in 
neurologic diseases. Seminars inNeurol, 12:1-9, 1992. 

89. Cheng-Mayer C, Shioda T, Levy JA. Small regions of the env and tat genes control 
cellular tropism, cytopathology and replicative properties of HTV-1. In: Science 
Challenging AIDS (eds. Rossi GB, Beth-Giraldo E, Chieco-Bianchi L, Dianzani F, 
Giraldo G, Verani P), S.Karger, Basel, pp 188-195, 1992. 

90. Mackewicz C, Levy JA. CD8+ cell anti-HIV activity: nonlytic suppression of virus 
replication. AIDS Res and Human Retroviruses 8:1039-1050, 1992. 

91. Levy JA. Pathogenesis of HIV-1: controversies and hypotheses. HIV Advances in 
Research and Therapy, 1:3-9, 1992. 

92. Levy JA. Viral and Host Factors Influencing AIDS Pathogenesis. (1991): The Present and 
Future of AIDS. Minophagen Medical Review 37:187-189, 1992. 

93. Mosier DE, Gulizia RJ, Maclsaac PD, Torbett BE, Levy JA. HIV-1 strain-dependent CD4 
T cell depletion in hu-PBL-SCID mice. Proc 8th Intl Congress of Immunol, pp 725-730, 
1992. 

94. Levy JA, Landay A, Jessop C, Lennette E. Chronic fatigue syndrome: Is it a state of 
chronic immune activation against an infectious virus? In: Contemporary Issues in 
Infectious Diseases, Volume 10 (Sande M, Root R, eds). Churchill Livingstone Inc., New 
York, pp 127-146, 1993. 



Jay A. Levy, M.D. 150 

95. Morrow WJW, Homsy J, Swanson CA, Levy JA. The influence of nutrition on 
experimental autoimmune disease: an overview with particular emphasis on the effects of 
dietary fat. In: Nutritional Regulation of Immune Responses. (Cunningham-Rundles S, 
ed). Marcel Dekker, Inc., New York, 1993, pp 153-158. 

96. Levy, JA. Features of human immunodeficiency virus infection and disease. Fed Res 
33:s63-s70, 1993. 

97. LevyJA. Pathogenesis of HIV infection. Microbiol Rev, 57:183-289, 1993. 

98. Levy JA. The transmission of HIV and factors influencing progression to disease. Am J 
Med. 95:86-100, 1993. 

99. Levy JA. HIV and host immune responses in AIDS pathogenesis. J Clin Apheresis, 8:19- 
28, 1993. 

100. Levy JA. Does AIDS portend epidemics to come? The conflict of macro- vs. micro- 
parasitism. In: Cancer, AIDS and Society (Jasmin C, Bez G, eds), Editions Tempo 
Medical, Paris, pp 47-56, 1993. 

101. Levy, JA. Le sida prefigure-t-il les epidemics a venir? In: Cancer, sida et societe: pour 
une approche globale de la sante, (Jasmin C, Bez G, eds), ESF, Paris, pp 75-87, 1993. 

102. Levy JA. Concepts in HIV neuropathogenesis. In: Focus on HIV, 1992 (Neu HC, Levy, 
JA, Weiss R, eds.). Churchill Livingstone, London, pp 51-67, 1993. 

103. LevyJA. HIV pathogenesis and long-term survival. AIDS, 7:1401-1410, 1993. 

104. Evans LA, Levy JA. The heterogeneity and pathogenicity of HIV. In: HIV Molecular 
Organization, Pathogenesis and Treatment (Morrow WJW, Haigwood NL, eds.). 
Elsevier Science Publishers, Amsterdam, pp 29-74, 1993. 

105. Levy JA. Viruses as the cause of chronic fatigue syndrome. Clin Infect Dis 18:S117- 
S120, 1994. 

106. Barker E, Fujimura S, Fadem MB, Landay A, Levy JA. Immunologic abnormalities 
associated with chronic fatigue syndrome. Clin Infect Dis 18:S136-S141, 1994. 

107. Levy JA. Human retrovirus infections. In: Internal Medicine (Fourth Edition). (Stein 
JH, ed). Little, Brown and Company, Boston, pp 2045-2050, 1994. 

