This is the html version of the file http://www.ias.ac.in/jbiosci/jun2003/383.pdf.
Google automatically generates html versions of documents as we crawl the web.
Page 1
383
Keywords. AIDS not contagious; AIDS not immunogenic; drug-free HIV survivors; HIV-free AIDS; mortality on anti-HIV drugs; non-
exponential AIDS epidemics; non-random US/European AIDS; pediatric drug-AIDS; random African AIDS; recreational drug-AIDS
________________
Abbreviations used: CDC, US Centers for Disease Control; NIH, US National Institutes of Health; FDA, US Food and Drug
Administration; WHO, World Health Organization.
J. Biosci. | Vol. 28 | No. 4 | June 2003 | 383–412 | © Indian Academy of Sciences
The chemical bases of the various AIDS epidemics: recreational
drugs, anti-viral chemotherapy and malnutrition
PETER DUESBERG
†
, CLAUS KOEHNLEIN* and DAVID RASNICK
Donner Laboratory, University of California Berkeley, Berkeley, CA 94720, USA
*Internistische Praxis, Koenigsweg 14, 24103 Kiel, Germany
†Corresponding author (Fax, 510-643-6455; Email, duesberg@uclink4.berkeley.edu)
In 1981 a new epidemic of about two-dozen heterogeneous diseases began to strike non-randomly growing
numbers of male homosexuals and mostly male intravenous drug users in the US and Europe. Assuming
immunodeficiency as the common denominator the US Centers for Disease Control (CDC) termed the epidemic,
AIDS, for acquired immunodeficiency syndrome. From 1981–1984 leading researchers including those from the
CDC proposed that recreational drug use was the cause of AIDS, because of exact correlations and of drug-
specific diseases. However, in 1984 US government researchers proposed that a virus, now termed human
immunodeficiency virus (HIV), is the cause of the non-random epidemics of the US and Europe but also of a
new, sexually random epidemic in Africa. The virus-AIDS hypothesis was instantly accepted, but it is burdened
with numerous paradoxes, none of which could be resolved by 2003: Why is there no HIV in most AIDS
patients, only antibodies against it? Why would HIV take 10 years from infection to AIDS? Why is AIDS not
self-limiting via antiviral immunity? Why is there no vaccine against AIDS? Why is AIDS in the US and
Europe not random like other viral epidemics? Why did AIDS not rise and then decline exponentially owing to
antiviral immunity like all other viral epidemics? Why is AIDS not contagious? Why would only HIV carriers
get AIDS who use either recreational or anti-HIV drugs or are subject to malnutrition? Why is the mortality of
HIV-antibody-positives treated with anti-HIV drugs 7–9%, but that of all (mostly untreated) HIV-positives
globally is only 1⋅4%? Here we propose that AIDS is a collection of chemical epidemics, caused by recreational
drugs, anti-HIV drugs, and malnutrition. According to this hypothesis AIDS is not contagious, not immuno-
genic, not treatable by vaccines or antiviral drugs, and HIV is just a passenger virus. The hypothesis explains
why AIDS epidemics strike non-randomly if caused by drugs and randomly if caused by malnutrition, why they
manifest in drug- and malnutrition-specific diseases, and why they are not self-limiting via anti-viral immunity.
The hypothesis predicts AIDS prevention by adequate nutrition and abstaining from drugs, and even cures by
treating AIDS diseases with proven medications.
[Duesberg P, Koehnlein C and Rasnick D 2003 The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemo-
therapy and malnutrition; J. Biosci. 28 383–412]
1. Origins of the AIDS epidemics of the US,
Europe and Africa
1.1 AIDS in the US and Europe
In the spring of 1981 the US Centers for Disease Control
(CDC), the nation’s sentinel of infectious diseases, first
reported a mysterious epidemic of previously known
diseases that selectively affected growing numbers of
young male homosexuals, intravenous drug users and a few
minor risk groups such as hemophiliacs and recipients of
blood transfusions (Centers for Disease Control 1981a, b,
1986). The diseases of the new AIDS epidemic included
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
384
Kaposi’s sarcoma, bacterial and fungal (pneumocystis
and candida) pneumonia, oral yeast infections, dementia,
diarrhea, herpes, tuberculosis, lymphoma, weight loss, toxo-
plasmosis, chronic fevers, etc. (table 1), (Centers for Disease
Control 1986). A similar, non-random epidemic was soon
also reported in Europe by the World Health Organization
(WHO), (Downs et al 1987). The selective distribution of
these epidemics in the US and European population imme-
diately suggested risk group- or lifestyle-specific causes.
However, the plethora of AIDS diseases was not, and
still is not randomly distributed even among the different
risk groups (table 2). For example, Kaposi’s sarcoma
was exclusively diagnosed in male homosexual risk
groups using nitrite inhalants and other psychoactive
drugs as aphrodisiacs (Newell et al 1984; Haverkos et al
1985; Selik et al 1987; Duesberg 1988; Haverkos and
Dougherty 1988; Beral et al 1990). Bacterial pneumonia
was primarily diagnosed in children from mothers using
psychoactive drugs during pregnancy (Novick and Rubin-
stein 1987; Duesberg 1988, 1992; Centers for Disease
Control and Prevention 1997). Tuberculosis and pneu-
monia were, and still are more prevalent in intravenous
drug users and “crack” (cocaine) smokers than in other
risk groups (Lerner 1989; Duesberg 1992; Duesberg and
Rasnick 1998). Pneumocystis pneumonia and dementia
are common in both of these risk groups (Selik et al
1987; Duesberg 1992; Duesberg and Rasnick 1998).
Hemophiliacs and other transfusion recipients from the
US and Europe exclusively present with pneumonia and
yeast infections (Curran et al 1984; Duesberg 1992,
1995c). The non-random distribution of these diseases in
different risk groups, then and now, again suggests risk
group-specific causes, rather than a common one.
Only 3 months after first detecting the new epidemics
of old diseases, the CDC named all of them, AIDS, for
Acquired Immune Deficiency Syndrome, assuming that
immunodeficiency was their common denominator (Cen-
ters for Disease Control 1981b). According to their most
recent AIDS definition of 1993, there are now 26 AIDS
defining diseases (Centers for Disease Control 1986, 1992).
However, about one third of the CDC’s collection of
AIDS diseases are neither caused by, nor necessarily
associated with immunodeficiency (table 1), (Duesberg
and Rasnick 1998). Examples are Kaposi’s sarcoma,
lymphoma, dementia, and weight loss (see table 1 for the
share of these among the AIDS diseases of the US in
1997). Although the rest of the CDC’s AIDS diseases are
indeed microbial diseases, they are typically opportunistic
microbial diseases, in which the causative microbe
depends on a defective immune system to cause disease.
Examples are tuberculosis, yeast infections and pneumo-
cystis pneumonia (Duesberg 1992), (table 1). By contrast,
in a normal immune system, opportunistic microbes are
harmless passengers – the reason why such diseases are
Table 1. CDC-defined AIDS diseases and “conditions” in the US in 1997, the last year the
Centers for Disease Control published the distribution of AIDS diseases.
Disease
AIDS-diagnosis
Percentage
of cases*
Case numbers
per 60,161
No disease
< 200 T cells and antibody against HIV
61
36,634
Microbial disease
Pneumocystis
38
9,145
Candidiasis
16
3,846
Tuberculosis and Mycobacteria
15
3,537
Cytomegalovirus
7
1,638
Pneumonia
5
1,347
Herpes virus
5
1,250
Cryptococcus
5
1,168
Toxoplasmosis
4
1,073
Non-microbial disease
Weight loss/wasting
18
4,212
Kaposi’s sarcoma
7
1,500
Dementia
6
1,409
Lymphoma/leukemia
4
850
Cervical cancer
1
144
*According to the CDC, “The sum of percentages is greater than 100 because some patients are
reported with more than one illness [disease or condition]. Of persons reported with AIDS-
defining opportunistic illnesses, 65% also were reported with severe HIV-related immunosup-
pression [corresponding almost exactly to the share of the microbial diseases among the total of
23,527 AIDS-defining diseases]. . . . The 36,634 adults/adolescents presented on this table are
those persons reported with immunosuppression as their only AIDS-indicator condition [rather
than disease]” (Centers for Disease Control and Prevention 1997).
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
385
not transmitted to healthy contacts, as for example to the
doctors that treat AIDS patients (see below, § 3, table 4).
Since 1981 the AIDS epidemics of the US and Europe
have increased steadily for a decade and, after reaching
peaks in the early 1990s, they have all decreased to about
1/2 of their peak levels now (figure 1a), (World Health
Organization 2001b). By 2001 the US epidemic had gene-
rated a total of 816,149 AIDS cases and the European
epidemic 251,021 AIDS cases (Centers for Disease Con-
trol and Prevention 2001; World Health Organization
2001b). To this day, the AIDS epidemics of the US and
Europe have remained highly non-random: 80% of all
patients from the US and 80% from Europe are males
(World Health Organization 2001a). In the US about 2/3
of all AIDS cases are male homosexuals and about 1/3
are male and female intravenous drug users. In Europe
about 1/2 are male homosexuals and about 1/2 are intra-
venous drug users [note that over 75% of intravenous
drug users are males (Duesberg and Rasnick 1998)]. In
addition both epidemics include fringe groups of hemo-
philiacs and other transfusion recipients (1%) and children
born to drug-addicted mothers (1%) (World Health
Organization 2001a).
