Rosenberg suggests, by contrast, that AIDS is a “postrelativist phenomenon,” exposing the
limitations of a purely biological model divorced from social interpretations, while at the
same time showing the inadequacy of an extreme focus on the creation of social meanings
that denies the existence of biological disease; Charles E. Rosenberg, “What Is an Epi-
demic? AIDS in Historical Perspective,” in Explaining Epidemics and Other Studies in the
History of Medicine (Cambridge: Cambridge University Press, 1992), 292. Taking Rosen-
berg’s point, the approach adopted in this book is one of “moderate” social construction.
It recognizes the existence of an underlying pathological process causing the disease that
became known as AIDS, yet also emphasizes the vital importance of investigating the so-
cially produced meanings surrounding it.
Introduction
7
can speak (or stay silent) and what they can say (or not). I shall return
to these questions near the end of this introduction, when I consider in
greater detail my own position as a historian in the construction of this
historical account.
* * *
The initial geographic focus, as Chabner mentioned, on New York, Los
Angeles, and San Francisco soon expanded to include Haiti, Canada,
and countries in Western Europe. By 1983, the syndrome was recog-
nized to exist at substantial levels in several countries in sub- Saharan
Africa. This ominous distribution became easier to monitor with the
discovery and isolation of a causative virus— eventually named the hu-
man immunodefi ciency virus (HIV)— during 1983 and 1984 and the de-
velopment and distribution of a test for antibodies to the virus in 1985.14
Reports from the Joint United Nations Programme on HIV/AIDS chart
the devastating consequences of this condition from then until now.
They estimate that HIV was responsible for the deaths of approximately
twenty- nine million people worldwide between 1970 and 2009, and that
nearly thirty- seven million people were living with the virus in 2014,
the most recent year for which data were available at the time of this
writing.15
HIV infection has traversed the world and infected people from all
races and ethnicities, exposing in the process the extreme diffi culties in
14. The virus— variously named lymphadenopathy- associated virus (LAV) by French
scientists in 1983, human T- cell lymphotropic virus type III (HTLV- III) by Robert Gallo’s
team in 1984, and AIDS- related virus (ARV) by another American team led by Jay Levy
in 1984— was eventually named HIV in 1986; for a review of the politics involved in such
a decision, see Paula Treichler, “AIDS, Homophobia, and Biomedical Discourse: An Epi-
demic of Signifi cation,” in Crimp, AIDS, 31– 70; Epstein, Impure Science, 45– 78.
15. Joint United Nations Programme on HIV/AIDS, Outlook 30 (Geneva: UNAIDS,
2011), 17, http:// www .unaids .org/ sites/ default/ fi les/ media _asset/ 20110607 _JC2069 _30Out
look _en _0 .pdf; Joint United Nations Programme on HIV/AIDS, AIDS by the Numbers
2015 (Geneva: UNAIDS, 2015), 4, http:// www .unaids .org/ sites/ default/ fi les/ media _asset/
AIDS _by _the _numbers _2015 _en .pdf. Hereafter, the word epidemic is used to describe a
higher than usual number of cases in areas as small as a single community and as large
as a single continent, and pandemic to refer to the global spread of AIDS across several
continents.
8
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addressing its spread across barriers of language and culture.16 In con-
trast to the diversity of social, cultural, and political reactions to the vi-
rus, within each individual body there is a relatively similar continuum
from infection to early death— particularly in the absence of antiretro-
viral therapy.17 When a person has become infected with HIV, the virus
enters the bloodstream and the individual’s cells. Many people develop
fl u- like symptoms during the primary, acute- infection stage, which can
last for up to two weeks, before returning to feeling normal. The virus
travels to the lymph nodes and replicates rapidly in the absence of anti-
bodies, which can take the body between one and three months to pro-
duce. After a person has seroconverted— that is, after his or her body
has begun to produce antibodies to combat the virus— the immune sys-
tem enters into a slow, silent, and gradually losing struggle with HIV.