108. Kliks SC, Levy JA.Matemal antibody response and maternal infant HIV-1 transmission 
(Letter). Lancet 343:1364, 1994. 

109. Levy JA. Long-term survival: HIV pathogenesis. Clinical Care Options for HIV 1:1-6, 
1994. 



Jay A. Levy, M.D. 151 

1 10. Levy JA. Long-term survivors of HIV infection. Hospital Practice 29:41-52, 1994. 

111. Stamatatos L, Levy JA. CD26 is not involved in infection of peripheral blood 
mononuclear cells by HIV-1 (Letter). AIDS, 8:1727-1728, 1994. 

112. Blackbourn DJ, Mackewicz C, Barker E, Levy JA. Human CD8+ cell non-cytolytic anti- 
HIV activity mediated by a novel cytokine. Res in Immunol, 145:653-658, 1994. 

1 13. Levy JA.HIV research: a need to focus on the right target. Lancet 345:1619-1621, 1995. 

1 14. Levy JA. A new human herpesvirus: KSHV or HHV8? Lancet 345:786, 1995. 

115. Levy JA. HTV interaction with the cell and effective humoral and cellular immune 
responses against the virus. In: Biotechnology and AIDS. Proceedings of the 
International Congress "Biotech 94 - AIDS - From Basic Science to Prevention, 
Diagnosis and Therapy" pp 21-32, 1995. 

116. Levy JA. HIV: a decade of research. In: Global Challenge of AIDS - Ten Years of 
HIV/AIDS Research. Proceedings of the Tenth International conference on AIDS, 
Kodansha Ltd, Tokyo, pp 274-286, 1995. 

1 17. Kliks S, Contag C, Corliss H, Wara D, Levy JA. Selection of HIV-1 variants in vertical 
transmission. In: Proceedings, International Symposium on Pediatric AIDS in Thailand: 
A Public Health and Social Dilemma. Harvard AIDS Institute, Cambridge, MA, pp 30- 
32, 1995. 

118. Mascolini, M. The CDS cell antiviral factor: An interview with immunologist Jay Levy, 
M.D. BETA, pp 18-24, June 1995. 

119. Levy JA. HIV heterogeneity in transmission and pathogenesis. In: AIDS in the World, 
(Mann J, Tarantola D, eds.), Oxford University Press, New York, pp. 177-185, 1996. 

120. Levy JA, Mackewicz CE, Barker E. Controlling HIV pathogenesis: the role of 
noncytotoxic anti-HP/ response of CD8+ T cells. Immunol Today, 17:217-224, 1996. 

121. Levy JA. Surrogate markers in AIDS Research. Is there truth in numbers? JAMA 
276:161-162, 1996. 

122. Locher CP, Blackbourn DJ, Castro BA, Brasky KM, Levy JA. Susceptibility of peripheral 
blood mononuclear cells from gorillas, orangutans and baboons in diverse HIV isolates. 
AIDS, 10:1438-1440, 1996. 

123. Levy JA. The value of primate models for studying human immunodeficiency virus 
pathogenesis. J Med Primatol 25: 163-174, 1996. 

124. Levy JA. Infection by human immunodeficiency virus - CD4 is not enough. New Engl J 
Med 335: 1528-1530, 1996. 



Jay A. Levy, M.D. 152 

125. Levy JA. Controversies: does the CD4+ cell count reflect clinical efficacy? (Reply). J Am 
Med Assoc 276: 1219-1220, 1996. 

126. Levy JA. En quoi la recherche fondamentale sur le cancer et le sida concerne-t-elle la 
qualite de vie? In: Cancer, Sida.. .la Qualite de Vie (Jasmin C, Levy JA, Bez G, eds.), 
Synthelabo Groupe, Paris:Le Plessis-Robinson, pp 187-196, 1996. 

127. Ffrench R, Stewart GJ, Penny R, Levy JA. How HIV produces immune deficiency. In: 
Managing HIV, (Stewart G, ed.), Australiasian Medical Publishing Co., North Sydney, 
Australia, pp 22-28, 1997. 