1.2 African epidemic
A new AIDS epidemic was also claimed to have emerged
in sub-Saharan Africa in 1984 (Bayley 1984; Piot et al
1984; Seligmann et al 1984; Van de Perre et al 1984;
Quinn et al 1986, 1987). In sharp contrast to its US/Euro-
pean namesakes, the African AIDS epidemic is randomly
distributed between the sexes and not restricted to beha-
vioural risk groups (Blattner et al 1988; Duesberg 1988;
World Health Organization 2001a). Hence sub-Saharan
African AIDS is compatible with a random, either micro-
bial or chemical cause.
The African epidemic is also a collection of long-establi-
shed, indigenous diseases, such as chronic fevers, weight
loss, alias “slim disease”, diarrhea and tuberculosis (table
2), (Colebunders et al 1987; Konotey-Ahulu 1987a, b,
1989; Pallangyo et al 1987; Duesberg 1992). However,
the distribution of AIDS-defining diseases in Africa dif-
fers strongly from those in the US and Europe (table 2).
For example, the predominant and most distinctive AIDS
diseases in the US and Europe, Pneumocystis carinii
pneumonia and Kaposi’s sarcoma, are almost never diag-
nosed in Africa (Goodgame 1990; Abouya et al 1992).
According to the WHO the African epidemic has in-
creased from 1984 until the early 1990s, similar to the
epidemics of the US and Europe, but has since leveled
off to generate about 75,000 cases annually (figure 1c),
(World Health Organization 2001b, and back issues). By
2001, Africa had reportedly generated a cumulative total
of 1,093,522 cases (World Health Organization 2001b).
However, there are three reasons for questioning these
numbers:
(i) During the African AIDS epidemic, the sub-Saharan
African population has grown, at an annual rate of about
2⋅6% per year – from 378 million in 1980 to 652 million
in 2000 (US Bureau of the Census International Data Base
2001). Thus Africa had gained since 1980 274 million
people, the equivalent of the whole population of the US!
Therefore, a possible, above-normal loss of 1 million
Africans over a period in which over 200 millions were
gained is statistically hard, if not impossible to verify –
unless the African AIDS diseases were highly distinctive.
(ii) However, the African AIDS-defining diseases are
clinically indistinguishable from conventional African
morbidity and mortality (see above).
(iii) Further the HIV-based definition of AIDS (see § 3)
can not be used in Africa to distinguish AIDS-defining
from otherwise indistinguishable diseases, because as of
1985 the WHO decided at a conference in Bangui, Africa,
to accept African AIDS diagnoses without HIV-tests (see
§ 3). This was done because these tests are unaffordable
Table 2. Risk group-specific AIDS diseases.
Risk groups
Disease
Male
homosexual
Intravenous
drugs
AZT
recipient
US, Europe
child
Hemophilia,
transfusion
African
Kaposi’s sarcoma
+ +*
Lymphoma
+
+
Bacterial pneumonia
+ +
+
Tuberculosis
+ +
+ +
+ +
Dementia
+
+
+
+
Weight loss
+
+
+
+
+ +
Yeast
+
+
+
+
+
+
Pneumocystis pneumonia
+ +
+
+
+
+
*+ and + + represent common and highly representative diseases respectively.
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
386
in most African countries (World Health Organization
1986; Fiala 1998; Fiala et al 2002). Thus without the
CDC’s HIV standard (§ 3), the diagnosis of African
AIDS is arbitrary.
In view of the many epidemiological and clinical distinc-
tions of African AIDS from its US/European namesakes
and the many uncertainties about the diagnosis of African
AIDS, both the novelty of African AIDS and its relation-
ship to the US/European AIDS epidemics have been cal-
led into question (Hodgkinson 1996; Fiala 1998; Shenton
1998; Gellman 2000; Stewart et al 2000; Malan 2001; Fiala
et al 2002; Gisselquist et al 2002; Ross 2003). Indeed, all
available data are compatible with an old African epide-
mic of malnutrition and poverty-associated diseases under
a new name (Konotey-Ahulu 1987a, b; Oliver 2000;
Stewart et al 2000).
In the following we will try to find the most probable
causes for the various AIDS epidemics based on epide-
miological, clinical, microbial and biochemical evidence.
2. 1981–1984: The “lifestyle”-AIDS hypothesis
Hardly anybody remembers now, that shortly after the
origins of the AIDS epidemics in the US and Europe sci-
entists had already discovered that illicit psychoactive
and aphrodisiac drugs, consumed at massive doses, were
the common denominators and probable causes of the
new AIDS patients. Drugs such as cocaine, heroin, nitrite
inhalants, amphetamines, steroids and lysergic acid had
become widely available and popular in the US and Europe
during and after the Vietnam war and the coincident era
of “gay liberation” (legal indemnity of homosexuality)
Figure 1. Time courses of (a) the American, European and Australian AIDS epidemics since 1985 according to Centers for Dis-
ease Control and Prevention 2001 and redrawn from the World Health Organization (1999), (b) the incidence of HIV antibody car-
riers in the US since 1985 according to the Centers of Disease Control (CDC), and (c) the incidence of AIDS and HIV antibody
carriers in Africa according to the WHO. See text for further explanations and references.
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
387
(Duesberg and Rasnick 1998). The phenomenon was dub-
bed the “drug explosion” in the US and Europe. Its chro-
nology is documented in figure 2 based on cocaine and
heroin hospital-emergencies and confiscations of cocaine.
Figure 2 extends drug use statistics described by us ear-
lier until 2001 (Duesberg and Rasnick 1998), and also
compares the chronologies of the drug and AIDS epidemics
in the US (see also figure 1a and § 4).
The first series of publications linking homosexual AIDS
with drugs, particularly aphrodisiac nitrite inhalants
(Gottlieb et al 1981), was published in the New England
Journal of Medicine in 1981 together with an editorial by
AIDS researcher David Durack suggesting that drugs are
the causes of AIDS (Durack 1981). Dozens of further drug-
AIDS studies soon followed from all prominent AIDS
researchers of the time, including Blattner, Bregman,
Curran, Dougherty, Des Jarlais, Drotman, Friedman-Kien,
Goedert, Haverkos, Jaffe, Marmor, McManus, Mildvan,
Moss, Newell, Oppenheimer, Ortiz, Rivera, and Stone-
burner (Goedert et al 1982; Marmor et al 1982; McManus
et al 1982; Jaffe et al 1983; Mathur-Wagh et al 1984;
Newell et al 1984; Haverkos et al 1985; Moss 1987;
Haverkos and Dougherty 1988; Stoneburner et al 1988;
Oppenheimer 1992).
Even the CDC, normally just a survey agency, conduc-
ted epidemiological studies of their own, which confir-
med that male homosexuals at risk for AIDS and with
AIDS were using batteries of recreational and aphrodisiac
drugs (table 3), (Jaffe et al 1983). Not even one male homo-
sexual at behavioural risk for AIDS or with AIDS was
found to be drug-free by the CDC. However, some CDC
investigators suggested that nitrites depend on “infectious
cofactors” to cause AIDS diseases (Haverkos 1988).
The perfect correlations between recreational drug use
and AIDS became the basis for the hypothesis that drugs,
or the drug use-“lifestyle” is the cause of AIDS (Shilts
Table 3. CDC 1983*: Drug use by American male
homosexuals with AIDS and at risk for AIDS.
Drugs
Percentage users among 50 AIDS cases
and 120 at risk for AIDS
Nitrite inhalants
96
Ethylchloride
35–50
Cocaine
50–60
Amphetamines
50–70
Phenylcyclidine
40
LSD
40–60
Metaqualone
40–60
Barbiturates
25
Marijuana
90
Heroin
10
Drug-free
None reported
*(Jaffe et al 1983).
Figure 2. (a) Chronology of the recreational drug epidemic in
the US since 1980, based on various indicators. The data for
cocaine confiscations are from the US Bureau of Justice Statis-
tics, table 4.36 Federal drug seizures (1988–2001), Federal
drugs seizures (1989–2001), (www.albany.edu/sourcebook) and
from Duesberg and Rasnick (1998). The data for cocaine and
heroin hospital emergencies are from the Substance Abuse and
Mental Health Services Administration-Office of Applied
Studies (2002), from Emergency Department Trends of the
Drug Abuse Warning Network, Final Estimates 1994–2001,
Rockville, MD (2002), and from the Drug Abuse Warning
Network, Dept. Health Human Services, August, DAWN
Series: D-21, DHHS Publication No. (SMA) 02-3635
(http://www.drugabusestatistics.samhsa.gov). (b) The chrono-
logy of the US AIDS epidemic according to the CDC (Centers
for Disease Control 2001).
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
388
1987; Oppenheimer 1992). Moreover, the findings that
specific drugs, as for example nitrite inhalants, correlated
with specific AIDS diseases, such as immune suppression
and Kaposi’s sarcoma, directly support the lifestyle hypo-
thesis (Goedert et al 1982; Marmor et al 1982; Haverkos
and Dougherty 1988).
By contrast, the African epidemic had been reduced
right from its presumed origin in 1984 to the consequences
of malnutrition and lack of drinkable water, alias poverty,
consistent with its random distribution in the population
(Mims and White 1984; Seligmann et al 1984).