This process, during which the body’s T cells are slowly depleted, hap-
pens over a period of years, and in many cases the only external sign is
an eventual swelling of the lymph nodes.
At a certain point, the T cells deplete more rapidly, allowing virus
levels in the body to rise substantially. Poverty, malnutrition, and co-
infec tions can bring on this stage sooner.18 At earlier stages of HIV
disease, often within fi ve to seven years of infection, the compromised
immune system might give rise to such moderate symptoms as rash,
tiredness, night sweats, weight loss, and fungal infections. As time
passes, more severe medical diffi culties might emerge, including recur-
rent thrush and herpes, persistent diarrhea, and extreme loss of weight.
Finally, severe damage to the immune system occurs, roughly ten years
following infection. This development will allow the invasion of oppor-
tunistic infections— illnesses that would not normally occur in healthy
16. The massive scope of the challenge and variety in the responses can be gleaned
from a review of the thousands of abstracts of the posters and presentations at each bi-
ennial International AIDS Conference. See, for example, the abstracts presented at the
21st International Conference in Durban, South Africa, in 2016: http:// www .aids2016 .org/
Portals/ 0/ File/ AIDS2016 _Abstracts _LOW .pdf ?ver = 2016– 08– 10– 154247– 087.
17. The description that follows holds true for most infected individuals, though about
5 percent of this population may become long- term nonprogressors, remaining healthy
with no apparent loss of T cell function for many years; see Jay A. Levy, “HIV Pathogene-
sis: 25 Years of Progress and Persistent Challenges,” AIDS 23, no. 2 (2009): 158.
18. Marie- Marcelle Deschamps et al., “HIV Infection in Haiti: Natural History and
Disease Progression,” AIDS 14, no. 16 (2000): 2515– 21.
Introduction
9
individuals— often in rapid succession. The most common of these con-
ditions, which now herald the designation of late- stage HIV disease or
AIDS, include PCP, Mycobacterium avium complex, cytomegalovirus,
toxoplasmosis, and candidiasis.19 An aggressive form of KS— a previ-
ously rare and relatively benign cancer typically affecting older men—
was also one of the most common complications seen in the gay com-
munities when the epidemic was fi rst recognized, and it was the chief
reason why the National Cancer Institute had expressed such interest in
the new syndrome.20 In the absence of effective treatment, the risk of
death increases with each passing year after seroconversion, with nearly
two- thirds of untreated patients in resource- rich countries dying within
fi fteen years of infection.21
The Origins of HIV/AIDS
“As I mentioned,” Chabner emphasized to the meeting’s attendees, “the
fi rst cases were seen in homosexual males in New York.” He continued,
“There are now cases in most major US cities and foreign countries. In
some of these instances the patients in foreign countries have known
contacts, homosexual contact, with people in New York or other Amer-
ican cities. There are fewer cases in number in foreign countries than
in the United States.” Alluding to the dramatic rise in reported cases,
Chabner explained, “At this point when the slide was made we had 600
19. This description of the stages of HIV infection has been drawn from the informa-
tive online HIV/AIDS resource, The Body. See San Francisco AIDS Foundation, “The
Stages of HIV Disease,” The Body: The Complete Online HIV/AIDS Resource, Au-
gust 22, 2008, http:// www .thebody .com/ content/ whatis/ art2506 .html.
20. Studies would note that the proportion of gay and bisexual men with AIDS who de-
veloped Kaposi’s sarcoma decreased from 79 percent in 1981 to 25 percent in 1989. In 1994,
a new herpes virus was isolated which was found to be a contributing factor for developing
KS; see Yuan Chang et al., “Identifi cation of Herpesvirus- Like DNA Sequences in AIDS-
Associated Kaposi’s Sarcoma,” Science 266, no. 5192 (1994): 1865– 69. One likely hypothe-
sis is that this virus was more widespread in the gay community in the late 1970s, leading to
a higher proportion of KS in the fi rst cases of AIDS in men who had sex with men.