128. Blackboum DJ, Levy JA. Human herpesvirus 8 in semen and prostate. AIDS 11: 249- 
250, 1997. 

129. Levy JA. Three new human herpesviruses (HHV6, 7, and 8). Lancet 349:558-562, 1997. 

130. Levy JA, Barker E, Mackewicz CE. Effect of cytokines on CD8+ cell anti-HTV activity. 
In: HIV and Cytokines (Geunounou M, ed.), INSERM, Paris, France, pp 199-205, 1997. 

131. Levy JA. How does basic research in cancer and AIDS approach the concern for quality 
of life? In: Cancer, AIDS and Quality of Life. (Levy JA, Jasmin C, Bez G, eds.) Plenum 
Publishing Corporation, New York, pp 17-36, 1997. 

132. Levy JA, Mackewicz C, Barker E. The CD8+ cell antiviral factor. J AIDS & Hum 
Retrovir, 15(Suppl. I): S23-S26, 1997. 

133. Levy JA. David A. Wood In: In Memoriam. University of California Academic Senate. 
pp 191-192, 1997. 

134. Levy JA. Human retrovirus infections, Chapter 256. In: Internal Medicine (Fifth 
Edition). (Stein JH, ed). Little, Brown and Company, Boston, pp 1531-1534, 1998. 

135. Barker E, Kahn J, Levy, J. Protease inhibitors do not increase the CD4+ cell count in 
HIV-uninfected individuals. AIDS 12:14, 1998. 

136. Levy JA. Conversations with Samuel Beckett. ln:The Critical Response to Samuel 
Beckett: Critical Responses in Arts and Letters, (Andonian, CC, Editor), Greenwood 
Press, Westport, 30:195-206, 1998. (Revised). 

137. Landay A, Levy JA. Basic Science: Report from the 12th World AIDS Conference, 
[JAMA HIV/AIDS Web Site]. July 20, 1998. Available at http://www.ama- 
assn.org/special/hiv/newsline/conferen/aidsl2/bassci.htm. Accessed July 20, 1998. 

138. Ambroziak J, Levy JA. Epidemiology, natural history and pathogenesis of HIV infection. 
In: Sexually Transmitted Diseases (Third Edition), (Holmes KK, Sparling PF, Mardh PA, 
Lemon SM, Stamm WE, Piot P, Wasserheit JN, eds.) McGraw-Hill, Inc., New York, pp 
251-258, 1998. 



Jay A. Levy,M.D. 153 

139. Levy JA. Caution: should we be treating HIV infection early? Lancet, 352:982-983, 1998. 

140. Levy JA. Early treatment of HIV-1 infection (Reply). Lancet, 352:1936, 1998. 

141. Levy JA. Xenotropism: The elusive viral receptor finally uncovered. Proc Natl Acad Sci 
(USA) , 96:802-804, 1999. 

142. Stranford SA, Levy JA. HIV immunology. In: Clinical Infectious Diseases: A Practical 
Approach (Root RK, Editor-in-Chief), Oxford University Press, Oxford, pp 927-936, 
1999. 

143. Levy JA, HIV/AIDS research at the millennium. Interviewed by L. Hanna In BETA, 
12(3) pp 9-1 1,34, 1999. 

144. Levy, JA. AIDS Fighters Must Find New Strategies to Control HIV. San Francisco 
Chronicle, October 25, 1999, p A23. 

145. Levy, JA. CDS cell antiviral factors: clinical relevance. In Basic Science in HIV/AIDS: 
an Update. (Mertens TE, Dias-Ferraro V, Wedel A, Pialoux G, Piketty C, Jayle D, 
Esparaza J, eds.), World Health Organization, Geneva, 1999. 

146. Blackbourn DF, Fujimura SH, Kutzkey T, Levy JA. Induction of HHV-8 gene expression 
by recombinant interferon-y. AIDS, 14:98-99, 2000. 

147. Mackewicz CE, Ridha S, Levy JA. Fas and Fas ligand are not involved in the 
suppression of HIV replication by CD8+ cells. AIDS, 14:204-205, 2000. 

148. Mackewicz CE, Ridha A, Levy JA. HIV virions and HIV replication are unaffected by 
granulysin. AIDS, 14:328-30, 2000. 