In sum all clinical and epidemiological data available
on AIDS in 1984 made a coherent case for lifestyle- or
chemical AIDS, caused by recreational drugs or malnu-
trition.
3. 1984: The virus-AIDS hypothesis takes over
By 1983 AIDS had become big enough in the American
and European press to pique the interest of the influential
infectious disease establishment, particularly the cancer
virus hunters. At that time the virus hunters had been enga-
ged for over a decade in president Nixon’s War on Can-
cer with unsuccessful attempts to find a human cancer
virus (Duesberg 1996b; Fujimura 1996; de Harven 1999).
Now they were looking for new diseases that could be
attributed to viruses (Duesberg 1987). Perhaps AIDS could
at last yield clinically relevant lymphoma-, Kaposi’s sar-
coma- or immunodeficiency-viruses (Duesberg 1996b).
Indeed, virus hunters from the CDC were the first to alert
the public that AIDS may be “transmissible” (Francis
et al 1983). A similar alert came from a French virus
team, which had discovered a retrovirus in a homosexual
man at risk for AIDS, which a year later became the
accepted cause of AIDS (Barre-Sinoussi et al 1983).
News, that the cause of AIDS may be a virus, and thus
transmissible to the general population, immediately set
off a national panic that opened the doors for new sur-
veillance programs by the CDC and predictably set off a
race among virus hunters for the AIDS virus (Shilts 1987).
According to an international press conference called
by the US Secretary of Health and Human Services in
Washington DC on 23 April 1984, that race was won by
government researchers from the NIH who had found in
some AIDS patients antibodies against a new retrovirus
closely related to a hypothetical human leukemia virus
(Altman 1984). The virus was introduced as fortunate
fallout of the failed War on Cancer. The next day the new
virus was already termed, the “AIDS virus”, by the New
York Times (Altman 1984). Overnight nearly all AIDS
researchers dropped the lifestyle-AIDS hypothesis to work
on the new “AIDS virus”, which was already endorsed by
the US government. The CDC’s director of the Task
Force on Kaposi’s Sarcoma and Opportunistic Infections,
James Curran, was the only one who later announced the
reason for his conversion to the new “AIDS virus”:
“That’s where the money is” (Shilts 1987).
The National Academy, the Institute of Medicine and
the CDC quickly united the infectious disease establish-
ment under the leadership of David Baltimore, who had
received a Nobel prize for his work on retroviruses, to
provide practical recommendations for the intimidated
public. Their recommendations were published in two
consecutive monographs of Confronting AIDS (Institute
of Medicine and National Academy of Sciences 1986;
Institute of Medicine 1988), and initiated history’s big-
gest and most expensive anti-viral program ever, costing
$ 93⋅3 billion by 2000 to the US taxpayer alone (Johnson
2000). At the same time an international committee of
retrovirologists officially sealed the seemingly tight
package of a new “AIDS virus” and the CDC’s assumption
that immunodeficiency was the common denominator of
the 26 AIDS-defining diseases (table 1) by naming it,
Human Immunodeficiency Virus (HIV) (Coffin et al 1986).
Even before the AIDS virus became the officially accep-
ted cause of AIDS, the CDC had already made antibodies
against the virus the only definitive criterion to diagnose
any of the heterogeneous diseases as AIDS in 1985 (Cen-
ters for Disease Control 1985, 1987, 1992). Their unortho-
dox decision to use antibodies against the virus (normally
functioning as a vaccine), instead of the virus, for the
diagnosis of AIDS was based on the flawed analogy with
some bacterial pathogens. For example, syphilis bacteria
can be pathogenic despite the presence of antibodies,
e.g. the Wassermann test for syphilis (Brandt 1988). But
viruses are typically unable to enter cells in the presence
of anti-viral antibodies – the basis for the effectiveness of
Jennerian vaccines. Because of the CDC’s decision,
AIDS is diagnosed worldwide if antibody against (!) HIV,
rather than HIV, is detectable in a patient along with any
of the CDC’s 26 diseases. Since 1992 even low T-cell
counts are diagnosed as a condition, termed “HIV/AIDS”,
which is treatable with anti-HIV drugs provided it occurs
in the presence of antibodies against HIV (Centers for
Disease Control 1992), (see table 1, and § 4.2).
3.1 Discrepancies between the predictions of
the virus-AIDS hypothesis and the facts
Despite its spectacular birthday the HIV-AIDS hypothe-
sis has remained entirely unproductive to this date: There
is as yet no anti-HIV-AIDS vaccine, no effective preven-
tion and not a single AIDS patient has ever been cured –
the hallmarks of a flawed hypothesis. Indeed the hypo-
thesis was born with several serious birth defects and has
developed further defects since; most of these should
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
389
have given pause to HIV-AIDS researchers to rethink and
reconsider. However, in the race to claim a share of the
new viral cause for AIDS and of virus-based AIDS treat-
ments, “The Trojan horse of emergency” (Szasz 2001) was
saddled so quickly that there was little time and no interest
to address these defects, not even the most fundamental
ones (Weiss and Jaffe 1990; Cohen 1994; O’Brien 1997).
An analysis of the defects of the HIV-AIDS hypothesis
based on its failure to predict AIDS facts is shown in
table 4. Our analysis is based on the most recent and
most authoritative case made for the HIV-AIDS hypothe-
sis since 1984, namely the Durban Declaration that was
published in Nature in 2000 and has been signed by
“over 5,000 people, including Nobel prizewinners” (The
Durban Declaration 2000). It can be seen in table 4 that
the HIV-hypothesis fails to predict 17 specific facts of
AIDS. The most fundamental discrepancy between the
HIV-AIDS hypothesis and the facts is the paradox, that a
latent, non-cytopathic and immunologically neutralized
retrovirus [a virus that is inherently not cytopathic
(Duesberg 1987)], that is only present in less than 1 out
of 500 susceptible T-cells and rarely expressed in a
few of those, would cause a plethora of fatal diseases in
sexually active, young men and women. And, that the
plethora of the diseases attributed to this virus would not
show up for 5–10 years after infection (table 4). As a re-
sult of the many discrepancies between the HIV hypothe-
sis and the facts, we conclude that HIV is not sufficient
for AIDS, and is most compatible with being a passenger
virus.
Surprisingly our conclusion is supported by a survey of
AIDS researchers conducted by the New York Times,
shortly after the publication of the Durban Declaration.
At the 20th anniversary of AIDS, on 30 January 2001,
the New York Times interviewed a dozen leading AIDS
researchers for an article that turned into a list of que-
stions, “The AIDS questions that linger” (Altman 2001a),
similar to those asked by us in table 4:
“In the 20 years since the first cases of AIDS were
detected, scientists say they have learned more about
this viral disease than any other, and few have dispu-
ted the claim. … Despite the gains … experts say
reviewing unanswered questions could prove useful
as a measure of progress for AIDS and other diseases.
Such a list could fill a newspaper, and even then would
create debate. (E.g.): How does H.I.V. subvert the
immune system? . . . Why does AIDS predispose infec-
ted persons to certain types of cancer and infections
and not others? . . . Dr Anthony S Fauci, the director
of the National Institute of Allergy and Infectious
Diseases, said, ‘It is the rare person who gets up and
strips himself of his personal agenda and articulates
what we really do not know because by saying that
they would diminish the impact of their own work,
which is their agenda’. (Regarding anti-HIV medica-
tions:) . . . the new drugs do not completely eliminate
H.I.V. from the body, so the medicines, which can
have dangerous side effects, will have to be taken for
a lifetime and perhaps changed to combat resistance.
The treatments are now so complicated that it is diffi-
cult, expensive and time-consuming to answer basic
and practical questions. What combinations of drugs
should be started first and when? Why do side effects
like unusual accumulations of fat in the abdomen and
neck develop? . . . Anti-H.I.V. drugs suppress replica-
tion of the virus, which should give the functioning
parts of the immune system a chance to eliminate re-
maining virus. That does not happen. ‘So something is
bizarre about that, that we don’t understand’, Dr Fauci
said. Is a vaccine possible? . . . many unanswered
questions exist about whether and when one can be
developed.”
Thus HIV-AIDS researchers have not solved the discre-
pancies and paradoxes of the HIV-AIDS hypothesis, but
still do not follow the scientific method of searching for
alternative explanations (Costello 1995).
Since 19 years of HIV-AIDS research have failed to
produce tangible benefits for AIDS patients and risk
groups, and since there are no paradoxes in nature only
flawed hypotheses, the scientific method calls for an
alternative, testable hypothesis. Here we offer one such
hypothesis. Our hypothesis extends the early, and now
abandoned “lifestyle” hypothesis (§ 2) and subsequent
drug-AIDS hypotheses from us and others (Duesberg
1992; Duesberg and Rasnick 1998).
4. Chemical AIDS
“Historically, the first step in determining the cause of
any disease has always been to find out if there is any-
thing, apart from the disease itself, that sufferers have in
common” (Cairns 1978). However, the traditional search
for the cause is only completed, if something that suf-
ferers have in common can also be shown to cause the
disease; in other words if Koch’s postulates can be ful-
filled (Merriam-Webster 1965). This is true for viruses
just as much as for drugs. Following this tradition, we try
here to provide proof of principle for our drug and mal-
nutrition hypothesis of AIDS – alias chemical AIDS.