21. Beryl A. Koblin et al., “Long- Term Survival after Infection with Human Immuno-
defi ciency Virus Type 1 (HIV- 1) among Homosexual Men in Hepatitis B Vaccine Trial Co-
horts in Amsterdam, New York City, and San Francisco, 1978– 1995,” American Journal of
Epidemiology 150, no. 10 (1999): 1027.
10
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known patients that had the disease, now the number is closer to 800
patients.”22
* * *
From the time he spoke those words to the present day, attempting to
locate the origins of HIV/AIDS has been a contentious issue— and one
which would be central to discussions of “Patient Zero” in the 1980s. As
readers shall see in chapter 1, epidemics throughout history have repeat-
edly been accompanied by attempts to locate origins and to lay blame.
Initially, with the vast majority of people diagnosed with AIDS located
in New York City, or with ties to that city, many observers assumed that
the origins of the epidemic lay there. Soon, the appearance of cases
among Haitian immigrants led to speculation that the immune disorder
was endemic in their home country, or, perhaps, that vacationing Amer-
ican homosexuals from New York had unwittingly spread an etiologi-
cal agent there.23 A joint Belgian and American research trip to Zaire in
1983 established that a similar condition, predominantly affecting het-
erosexual men and women, was widespread there. This realization chal-
lenged the notion that the etiological agent thought to cause AIDS had
initially come into existence in the United States or that the disease was
predominantly one affecting gay men.24 Primate hosts of a more ancient
deadly virus that might have been passed to humans were sought. Afri-
can green monkeys were proposed as likely hosts, before eventually ced-
ing this position to chimpanzees in central Africa.25
After scientists developed a blood test for HIV, attempts to locate the
22. “NCAB Meeting,” 3.
23. See Renée Sabatier, Blaming Others: Prejudice, Race and Worldwide AIDS (Lon-
don: Panos Institute, 1988); Paul Farmer, AIDS and Accusation: Haiti and the Geography
of Blame, rev. ed. (Berkeley: University of California Press, 2006).
24. Peter Piot et al., “Acquired Immunodefi ency Syndrome in a Heterosexual Popula-
tion in Zaire,” Lancet 324, no. 8394 (1984): 65– 69. Piot, the Belgian physician who headed
this trip and later became the head of the United Nations AIDS Programme, describes the
experience in his memoir, No Time to Lose: A Life in Pursuit of Deadly Viruses (W. W.
Norton, 2012), 121– 32.
25. This appears to be true for HIV- 1; HIV- 2, a far less widely distributed form of the
virus, is believed to have crossed into humans from the sooty mangabey monkey; Justin
Stebbing and Graeme Moyle, “The Clades of HIV: Their Origins and Clinical Signifi -
cance,” AIDS Reviews 5, no. 4 (2003): 205– 13.