149. Levy JA. Uncloaking hidden viruses. In: Many Faces, Many Microbes (Atlas, RM, ed.) 
ASM Press, pp 138-145, Washington, DC, 2000. 

150. Levy JA, Padian N, Sheehy J. Proven Connection - HIV causes AIDS. San Francisco 
Chronicle, May 30, 2000, p A25. 

151. Levy JA. Preface. In: HIV and the Pathogenesis of AIDS (Chinese Edition). (Shao Y, 
trans.) pp iii-v, 2000. 

152. Landay A, Levy JA. Basic Science: Report from the 13th World AIDS Conference, 
[JAMA HIV/AIDS Web Site]. August 20, 2000. Available at http://www.ama- 
assn.org/special/hiv/newsline/conferen/iacOO/basicsci.htm. Accessed August 31, 2000. 

153. Levy JA. Forward. In: Manuale Pratico di Terapia Antivirale, (Milazzo F. ed.) Periodici 
Scientifici, Milano, Italy, pp VH-IX, 2000. 

1 54. Levy JA. What can be achieved with an HIV vaccine? Lancet, 357:223-224, 2001 . 

155. Levy JA. Harness the immune system. AIDS at 10 years series. San Francisco Chronicle, 
June 4, 2001, p. A19. 



Jay A. Levy, M.D. 154 

156. Levy JA. The role of the innate immune system in controlling HIV infection and disease, 
Trends in Immunology, 22:312-316, 2001. 

157. Levy JA. The AIDS vaccine: Who can take the lead? Book Review Shots in the dark: The 
wayward search for an AIDS Vaccine by Jon Cohen. Lancet,357:1986, 2001. 

158. Levy JA, Zucker-Franklin D. Acquired Immunodeficiency Syndrome In: Atlas of Blood 
Cells. Function and Pathology (Zucker-Franklin D, Greaves MF, Grossi CE, Marmont 
AM, eds.) 3 rd ed., Edi-ermes, Milan, in press, 2001. 

159. Levy JA. Forward. In: Techniques in Quantification and Localization of Gene 
Expression. (Patterson B, ed) Springer- Verlag, New York, in press, 2001. 

160. Castelli JC, Levy JA. Human immunodeficiency virus In: Encyclopedia of 
Cacer(Bertino, JR, et. al. eds.), Academic Press, San Diego, in press, 2001. 

161. Levy JA. Forward. In: Human AIDS, (Zeng Q-P, ed.), Chinese Academy of Sciences, 
China, in press, 2001. 

162. Levy JA, Murphy EL. Human T cell leukemia virus. In: Cancer Research: An 
Encyclopedic Reference (Schwab, M, et. al. eds.) Heidelberg, in press 2001. 



Jay A. Levy, M.D. 155 



Books 

1. Fraenkel-Conrat H, Kimball PC, Levy JA: Virology. 2nd ed. Englewood Cliffs: Prentice 
Hall, 1988. 

2. Levy JA (ed). AIDS: Pathogenesis and Treatment. New York: Marcel Dekker, Inc., 
1989. 

3. Levy JA (ed). The Retroviridae (Volume 1) New York: Plenum Press, 1992. 

4. Levy JA (ed). The Retroviridae (Volume 2) New York: Plenum Press, 1993. 

5. Neu HC, Levy JA, Weiss R (eds.). Focus on HIV, 1992, London: Churchill Livingstone, 
1993. 

6. Levy JA (ed). The Retroviridae (Volume 3) New York: Plenum Press, 1994. 

7. Levy JA, Fraenkel-Conrat H, Owens R. A. Virology. 3rd. ed. Englewood Cliffs: Prentice 
Hall, 1994. 

8. Levy JA. HIV and the Pathogenesis of AIDS. ASM Press, Washington, DC, 1 994. 

9. Major E, Levy JA (eds). Technical Advances in AIDS Research in the Human Nervous 
System, New York: Plenum Press, 1995. 

1 0. Levy JA (ed). The Retroviridae (Volume 4) New York: Plenum Press, 1 995 . 