4.1 The chemical-AIDS hypothesis and its predictions
The chemical-AIDS hypothesis proposes that the AIDS
epidemics of the US and Europe are caused by recreatio-
nal drugs, alias lifestyle, and anti-HIV drugs (Duesberg
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
390
Table 4. The HIV-AIDS hypothesis*: 17 predictions versus the facts.
No.
Prediction
Fact
1. Since HIV is “the sole cause of AIDS”, it must be abundant
in AIDS patients based on “exactly the same criteria as for
other viral diseases.”
But, only antibodies against HIV are found in most
patients (1–7)**. Therefore, “HIV infection is identified in
blood by detecting antibodies, gene sequences, or viral
isolation.” But, HIV can only be “isolated” from rare, la-
tently infected lymphocytes that have been cultured for
weeks in vitro – away from the antibodies of the human
host (8). Thus HIV behaves like a latent passenger virus.
2. Since HIV is “the sole cause of AIDS”, there is no AIDS in
HIV-free people.
But, the AIDS literature has described at least 4621 HIV-
free AIDS cases according to one survey – irrespective of,
or in agreement with allowances made by the CDC for
HIV-free AIDS cases (55).
3. The retrovirus HIV causes immunodeficiency by killing
T-cells (1–3).
But, retroviruses do not kill cells because they depend on
viable cells for the replication of their RNA from viral
DNA integrated into cellular DNA (4, 25). Thus, T-cells
infected in vitro thrive, and those patented to mass-pro-
duce HIV for the detection of HIV antibodies and diag-
nosis of AIDS are immortal (9–15)!
4. Following “exactly the same criteria as for other viral disea-
ses”, HIV causes AIDS by killing more T-cells than the body
can replace. Thus T-cells or “CD4 lymphocytes . . . become
depleted in people with AIDS”.
But, even in patients dying from AIDS less than 1 in 500
of the T-cells “that become depleted” are ever infected by
HIV (16–20, 54). This rate of infection is the hallmark of
a latent passenger virus (21).
5. With an RNA of 9 kilobases, just like polio virus, HIV
should be able to cause one specific disease, or no disease if
it is a passenger (22).
But, HIV is said to be “the sole cause of AIDS”, or of 26
different immunodeficiency and non-immunodeficiency
diseases, all of which also occur without HIV (table 2).
Thus there is not one HIV-specific disease, which is the
definition of a passenger virus!
6. All viruses are most pathogenic prior to anti-viral immunity.
Therefore, preemptive immunization with Jennerian vaccines is
used to protect against all viral diseases since 1798.
But, AIDS is observed – by definition – only after anti-
HIV immunity is established, a positive HIV/AIDS test
(23). Thus HIV cannot cause AIDS by “the same criteria”
as conventional viruses.
7. HIV needs “5–10 years” from establishing antiviral immu-
nity to cause AIDS.
But, HIV replicates in 1 day, generating over 100 new HIVs
per cell (24, 25). Accordingly, HIV is immunogenic, i.e. bio-
chemically most active, within weeks after infection (26, 27).
Thus, based on conventional criteria “for other viral disea-
ses”, HIV should also cause AIDS within weeks – if it could.
8. “Most people with HIV infection show signs of AIDS within
5–10 years” – the justification for prophylaxis of AIDS with
the DNA chain terminator AZT (§ 4).
But, of “34⋅3 million . . . with HIV worldwide” only 1⋅4%
[= 471,457 (obtained by substracting the WHO’s cumulative
total of 1999 from that of 2000)] developed AIDS in 2000,
and similarly low percentages prevailed in all previous years
(28). Likewise, in 1985, only 1⋅2% of the 1 million US citizens
with HIV developed AIDS (29, 30). Since an annual incidence
of 1⋅2–1⋅4% of all 26 AIDS defining diseases combined is no
more than the normal mortality in the US and Europe (life ex-
pectancy of 75 years), HIV must be a passenger virus.
9. A vaccine against HIV should (“is hoped” to) prevent
AIDS – the reason why AIDS researchers try to develop an
AIDS vaccine since 1984 (31).
But, despite enormous efforts there is no such vaccine to
this day (31). Moreover, since AIDS occurs by definition
only in the presence of natural antibodies against HIV
(§ 3), and since natural antibodies are so effective that no
HIV is detectable in AIDS patients (see No. 1), even the
hopes for a vaccine are irrational.
10. HIV, like other viruses, survives by transmission from host
to host, which is said to be mediated “through sexual con-
tact”.
But, only 1 in 1000 unprotected sexual contacts transmits
HIV (32–34), and only 1 of 275 US citizens is HIV-infec-
ted (29, 30), (figure 1b). Therefore, an average un-infected
US citizen needs 275,000 random “sexual contacts” to get
infected and spread HIV – an unlikely basis for an epidemic!
(Table 4. Cond.)
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
391
Table 4.
No.
Prediction
Fact
11. “AIDS spreads by infection” of HIV.
But, contrary to the spread of AIDS, there is no “spread”
of HIV in the US. In the US HIV infections have remained
constant at 1 million from 1985 (29) until now (30), (see
also The Durban Declaration and figure 1b). By contrast,
AIDS has increased from 1981 until 1992 and has decli-
ned ever since (figure 1a).
12. Many of the 3 million people who annually receive blood trans-
fusions in the US for life-threatening diseases (51), should have
developed AIDS from HIV-infected blood donors prior to the
elimination of HIV from the blood supply in 1985.
But there was no increase in AIDS-defining diseases in
HIV-positive transfusion recipients in the AIDS era (52),
and no AIDS-defining Kaposi’s sarcoma has ever been
observed in millions of transfusion recipients (53).
13. Doctors are at high risk to contract AIDS from patients, HIV
researchers from virus preparations, wives of HIV-positive
hemophiliacs from husbands, and prostitutes from clients –
particularly since there is no HIV vaccine.
But, in the peer-reviewed literature there is not one doctor or
nurse who has ever contracted AIDS (not just HIV) from the
over 816,000 AIDS patients recorded in the US in 22 years
(30). Not one of over ten thousand HIV researchers has con-
tracted AIDS. Wives of hemophiliacs do not get AIDS (35).
And there is no AIDS-epidemic in prostitutes (36–38). Thus
AIDS is not contagious (39, 40).
14. Viral AIDS – like all viral/microbial epidemics in the past
(41–43) – should spread randomly in a population.
But, in the US and Europe AIDS is restricted since 1981
to two main risk groups, intravenous drug users and male
homosexual drug users (§ 1 and 4).
15. A viral AIDS epidemic should form a classical, bell-shaped
chronological curve (41–43), rising exponentially via virus
spread and declining exponentially via natural immunity,
within months (see figure 3a).
But, AIDS has been increasing slowly since 1981 for 12
years and is now declining since 1993 (figure 1a), just like
a lifestyle epidemic, as for example lung cancer from
smoking (figure 3b).
16. AIDS should be a pediatric epidemic now, because HIV is
transmitted “from mother to infant” at rates of 25–50% (44–
49), and because “34⋅3 million people worldwide” were al-
ready infected in 2000. To reduce the high maternal trans-
mission rate HIV-antibody-positive pregnant mothers are
treated with AZT for up to 6 months prior to birth (§ 4).
But, less than 1% of AIDS in the US and Europe is pedia-
tric (30, 50). Thus HIV must be a passenger virus in new-
borns.
17. “HIV recognizes no social, political or geographic bor-
ders” – just like all other viruses.
But, the presumably HIV-caused AIDS epidemics of
Africa and of the US and Europe differ both clinically and
epidemiologically (§ 1, table 2). The US/European epi-
demic is highly nonrandom, 80% male and restricted to
abnormal risk groups, whereas the African epidemic is
random.
*All quotes are from The Durban Declaration, the most authoritative edition of the HIV-AIDS hypothesis to date, which was signed
“by over 5000 people, including Nobel prizewinners” and published in Nature in 2000 (The Durban Declaration 2000). **Numbers
in parentheses are for the following references: (1) (Marx 1984); (2) (Gallo et al 1984); (3) (Altman 1984); (4) (Duesberg 1987);
(5) (Duesberg 1988); (6) (Duesberg 1994); (7) (Duesberg and Bialy 1996); (8) (Levy et al 1984); (9) (Hoxie et al 1985); (10)
(Anand et al 1987); (11) (Langhoff et al 1989); (12) (Duesberg 1996b); (13) (Weiss 1991); (14) (Cohen 1993); (15) (McCune
2001); (16) (Harper et al 1986); (17) (Schnittman et al 1989); (18) (Hazenberg et al 2000); (19) (Duesberg 1988); (20) (Blattner
et al 1988); (21) (Enserink 2001); (22) (Fields 2001); (23) (Centers for Disease Control 1992); (24) (Duesberg and Rasnick 1998);
(25) (Duesberg 1992); (26) (Clark et al 1991); (27) (Daar et al 1991); (28) (World Health Organization 2001b); (29) (Curran et al
1985); (30) (Centers for Disease Control and Prevention 2001); (31) (Cohen 2003); (32) (Jacquez et al 1994); (33) (Padian et al
1997); (34) (Gisselquist et al 2002); (35) (Duesberg 1995c; Hoots and Canty 1998); (36) (Mims and White 1984); (37) (Rosenberg
and Weiner 1988); (38) (Root-Bernstein 1993); (39) (Hearst and Hulley 1988); (40) (Sande 1986); (41) (Bregman and Langmuir
1990); (42) (Anderson 1996); (43) (Fenner et al 1974); (44) (Blattner et al 1988); (45) (Duesberg 1988); (46) (Blanche et al 1989);
(47) (Rogers et al 1989); (48) (European Collaborative Study 1991); (49) (Connor et al 1994); (50) (World Health Organization
2000); (51) (Duesberg 1992); (52) (Ward et al 1989); (53) (Haverkos et al 1994); (54) (Simmonds et al 1990); (55) (Duesberg
1993d).