Introduction 11
virus in decades- old stored samples yielded contested results. In Octo-
ber 1987, preserved samples from a teenaged male from St. Louis who
died of an AIDS- like condition in 1969 were reported to have tested
positive for HIV antibodies. Samples from a British sailor who had died
in 1959 after a devastating series of infections including pneumocystis
carinii pneumonia yielded similar positive rest results.26 Experts would
later cast doubt on the validity of these two examples due to subsequent
diffi culties in reproducing the results with tests that searched for the ac-
tual genetic presence of the virus, as opposed to antibodies.27 However,
tests repeatedly detected the virus in another archival sample: blood
drawn in 1959 from an individual in the vicinity of Léopoldville, the cap-
ital of what was then the Belgian Congo.28
Throughout the 1980s and 1990s, suggestions that HIV had origi-
nated in Africa were met from a number of quarters as a further ex-
ample of Western fascination with the continent as a diseased and dan-
gerous landmass. Meanwhile, during this period, most scientists came
to believe that HIV had resulted from the cross- species transmission of
a simian immunodefi ciency virus (SIV) to a single human during the
hunting and/or consumption of chimpanzee meat. Some AIDS activ-
ists and African offi cials mounted resistance, however, citing a lack of
evidence and racist insinuations of bestiality.29 An alternative and more
marginalized explanation to this “cut hunter” theory also arose, which
alleged that a laboratory based in the Belgian Congo unwittingly used
SIV- infected chimpanzee tissue in the local preparations of an oral po-
lio vaccine (OPV) in the late 1950s. Between 1957 and 1960, these oral
doses were fed to several hundred thousand individuals in the Belgian
Congo and in the Belgian- administered areas near Lake Victoria and
26. John Crewdson, “Case Shakes Theories of AIDS Origin,” Chicago Tribune, Octo-
ber 25, 1987, 1, 20; Gerald Corbitt, Andrew S. Bailey, and George Williams, “HIV Infec-
tion in Manchester, 1959,” Lancet 336, no. 8706 (1990): 51.
27. Edward Hooper and William D. Hamilton, “1959 Manchester Case of Syndrome
Resembling AIDS,” Lancet 348 (1996): 1363– 65; Edward Hooper, The River: A Journey
Back to the Source of HIV and AIDS (London: Allen Lane, 1999), 133– 37, 741, 1006n5.
28. A. Nahmias et al., “Evidence for Human Infection with an HTLV- III/LAV- like Vi-
rus in Central Africa, 1959,” Lancet 1 (1987): 1279– 80. Following decolonization, Léo-
pold ville was renamed Kinshasa and the former colony took on the nam
e Zaire, before
changing its name again in 1997 to the Democratic Republic of the Congo.
29. Treichler, Theory in an Epidemic, 121– 22.
12
chapter 0
Lake Tanganyika, regions which would later see early and extensive
HIV epidemics.30
Mainstream scientists have rejected the OPV theory, particularly fol-
lowing reports describing a scientifi c debate in 2000 at the Royal Society
in London, which declared that there was no fi rm evidence to support it.31
The theory’s most prominent supporter, Edward Hooper, continues to
vigorously defend the theory and respond to its critics from his personal
website.32 Some scientists, including several associated with the OPV re-
search, have answered forcefully with counterclaims and legal threats.
They asserted that the OPV theory was dangerous and that it directly
contributed to fears worldwide about the dangers of vaccination cam-
paigns and jeopardized the global eradication of polio.33 Other research-
ers have pushed past Hooper’s increasingly lonely objections. Some have
used computer models of HIV mutation rates to estimate the date of the
crossover event, that of an immunodefi ciency virus passing from a chim-
30. A lengthy account of this theory of accidental iatrogenic introduction, as well as
many other origin theories, is Edward Hooper’s The River. A more succinct and up- to-
date version of his main points in support of the OPV theory can be found in his article
“The Origins of the AIDS Pandemic: A Quick Guide to the Principal Theories and the
Alleged Refutations,” AIDS Origins (blog), April 25, 2012, http:// www .aidsorigins .com/
origins - aids - pandemic.
31. Brian Martin offers an intriguing analysis of the ways in which the scientifi c com-
munity has worked to discredit Hooper and the OPV theory: “The Politics of a Scientifi c
Meeting: The Origin- of- AIDS Debate at the Royal Society,” Politics and the Life Sci-
ences 20, no. 2 (2001): 119– 30.
32. In her book The AIDS Conspiracy: Science Fights Back (New York: Columbia Uni-
versity Press, 2012), 29– 31, Nicoli Nattrass suggests that Hooper’s actions— which include
personal attacks and often verbose and angry writing on his personal website— resemble
those of a conspiracy theorist. Some fairness to Hooper, though, might allow the acknowl-
Patient Zero and the Making of the AIDS Epidemic Page 3