11. Jasmin C, Levy JA, Bez G (eds.) Cancer, SID A ...la Qualite de Vie, Synthelabo Groupe, 
Paris: Le Plessis-Robinson, 1996. 

12. Levy JA, Jasmin C, Bez G (eds.) Cancer, AIDS and Quality of Life, Plenum Publishing 
Corporation, New York, 1997. 

13. Levy JA. HIV and the Pathogenesis of AIDS (Second Edition). ASM Press, Washington, 
DC, 1998. 



156 

INDEX--The AIDS Epidemic in San Francisco: The Medical Response, 1981-1984: 
Volume VIII 



Abrams, Donald, 35, 37 
AIDS/HIV disease 

grants /funding, 36-37, 42, 44- 

46, 53, 58, 67, 70, 84 
immune deficiency, 41, 66, 67- 

68, 75 

in Dominican Republic, 38-42 
in Haiti, 38-42 
legislation, 44-45 
Levy research on CDS cells, 85- 

86 
publication/publicity, 78, 82, 

86, 90, 91, 96 
research in primates, 55-56, 64, 

93 
seropositivity without AIDS, 68- 

69 

vaccine, 90-91 
viral/retroviral etiology, 35, 

37, 38, 40-42, 44-45, 46-49, 60, 

74-78 

and voodoo, 40 

See also specific AIDS-related 
diseases 
AIDS research/medical practice 

in San Francisco, 42-44 
AIDS Specimen Bank, UCSF, 64-65 
AIDS virus 

blood tests, 43, 53, 54, 70, 74, 

77, 78, 79, 80-83 
cell lines, 79-80, 95-96, 99 
cloning /sequencing, 87-92 
electron microscopy studies, 60, 

76, 87 
heat treatment of blood products, 

46-51 
in hemophiliacs /blood products, 

41, 46-51, 54, 70, 73-76 
and human T cell leukemia virus 

[HTLV], 51-52, 53, 57, 59, 60, 

73-74, 87, 88-90, 91, 93-99 
isolating/ identifying the virus 

(Gallo, Levy, & Pasteur labs), 

51-64, 72-83, 
naming the virus, 97-99 
patent/patenting, 92, 99-100 



AIDS virus (continued) 
reverse transcriptase 

assays /enzyme, 27, 46, 53, 54, 

61-62, 71, 72 
Alizon, Marc, 52, 53, 74 
American Tissue Culture Collection, 

79 

Ammann, Arthur, 44, 46 
amyl nitrate, 42 
Arnstein, Paul, 76 



bacteriophage, research on, 4-5 
Banghardt, Harry, 54, 61 
Barnes, Ron, 28 
Barre-Sinoussi, Frangoise, 31, 51, 

53, 60, 73, 85 
Bell, Thomas, 5-6 
Berman, Phil, 90 
Bertani, Elizabeth & Giovanni, 4 
Bielschovsky, Franz, 21 
Bielschovsky, Marianne, 21 
Bishop, Michael, 20, 24, 27, 28 
Blanchard, Max, 39, 40 
Boiron, Michel, 17-18 
Boyer, Herbert, 87 
Brown, Paul, 55, 56 
Brown, Willie, 44, 45 
Bryant, Marty, 88, 92, 93, 96 
Burkitt, Denis, 5 
Burkitt's lymphoma, 5-6, 7, 8, 10, 

35, 77 
Burnet, Macfarlane, 28 



Cadman, Ed, 34, 46, 55 
California State Legislature 

AIDS funding, 44-47, 58, 67 
Cancer Research Institute, UCSF, 

19, 24, 33-34 

cancer, viral cause of, 4, 5, 12-16 
carcinogenesis/ trans format ion, 14- 

19, 30-31 

Casavant, Conrad, 71 
Centers for Disease Control [CDC], 

50 



157 



Chanock, Robert, 16 

Chermann, Jean-Claude, 31, 49, 51, 

53, 56-57, 60, 73 
Chiron Corporation, 86-91 
Clark, Margaret, 72 
Cochrane, Vince, 1-2 
Conant, Marcus, 36, 37-38, 42, 44, 