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
392
1992, 1996b; Duesberg and Rasnick 1998), and by other
non-contagious risk factors such as immunosuppressive
proteins associated with transfusions of blood clotting fac-
tors (Duesberg 1995c; Hoots and Canty 1998). According
to our hypothesis pediatric AIDS is due to prenatal con-
sumption of recreational and anti-HIV drugs by unborn
babies together with their pregnant mothers (Duesberg
1992; Duesberg and Rasnick 1998). The chemical basis
of African AIDS is proposed to be malnutrition and lack
of drinkable water (Duesberg 1992, 1996b; Duesberg and
Rasnick 1998) – exactly as proposed originally by the
now leading HIV-AIDS researchers Fauci and Seligmann:
“The commonest cause of T-cell immunodeficiency
worldwide is protein-calorie malnutrition” (Seligmann et al
1984) and others (Mims and White 1984), (see also § 1).
The chemical AIDS hypothesis makes the following
testable predictions:
(i) Patients of the various epidemics have drug use,
medications, malnutrition or other chemical pathogens in
common.
(ii) Distinct chemical pathogens cause distinct AIDS-defin-
ing diseases. Since chemicals are not self-replicating,
like viruses, pathogenicity is dose- and thus also time-
dependent (Duesberg and Rasnick 1998). Take for exa-
mple the average 20 years of smoking to cause cancer
(figure 3b), (Cairns 1978).
(iii) Since there is no immunity against drugs or malnutri-
tion, neither drug-, nor malnutrition-diseases, nor the cor-
responding epidemics are self-limiting. In contrast to an
infectious epidemic, the time curves of chemical epi-
demics are not bell-shaped (see figure 3).
(iv) People who are not subject to drugs or malnutrition,
or discontinue drug use or malnutrition before irrever-
sible damage has occurred, do not develop AIDS, regard-
less of antibodies against HIV.
Here, we will focus on new and poorly known evidence
confirming each of these predictions, but also make refe-
rences to prior supportive evidence by others and us.
4.2 Prediction 1: AIDS coincides with recreational
and anti-viral drugs in the US and Europe
and with malnutrition in Africa
4.2a Recreational drugs: Annually, the CDC and the
WHO confirm that about 1/3 of all AIDS patients from
the US and about 1/2 of those from Europe are intra-
venous users of cocaine, heroin, amphetamines and other
illicit, psychoactive drugs, since the beginning of the AIDS
epidemics (see § 1). Most babies with AIDS in the US
and Europe are also born to mothers who have used rec-
reational drugs (and antiviral drugs, see below) during
pregnancy according to the CDC, the WHO and inde-
pendent publications reviewed below and previously
(Duesberg 1992; Duesberg and Rasnick 1998). In addition
the CDC and WHO confirm that about 2/3 of the AIDS
patients in the US and 1/2 of those in Europe are male homo-
sexuals (§ 1), but, after the lifestyle hypothesis was aban-
doned in 1984, they did no longer report their drug use.
However, rare independent investigations have confir-
med continued use of illicit recreational drugs by male
homosexuals ever since the origins of the epidemic
(Lauritsen and Wilson 1986; Haverkos and Dougherty
1988; Rappoport 1988; Duesberg 1992; Lauritsen 1994;
Duesberg and Rasnick 1998). Since there is no general
knowledge about the male-homosexual-AIDS-drug con-
nection now, we have summarized in table 5 rare, post-
1984 studies which demonstrate that male homosexuals
with AIDS or at risk for AIDS have continued to use
nitrite inhalants, amphetamines, cocaine, heroin, steroids,
and other recreational drugs to this date, just as originally
shown by the proponents of the lifestyle hypothesis in-
cluding the CDC (see § 2, table 3) (Duesberg and Rasnick
1998). As this article went to press, the San Francisco
Chronicle published a 3-part front-page story on how
Figure 3. The time course of (a) a classical microbial epi-
demic, the plague in London of 1665 adapted from Anderson
(1996), and (b) of the classical behavioural, or “lifestyle” epi-
demics of smoking and lung cancer in men and women in Eng-
land in the 20th century, adapted from Cairns (1997).
(a)
(b)
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
393
“Crystal Meth (amphetamine) fuels HIV”. According to
the article “the state’s top AIDS and HIV prevention
officials came up with the smoking gun of all statistics:
Gay men in California who use speed are twice as likely
to be HIV-positive . . .” (Heredia 2003a). But the ques-
tion whether meth “fuels” AIDS without HIV was not
asked, even though the featured case of a gay meth-addict
had AIDS-defining dementia and opportunistic infections
(Heredia 2003a, b). Further, we confirm and extend, in tables
6 and 7, the correlations between maternal drug use and
baby-AIDS documented previously (Novick and Rubin-
stein 1987; Duesberg 1992; Root-Bernstein 1993; Duesberg
and Rasnick 1998; Farber 1998). The continuation of drug
use in the HIV era is not surprising in the absence of any
advice from the medical establishment, that nitrite inhalants
and other drugs may cause AIDS (Lerner 1989).
4.2b Anti-viral DNA chain terminators and protease
inhibitors: It is also little known that since 1987 thou-
sands of US citizens and Europeans with AIDS (Kolata
1987), and that since 1990 even larger numbers of heal-
thy HIV antibody-positives are on lifetime prescriptions
of inevitably toxic DNA chain-terminators, such as azi-
dothymidine (AZT), and protease inhibitors as anti-HIV
drugs (Volberding et al 1990). The original doses of these
prescriptions were 1⋅5 g per day of AZT or other DNA
chain-terminator for clinically ill patients (Fischl et al
1987) and 0⋅5 g per day for asymptomatic, HIV-positives
with low T-cell counts (Volberding et al 1990). As of
1996 the DNA chain-terminators were mixed with HIV-
protease inhibitors to generate so-called “drug cocktails”
(Ho 1995; Stolberg 2001). By 1996 200,000 US citizens
(Hall 1996), and by 2001/2002 over 450,000 (France 2001;
Altman 2002), were taking prescriptions of such drugs to
prevent or cure AIDS (Stolberg 2001). Due to the CDC’s
1993-definition of AIDS, well over half of these 450,000
treated subjects were clinically healthy at the time they started
taking the anti-HIV drugs (table 1) and are thus not patients
(Centers for Disease Control 1992; Centers for Disease Con-
trol and Prevention 1997). The asymptomatic HIV-positives
are treated according to the slogan, “Time to hit HIV, early
and hard”, that was introduced by the New England Journal
of Medicine in 1995 (Ho 1995). Thus recreational and anti-
HIV drugs are the common denominator of AIDS in the
US, and also in Europe (see below).
4.2c African AIDS coincides with malnutrition: The case
for malnutrition and lack of drinkable water as the com-
mon denominator and probable cause of African AIDS in
the HIV-era has been made by scientific (Mims and White
1984; Seligmann et al 1984; Konotey-Ahulu 1987a, b,
1989; Fiala 1998; Oliver 2000; Stewart et al 2000; Ross
2003) and non-scientific observers (Hodgkinson 1996;
Shenton 1998; Malan 2001). The non-scientific observers
even include the United Nations (Namango and World
Food Program of the United Nations 2001) and president
Mbeki of South Africa (Cherry 2000; Gellman 2000).
4.3 Prediction 2: Drugs cause AIDS and other diseases
4.3a Literature confirms that illicit recreational drugs
cause AIDS defining and other drug-specific diseases:
We have recently summarized the evidence from over 60
publications, beginning in 1909 (Achard et al 1909),
which prove that regular consumption of illicit recreatio-
nal drugs causes all AIDS defining and additional drug-spe-
cific diseases at time and dose-dependent rates (Duesberg
1996b; Duesberg and Rasnick 1998). At recreational doses,
addictions ranging from years to over a decade are typically
required to reach pathogenic thresholds. Thus the literature
confirms the original “lifestyle”- or drug AIDS hypothesis.
4.3b Epidemiological drug dose-AIDS-response curves:
In figure 2 (§ 2) we have already shown that the chrono-
logy of the epidemic of illicit drug-use in the US during
the 1980s and 1990s closely paralleled the US AIDS epi-
demics, see also Duesberg and Rasnick (1998). A report
from the White House, underwritten by president Clin-
ton, provides additional data: It states in 1996 that the
number of regular users of illicit recreational drugs in the
US soared from a negligible background in the early
1960s to a high of 25 million, or about 10% of the US
population, in the late 1980s (Clinton and The White
House 1996; Duesberg and Rasnick 1998). Since its peak
Table 5. Studies describing illicit recreational (IR) and
antiviral (AV) drug use by male homosexuals with AIDS
and at risk for AIDS in the HIV era, since 1984.