64, 78 

Cooper, Geoff, 20 
Council for Tobacco Research, 16 
Crede, Robert H. , 32 
Crewdson, John, 53, 79, 92, 93, 94 
Crocker, Tim, 16 
Curnen, Ed, 7 
Cutter Laboratories, 48-49, 54, 75- 

76 



Defendi, Vittorio, 8-9, 11 

DeVita, Vince, 47 

Dina, Dino, 88 

Dirksen, Ellen, 24-25, 33 

Dixon, Frank, 17 

Drew, Larry, 37, 42 

Dritz, Selma, 37 

Duesberg, Peter, 42, 69, 74-75 



Eleanor Roosevelt Foundation, 30 
Elie, Bob, 39 

Essex, Myron, 48, 53, 59, 98 
Evatt, Bruce, 48 



Fauci, Tony, 58 
Fieldsteel, Howard, 76 
Finkel, Miriam, 14 
Fischinger, Peter, 92-93 
flow cytometry, 71-72 
Freedom of Information Act, 93 
Fulbright Fellowship, 2 



Gazdar, Adi, 79, 99 

Gelman, Edward, 59 

Genentech, 87, 89-90 

Giraldo, Gaetano, 35 

Gladstone Institute of Virology and 

Immunology, UCSF, 42 
Golde, David, 45 
Graham, Angus, 8 
Greenspan, John, 42, 43, 44 
Gruber, Jack, 47 



Haitian American Foundation, 39, 41 
Haran-Ghera, Nechama, 30, 33 
Hartley, Janet, 13, 14, 15, 22, 88 
hemophilia /hemophiliacs and AIDS, 

41, 46-51 
Henle, Gertrude (Brigitta) , 9, 10- 

11, 23, 24, 77, 80, 84, 86 
Henle, Werner, 9, 10, 23, 24, 29, 

56, 77, 80, 84, 86 

hepatitis B/model for AIDS, 50, 56 
Herzenberg, Lee, 71 
Hetzenberg, Len, 71 
Hill, Mirek, 18-20 
Hillova, Jana, 18 
Hirsch, Marty, 62, 69 
HIV/HIV disease. See AIDS 
Hoffman, Tony, 53-54 
Hopital Paul Brouse, Villejuif, 18- 

19, 31 

Hopital St. Louis, Paris, 17 
Huebner, Harriet, 28 
Huebner, Robert, 8, 12, 14, 15, 20, 

23, 24, 28-29 



immune deficiency, 41, 66, 67-68, 

75 

International Committee on the 
Taxonomy of Viruses, 97-99 



Gajdusek, Carlton, 55-56 

Gallo, Robert, 47, 48, 51, 53, 56, 

57-59, 60, 63, 64, 73, 78, 81, 83, 

89, 91, 92, 93, 95, 97-99 
Gardner, Murray, 22, 44, 88, 92, 

93, 96 



Jacob, Francois, 30 
Jasmin, Claude, 18, 31 



Kalter, Sy, 24-25, 44, 55 
Kaminsky, Larry, 47, 81 



158 



Kane, John, 29 

Kaposi's sarcoma, 35-38, 45, 65-67, 

68, 69-70, 76, 83 
Kaposi's Sarcoma Clinic, UCSF, 37- 

38, 40, 70 
Karpas, Abe, 57 
Klein, Marty, 19 

Koenig, Ellen Levy, 10, 23, 38, 39 
Koprowski, Hilary, 8, 9 
Krause, Richard, 58 
Krevans, Julius, 23-24, 33, 44 
Kuerper, Marion, 81 