Drugs
Reference and Year
IR
(Haverkos et al 1985; Newell et al 1985)
IR
(Lauritsen and Wilson 1986)
IR
(Darrow et al 1987)
IR
(Haverkos and Dougherty 1988; Rappoport 1988)
IR
(Adams 1989; Archer et al 1989; Kaslow et al 1989)
IR
(Lifson et al 1990; Ostrow et al 1990)
IR
(Eggers and Weyer 1991)
IR
(Archibald et al 1992)
IR + AV (Ascher et al 1993b; Ostrow et al 1993; Schechter
et al 1993)
IR + AV (Lauritsen 1994; Sadownick 1994; Veugelers et al 1994)
IR
(Haverkos and Drotman 1995)
IR
(Gibbons 1996; Haverkos 1996; Haverkos and Drot-
man 1996)
IR
(McNall and Remafedi 1999)
IR
(Craib et al 2000; Dukers et al 2000; Pauk et al 2000)
IR
(Colfax et al 2001; Diamond et al 2001; Mansergh
et al 2001; Mattison et al 2001; Woody et al 2001)
IR + AV (Botnick et al 2002; Bull et al 2002)
IR, Illicit recreational drugs such as nitrite and other inhalants,
amphetamines, cocaine, heroin, steroids; AV, antiviral drugs
such as DNA chain terminators, protease inhibitors and others.
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
394
in the late 1980s-early 1990s, the US drug epidemic has
declined to an estimated 13 million regular users in 1996
(Los Angeles Times 1998; White House Office of Natio-
nal Drug Control Policy 1998), again roughly paralleling
the course of the AIDS epidemic (figure 2).
In addition, a fast-rising epidemic of volatile nitrite
inhalants, primarily among male homosexuals, was iden-
tified in the US by Newell et al, Lauritsen and Wilson,
and the National Institute on Drug Abuse (Lauritsen and
Wilson 1986; Haverkos and Dougherty 1988; Newell
et al 1988). It started in the late 1970s – immediately
preceding the male homosexual AIDS sub-epidemics of
Kaposi’s sarcomas and pneumonias (§ 1). Newell et al
(1988) documented that recreational nitrite inhalant –
alias “popper” – use had increased from negligible numbers
in the 1960s to 5 million users of one ounce per week (!)
Table 6. Diseases and mortality of HIV antibody-positive people on anti-HIV drugs that do not occur in,
or exceed the rates of untreated controls.
AIDS-defining
Other
References
Immunodeficiency,
Leukopenia
Anemia, Neutropenia
(Gill et al 1987; Kolata 1987; Richman et al 1987; Dournon et al 1988; Jacobson
et al 1988; Mir and Costello 1988; Alcabes et al 1993; Poznansky et al 1995;
Kline et al 1998; Levy 1998; Anonymous 1999; Blanche et al 1999; Mocroft et al
1999)
Fever
Nausea
(Richman et al 1987; Volberding et al 1990; Smothers 1991; Race et al 1998; Fel-
lay et al 2001)
Dementia
(Hitchcock 1991; Smothers 1991; Bacellar et al 1994)
Weight loss
(Poznansky et al 1995; Moye et al 1996; Anonymous 1999)
Lymphoma
(Pluda et al 1990)
Diarrhea
Lipodystrophy,
“protease paunch”
(Duesberg and Rasnick 1998; Levy 1998; Brinkman et al 1999; Carr et al 2000;
Fellay et al 2001)
Muscle atrophy
(Richman et al 1987; Dalakas et al 1990; Till and MacDonnell 1990; Hitchcock
1991; Blanche et al 1999)
Mitochondrial dysfunction (Dalakas et al 1990; Blanche et al 1999; Carr et al 2001)
Hepatitis
(Braeu et al 1997; Saves et al 1999; Carr et al 2000, 2001; France 2001)
Birth defects
(Kumar et al 1994; Newschafter et al 1999)
Nephritis
(Fogelman et al 1994)
Lactic acidosis
(Scalfaro et al 1998)
Heart infarct
(Levy 1998; Altman 2001a; Carr et al 2001)
Death
Death
(Dournon et al 1988; Goedert et al 1994; Seligmann et al 1994; Veugelers et al
1994; Fischl et al 1989, 1995; Duesberg 1995c, 1996a; Sabin et al 1996; Anony-
mous 1999; Mocroft et al 1999; de Souza et al 2000; Kuhn et al 2000)
Table 7. Diseases and mortality in HIV-free human babies, and in HIV-free animals
treated with anti-HIV drugs before and after birth (BB, AB).
Species
AIDS-defining
Other disease
References
Human
Babies (AB)
Fever,
Pneumonia
Anemia,
Mitochondrial dysfunction
(Blanche et al 1999), (Heresi et al 1997)
Animals (AB):
Mice, rats,
dogs, monkeys
Lymphopenia,
Weight loss,
Leukemia, T-cell depletion,
Thymic atrophy,
Death of 25/30 mice
Anemia, neutropenia,
Thrombocytopenia, Bone marrow
depletion, Lymphotoxicity, Myelo-
dysplasia,
Muscle atrophy,
Nephrotoxicity
Hepatotoxicity
(Ayers 1988; Cronkite and Bullis 1990;
Thompson et al 1991; McKallip et al
1995; Omar et al 1996; Grossman et al
1997; Inoue et al 1997; Gerschenson et al
2000)
Animals (BB)
Death
Lung, liver, vaginal cancer
Retarded development, Abortion
(Toltzis et al 1993; Olivero et al 1997)
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
395
in 1979 in the US. They even recorded the first nitrite-linked
Kaposi-cases, 3 years before the first description of AIDS.
The following surveys lend further support to the many syn-
chronies between the drug and AIDS epidemics: Duesberg
(1988), Haverkos and Dougherty (1988), Rappoport (1988),
Duesberg (1992), Oppenheimer (1992), Lauritsen (1994),
Haverkos (1996), and Duesberg and Rasnick (1998).
We think that the chronological overlaps between the
epidemics of drug-use and drug-specific AIDS diseases
are epidemiological dose-response curves, and thus cor-
relative proof of principle that drugs cause AIDS.
4.3c HIV-AIDS researchers confirm that recreational
drugs cause AIDS and other diseases – despite efforts to
suppress this information: In their efforts to promote the
view that “HIV is the sole cause of AIDS” (The Durban Dec-
laration 2000), the proponents of the HIV hypothesis try to
exclude all non-HIV causes, particularly the illicit drugs that
are the basis of the competing “lifestyle”-AIDS hypothesis.
For example, the Lancet published in 1993 a Canadian
epidemiological study, “HIV and the etiology of AIDS”,
which found that 88% of AIDS cases in a cohort of
male homosexuals at risk for AIDS had used nitrite inha-
lants and that 75–80% of the same cohort had also used
“cocaine, heroin, amphetamines, lysergic acid dimethyl
amide, or methylenedioxy amphetamine” (Schechter et al
1993). One of the subjects even passed away on an “over-
dose” of recreational drugs during the study. In addition
an undisclosed percentage (but in 1993 certainly a high
percentage, see above) was also prescribed the DNA
chain-terminator AZT as anti-HIV drug (Duesberg 1993a,
c). Thus not a single drug-free AIDS patient was identi-
fied. But, the study concluded, “drugs and sexual activity
is rejected by these data” as causes of AIDS. Neverthe-
less, the authors acknowledged that their study “does not
rule out a role for cofactors . . .”.
Publishing in a high-profile commentary in Nature a
Californian HIV-AIDS team also investigated the ques-
tion, “Does drug use cause AIDS?” (Ascher et al 1993a).
The authors studied 215 HIV-positive homosexual AIDS
patients of which all were either “heavy” or “light” users
of nitrites, of which unnamed percentages had also con-
sumed amphetamines, cocaine and marijuana, and of
which an unnamed percentage was also prescribed the
DNA chain-terminator AZT as anti-HIV drug (Ascher
et al 1993a; Duesberg 1993a, c, 1995a). Thus again, not a
single drug-free patient was identified (Duesberg 1993a,
c; Ascher et al 1995; Ellison et al 1996; Duesberg and
Rasnick 1998). But, the authors concluded that, “when
controlled for HIV serostatus, there is no overall effect
of drug use on AIDS”. Moreover, the authors did not in-
form the reader that their unpublished databank included
45 patients which had used drugs and had AIDS-defining
diseases, but were HIV-free, and thus did not support
their conclusion (Ellison et al 1996). But the authors did
inform the reader that, “The energies of Duesberg and his
followers could better be applied to unraveling the enig-
matic mechanism of the HIV pathogenesis of AIDS”.
Despite numerous other ad hominems, and the fact that
Duesberg was named 13 times, the editor of Nature
vetoed a response, and even published his veto in an arti-
cle, “Has Duesberg a right of reply?” (Maddox 1993).
Science also quoted a toxicologist ready to blame all
consequences of heroin addiction on HIV, because “heroin
is a blessedly untoxic drug” (Cohen 1994).
In an anonymous response to our hypothesis that drugs
cause AIDS (Duesberg 1995b; Duesberg and Rasnick
1998), the National Institutes of Health (NIH) acknow-
ledge drug-AIDS correlations on their website, The evidence
that HIV causes AIDS, but reject causation: “Because
many HIV-infected mothers abuse recreational drugs,
some (unnamed researchers) have argued that maternal
drug use itself causes pediatric AIDS. However, studies
(un-referenced) have consistently shown that babies who
are not HIV-infected do not develop AIDS (per HIV-
AIDS definition), regardless of their mothers’ drug use.”
Despite, “similar rates of alcohol, tobacco, cocaine, heroin
and methadone use …” none of “248 uninfected children”
would develop AIDS (National Institute of Allergy and
Infectious Diseases and National Institutes of Health 2001).
However, the NIH does not mention even one study that
has ever described an AIDS-baby born to an HIV-posi-
tive, but drug-free mother, to prove their website’s claim
that “HIV causes AIDS”. The NIH also does not mention
the AIDS-defining and other birth defects of HIV-free
“crack” (cocaine) babies born to HIV-free drug-addicted
mothers that are described in the literature (Toufexis
1991; Duesberg 1992; Duesberg and Rasnick 1998).
In contrast to the studies selected and promoted by the
NIH, the scientific literature has shown that nearly all
AIDS-babies from the US and Europe were born to
mothers who had used either recreational or anti-HIV
drugs or both during pregnancy (Duesberg and Rasnick
1998), (§ 4.2a and 4.3d, e, table 7).
4.3d Anti-HIV drugs cause AIDS defining and other drug-
specific diseases – regardless of the presence of antibodies
to HIV: The fundamental problem of any chemical anti-
virus “therapy” is that the cell carries out all viral bio-
chemical functions. Thus all anti-viral treatments are
inevitably anti-cell treatments. In the case of HIV, this
problem is compounded by the notorious biochemical
inertia of HIV in antibody-positive people, and by the
extremely low multiplicity of infection of only 1 in 500
T-cells (table 4). Thus in antibody-positive people there
are no HIV functions that could be targeted by DNA
chain-terminators. As a result all treatments designed to
inhibit nucleic acid and protein synthesis of HIV with
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
396
DNA chain-terminators only inhibit cellular nucleic acid
and protein synthesis. Since elimination of the few cells
that are latently infected is clinically not detectable,
“therapeutic” results are typically reported in terms of
various lab markers, primarily the “viral load”, rather
than in restored health (Ho et al 1995; Wei et al 1995;
Palella et al 1998; Hogg et al 2001). Even the term “viral
load” is deceptive, because it suggests that there is a high
virus titer, although infectious virus is typically not detec-
table. Instead this term describes the amount of viral
DNA fragments that can be generated in vitro by the
polymerase chain reaction from RNA of rare, antibody
neutralized virus or of DNA of rare, latently infected
cells isolated from the patient (table 4), (Duesberg 1993b;
Duesberg and Bialy 1996). Nevertheless, the anti-HIV
drugs have the unintended benefits of functioning as true
“anti-biotics”, because of their general toxicity to all
living things. As such they will also reduce the load of
opportunistic microbial diseases that affect most AIDS
patients (table 1), (Cohen 1987; Palella et al 1998). In the
following we briefly review the primary effects of the
DNA chain-terminators and protease inhibitors on the
biochemistry of the cell.
(i) DNA chain-terminators: Currently nearly all anti-HIV
prescriptions include DNA chain-terminators, that were
originally developed 40 years ago, long before AIDS, to
kill growing human cells as cancer therapy by terminat-
ing DNA synthesis (Horwitz et al 1964). Considering
their mechanism of action, the DNA chain-terminators
are inevitably cytotoxic, and thus immunotoxic like most
other chemotherapies (Stedman’s Medical Dictionary
1982; Oliver 2000). DNA chain-terminators were first
licensed as anti-HIV drugs in 1987, although their immu-
notoxicity or bone ”marrow suppression” was immedia-
tely recognized (Kolata 1987; Richman et al 1987), see
also (Nussbaum 1990; Duesberg 1996b). The inevitable
immunotoxicity and lethality of AZT was confirmed in
AIDS patients within less than a year after its licensing as
anti-HIV-AIDS drugs (Kolata 1987; Richman et al 1987;
Dournon et al 1988; Mir and Costello 1988). The label of
a 100 mg-sample from the Sigma Chemical Co, a non-
medical supplier, even advertises the inevitable toxicity
of the DNA chain-terminator AZT with a scull and cross
bones (figure 4a).
Yet, the DNA chain-terminators are currently prescri-
bed at doses of about 500 mg per day (§ 4.2, and below).
For example, a typical prescription flask with 100 capsu-
les of 100 mg Retrovir (AZT) from the medical supplier
Burroughs Wellcome instructs its late user (see below),
“Take 1 capsule 5 times daily”, but does not mention
cellular or human toxicity (see figure 4b). Even HIV-
positive pregnant mothers are prescribed 500 mg of AZT
per day during the second and third trimester of preg-
nancy to reduce the probability of transmission of HIV to
their babies by 17% (from 25% to 8%) – at the cost of
having to treat 100% of the pregnant mothers and babies
with AZT (Connor et al 1994), (see table 6 and particu-
larly table 7 below for consequences).
(ii) HIV protease inhibitors: The HIV protease inhibitors
were designed to inhibit specifically auto-proteolytic
processing of HIV proteins, which is necessary for HIV
assembly (Fields 2001). But since no therapeutic effects
were observed at the low doses at which these inhibitors
“block HIV replication in the test tube” (The Durban
Declaration 2000), the “anti-viral” doses were increased
4–5 orders of magnitude above what is needed to render
HIV noninfectious in vitro, or to 1 to 2 g of inhibitor per
day (Rasnick 1997). The high doses of protease inhibitors
currently administered to patients are at minimum 50
times that needed to completely inhibit the cellular, inte-
stinal aspartyl protease cathepsin D (calculation based
on the Roche inhibitor Saquinavir; the Abbott inhibitor
Ritonivar is 1000 times more potent against cathepsin D
than Saquinavir), (Deeks et al 1997).
Mice in which cathepsin D is deleted develop anorexia,
their “Thymus and spleen undergo massive destruction with
fulminant loss of T and B cells”, and die about 26 days after
birth (Saftig et al 1995). Thus protease inhibitors can cause
at least three AIDS defining diseases, anorexia (weight
loss), T-cell deficiency and death (see § 4e). In addition,
diarrhea – which is also an AIDS defining disease (Centers
for Disease Control 1985, 1986, 1987) – is a common pro-
blem with all the protease inhibitors (table 6).
(iii) Drug cocktails: AZT and other DNA chain-termi-
nators are now typically supplemented by inhibitors of
proteases to form drug “cocktails” (Ho 1995; Palella et al
1998; Day 2000; Stolberg 2001). A daily dose of these
includes about 1 g of one or more DNA chain-terminators
per clinically ill person and 0⋅5 g per asymptomatic HIV-
positive per day (Stolberg 2001) (see also § 4.2b), which
is the equivalent of 1⋅5–3 × 106 molecules of DNA chain-
terminators per body cell!
Here, we present evidence that anti-HIV drugs cause
AIDS defining diseases, other diseases and death, both (i)
in the presence and (ii) in the absence of HIV.
(i) Diseases and death in HIV-positives treated with anti-
HIV drugs: A sudden 10-fold increase in the mortality of
HIV-positive British hemophiliacs, right after the intro-
duction of AZT in 1987, made scientific headlines in
1995, because the increased mortality was attributed to
HIV by the authors of the study, i.e. Darby et al (1995),
as well as by the editor of Nature, “More conviction on
HIV and AIDS” (Maddox 1995). Even the editor of the
Lancet wrote an editorial asking, “Will Duesberg now
concede defeat” (Horton 1995)? Darby et al based their
conclusion on the sudden 10-fold increase of the hemo-
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
397
philiacs’ mortality in 1987, shown in figure 5, on the
facts that the increased mortality was restricted to HIV-
positive hemophiliacs and that the increase was inde-
pendent of the degree of hemophilia (which is inversely
proportional to the life expectancy of the patient).
But, by 1987 transfusions of blood and factor VIII had
already infected most hemophiliacs for a long time. Most
of them were already infected before 1984 (about 75% in
the US), because all blood supplies with HIV antibodies
were banned after the introduction of the HIV-antibody
Figure 4. (a) The label on a bottle containing 100 mg of the DNA chain-terminator AZT from the
Sigma Chemical Co, USA. The advisory on the label reads: “TOXIC. Toxic by inhalation in contact with
skin and if swallowed. Target organ(s): Blood bone marrow. If you feel unwell, seek medical advice
(show the label where possible). Wear suitable protective clothing”. The amount of AZT in the bottle is
one fifth of the daily dose recommended for asymptomatic HIV-positives (§ 4.2b), and of the daily dose
prescribed to pregnant, HIV-positive mothers (§ 4.3d). (b) The label on a prescription flask containing
100 capsules of 100 mg AZT, termed Retrovir, by the medical manufacturer, Burroughs-Wellcome. The
prescription of five daily doses of 100 mg AZT was written in 1992 for the HIV-positive but then AIDS-
free Cesar Schmitz (§ 4.3d). In contrast to the biochemical manufacturer, the medical manufacturer does
not warn about the toxic effects of AZT.