Laguerre, Michel, 39-40 

Landau, Susan, 57 

Latarjet, Raymond, 4, 31 

Lender, Theodore, 2 

Lennette, Evelyne, 81 

Leong, JoAnn, 26-27, 28 

leukemia research, 30, 33 

Levine, Peter, 49 

Levy, Sharon, 29, 30, 31, 32, 53 

Levy, Stuart, 4, 22, 31 

Little John, Dick, 46 

Luce, Judy, 35, 43 

Luciw, Paul, 88, 89 

lymphadenopathy, 37, 38 

lysogeny, 4, 35 



National Hemophilia Foundation, 49, 

51 
National Institutes of Health 

[NIH] /National Cancer Institute, 

8, 12-16, 47, 96 
Nelson, Jay, 27 
Neumann, Sigmund, 3 



Office of Scientific Integrity, NIH, 

93, 96 

oncogene research, 19-20 
Oshiro, Lyndon, 76 
Oxman, Mike, 13 



Parkman, Robertson, 15 

Pasteur Institute, Paris, and AIDS 

research team, 30, 92 
patents /patenting, 92, 99 
Paucher, Kurt, 10 
Perkins, Herbert, 81 
Perlman, David, 23 
Petrakis, Marty, 32 
Pincus, Ted, 16 
Pneumocystis carinii pneumonia, 36, 

37, 65, 67, 69-70 
Popovic, Mikula, 93-94, 95, 96 
Prusiner, Stanley, 55 



Martin, Malcolm, 88-89 
McElhatton, David, 86 
McHugh, Tom, 71 
mice strains, laboratory 

C57 Black, 21 

New Zealand Black [NZB], 14, 17, 
21-22, 24 

NIH Swiss, 22 
Mills, John, 16, 37 
Mintz, Beatrice, 21 
Mitra, George, 48 
Montagnier, Luc, 31, 51, 53, 56, 60, 

63, 64, 70, 73, 91, 92, 97, 99 
Morrow, John, 43, 47 
Moss, Andrew, 42 
Mozen, Milt, 48, 49 



Ramirez, Michelle, 32, 43 

Rasheed, Suraya, 22 

Rauscher, Dick, 34 

recombinant DNA, 27 

Reichman, Michele, 90 

research funding cutbacks, 27, 32- 

34, 35 

Rich, Marvin, 64 
Rose, Harry, 5 
Rosenkranz, Herbert, 4 
Rowe, Wallace, 13-16, 22, 23 
Rutter, William J., 87 



Salk, Jonas, 100 

Salmon, Sid, 19 

Schmid, Rudi, 46, 53, 63, 67, 85 

Sheppard, Chip, 81 



159 



Shilts, Randy, 43, 78 

Shohet, Stephen, 33-34, 46, 72 

Smith, Lloyd H. , 16, 85 

Stites, Dan, 44, 71 

suramin treatment of AIDS, 54 

Szoenyi, Martha, 43 



Talal, Norman, 21 

Tanabe, Eru, 7 

Teas, Jane, 40 

Temin, Howard, 20 

Terry, Luther, 8 

Tobler, Leslie, 44 

Todaro, George, 22 

Trent in, John, 12 

Tumor & Virus Group of the West, 

Turner, Dan, 36, 37, 65 



University of California, San 
Francisco 

AIDS research/patient policy, 
32-34, 46, 63, 67, 83, 85 



76 



viruses, specific types, and 
research on (continued) 

xenotropic, 14-16, 20-29, 43, 

47, 80, 83-84 
See also AIDS /HIV disease; AIDS 

virus 
Volberding, Paul, 35, 36-37, 44, 67 



Wain-Hob son, Simon, 89 
Walker, Chris, 86 
Weinberg, Robert, 19 
Wesley an University, 1-2, 3 
Wilbur, Judy, 81 
Wistar Institute, 8-11 
Wolff, Etienne, 2 
Wood, David, 19, 29, 32, 34 



Ziegler, John, 36, 42, 66 
Zolla-Pazner, Susan, 52 



Varmus, Harold, 20, 24, 27, 96, 97- 

99 

Virolab, 81 

viruses, specific types, and 
research on 

adenovirus, 12, 13 
amphotropic viruses, 22-23 
cytomegalovirus, 35 
Epstein-Barr, 8, 11, 12, 13, 35, 

86 
human immunodeficiency virus 

[HIV] . See AIDS virus 
human T cell leukemia virus 
[HTLV], 51-52, 53, 57, 59, 60, 
73-74, 87, 88-90, 91, 93-99 
New Zealand Black [NZB] virus, 

15, 16, 17, 21-23, 43 
reovirus , 6 , 7 , 8 , 9 , 11 
retroviruses , 12, 17-18, 22, 23, 
26-27, 31, 35, 47, 48-49, 60 



3412 



77/37 
C