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
398
test in 1984 (Duesberg 1995c, 1996a). Moreover, the
mortality of hemophiliacs was steadily decreasing since
the 1970s until 1987 – despite the presence of HIV
(Duesberg 1995c)! Thus the only new risk of mortality,
in and after 1987, was not HIV, but AZT. Darby et al
even acknowledged “treatment, by prophylaxis against
P. carinii pneumonia or with zidovudine (AZT), has
been widespread for HIV-infected haemophiliacs since
about 1989 (more accurately since 1987)”. The editor
of Nature also pointed out that, “Darby et al failed to
provide full details of the drug regimen followed”
(Maddox 1995). The AZT-mortality hypothesis would of
course also explain why the new hemophilia mortality
was independent of the severity of the hemophilia, as
Darby et al observed. Nevertheless Nature, did not accept
an alternative interpretation, specifically not from “Those
who have made the running in the long controversy over
HIV in AIDS, Dr Peter Duesberg of Berkeley, California,
in particular . . .” (Maddox 1995). But, the Lancet accep-
ted a response, which proposed that AZT treatments were
the probable cause of the sudden increase in mortality of
hemophiliacs (Duesberg 1995d).
According to researchers from the NIH, AZT also in-
creased the mortality of US hemophiliacs 2⋅7 times and
their AIDS risk 4⋅5 times compared to untreated controls
(Goedert et al 1994; Duesberg 1995c). The medical lite-
rature describes many more examples of AIDS defining,
other diseases and deaths that developed in HIV-positive
asymptomatic people or in AIDS patients treated with
anti-HIV drugs, which were not observed in untreated
controls; some of these are summarized in table 6.
The case of Cesar Schmitz, married to an HIV-free
wife and father of an HIV-free healthy child in Miami,
FL, is an example of AZT-mediated mortality that did
not appear in the medical literature (Duesberg 1996b). But
his wife Teresa has recorded his case in sufficient
detail for inclusion in this article. In March 1992, an
asymptomatic Schmitz was found to be HIV-positive at
a medical check-up and pressured by his doctor to start
AIDS prophylaxis by AZT (figure 4b). Immediately after
initiation of AZT treatment, Schmitz developed “nausea,
diarrhea and weight loss”. In 1994 he decided, “against his
doctors will,” to discontinue AZT medication, and “All
of a sudden, like magic, no more symptoms” (Duesberg
1996b). But, in 1998 Schmitz developed lymphoma,
which is a typical, late “side effect” that appears in 46%
of patients 36 months after initiation of AZT therapy
(Pluda et al 1990). In view of this and pressure from his
doctors Schmitz started AZT therapy again. Within months
he was “paralyzed”, suffered from “unbearable cramps”
and became incontinent (probably from mitochondrial
dysfunction, see table 6), which his doctor explained as
“side effects of one of the drugs he was taking”. And in
October 1998 Schmitz passed away (T Schmitz, personal
communication).
(ii) Diseases and death in HIV-free humans and animals
treated with anti-HIV drugs: Table 7 lists rare studies
reporting AIDS-defining and other diseases in HIV-free
humans and animals treated with anti-HIV drugs. Since
all HIV-positive, pregnant mothers are now treated with
AZT during the last 6 months of their pregnancy to reduce
the natural transmission of HIV to 25 to 50% of their
babies, there are now over 50% HIV-free babies born to
these mothers who have all been treated with AZT (Connor
Figure 5. Mortality of HIV antibody-positive (+) and nega-
tive (–) British hemophiliacs after the introduction of the DNA
chain-terminator AZT, alias zidovudine, in 1987 as anti-HIV
therapy. The data are from a study by Darby et al (1995) that
considered HIV to be the cause of the sudden increase of he-
mophilia mortality after 1987. Instead of HIV, which has been
diagnosed in hemophiliacs since 1984, the introduction of AZT
as anti-HIV drug explains the sudden rise in mortality in 1987,
and also the increase in mortality irrespective of the degree of
hemophilia (see § 4.3d).
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
399
et al 1994; The Durban Declaration 2000). Table 7 lists
two rare publications that describe the diseases of these
HIV-free, AZT-treated babies, such as fevers, pneumo-
nia, anemia, and mitochondrial dysfunction. In addition
the table lists studies, which have observed numerous
diseases and deaths in HIV-free animals treated with
anti-HIV drugs. All of these animal studies were publi-
shed after the drugs had been licensed for humans (per-
haps because licenses once issued are almost impossible
to withdraw) and only in specialty journals. Therefore,
these results are not known and not discussed in the
popular and medical AIDS literature.
The anti-HIV treatment-specific diseases and death
summarized in tables 6 and 7 directly support the hypo-
thesis that anti-HIV drugs are at least necessary in the
presence of HIV, and are sufficient in its absence to
cause most AIDS defining-diseases, other drug-specific
diseases, and death. Since about 450,000 US citizens are
currently on DNA chain-terminators and protease inhi-
bitors as prophylaxis against, or therapy of AIDS (see
above), these drugs alone could have been sufficient to
generate all of the 43,158 new AIDS patients reported in
the US in 2001 (Centers for Disease Control and Preven-
tion 2001).
4.3e The AIDS treatment dilemma: Do anti-HIV drugs,
that cause AIDS defining and other diseases, delay pro-
gression to AIDS and reduce mortality?: Despite the
inevitable toxicity of anti-HIV drugs, the over 5000 sig-
natories of the Durban Declaration assert that, “drugs that
block HIV replication in the test tube also” (i) “delay
progression to AIDS”, and (ii) “have reduced AIDS mor-
tality by more than 80%”. However, the authors of the
Declaration have not provided a reference for controlled
studies in support of their assertion. But, they do acknow-
ledge “That it is crucial to develop new antiviral drugs that
. . . have fewer side effects” (The Durban Declaration
2000). Since many doctors share the views of the Declara-
tion, we investigate here the evidence for these claims.
(i) Controlled studies investigating the ability of anti-HIV
drugs to “reduce mortality” and “delay progression to
AIDS”: The licensing study of AZT, performed in 1987 by
the NIH in collaboration with the drug’s manufacturer
Burroughs Wellcome in the US, is the primary placebo-
controlled study set-up to test the ability of AZT to reduce
the mortality of AIDS (Fischl et al 1987; Richman et al
1987). The study showed that, after 4 months on AZT, 1
out of 145 AIDS patients died, whereas 19 out of 139
died in the placebo group. The study interpreted this re-
sult as evidence for reduced mortality by AZT. However,
this interpretation failed to consider that among the 4-
month-survivors of AZT, 30 could only be kept alive
with multiple blood transfusions because their red cells
had been depleted by AZT below survivable levels
(Fischl et al 1987; Duesberg 1992). Thus, without life-
saving transfusions 30 more AZT-recipients would have
died from anemia. In addition many AZT recipients had
developed life-threatening bone marrow suppression, neu-
tropenia, macrocytosis, headaches, insomnia and myalgia,
that augured poorly for their future survival (Richman
et al 1987). Indeed, the low mortality of 1/145 reported
for the first 4 months on AZT, could not be maintained in
a follow-up study, which found the “survival benefits” of
AZT rapidly declining after the original 4 months period.
By 21 months, 42% of the original AZT group had died
and 35% of the control group, which by then had also
received AZT for 12 months on a “compassionate” basis
(Fischl et al 1989). Thus the placebo-controlled, licensing
study did not prove that AZT “reduces AIDS mortality by
more than 80%” compared to the untreated control.
The ability of AZT to “delay the progression to AIDS”
was investigated in 1994 by the largest, placebo-control-
led study of its kind, the British-French Concorde study
(Seligmann et al 1994). This study investigated 1749
HIV-positive, mostly male homosexual subjects divided
into untreated and AZT-treated subgroups for the onset
of AIDS and death. The Concorde study found in 1994
that AZT is unable to prevent AIDS and increases the
mortality of recipients by 25%. In view of this it conclu-
ded, “The results of Concorde do not encourage the early
use of zidovudine (AZT) in symptom-free HIV-infected
adults.” (Seligmann et al 1994). Thus there is no control-
led evidence that anti-HIV drugs “reduce the mortality of
”or “delay progression to AIDS”.
(ii) Uncontrolled studies investigating the mortality of
HIV-positives on HIV drugs: Despite the discouraging
results of these controlled studies, AIDS researchers now
credit the more recently developed anti-HIV drug cock-
tails for a “declining morbidity and
AIDS (Palella et al. 1998). However, the evidence for
“declining morbidity and mortality” is only based on un-
controlled survey studies that investigated how long
HIV-positive, clinically healthy subjects, but mostly from
AIDS risk groups, survived on various anti-HIV drugs.
The largest and most influential of these surveys was
conducted by Palella et al (1998) who investigated in
1998 1255 anti-HIV drug-treated “patients, each of which
had at least one CD4+ count below 100” from nine clin-
ics in the US. However, all of these “patients” were
“nonhospitalized”, AIDS-free subjects. “Patients with a
diagnosis of cytomegalovirus retinitis or M. aviarum
complex disease before study entry or during the first 30
days of follow-up and patients with active P. carinii
pneumonia at the beginning of follow-up were excluded.”
A similar survey investigated in 2001 1219 anti-HIV drug-
treated Canadian HIV-positives with less than 200 CD4+
cells, of which 87% were AIDS-free (Hogg et al 2001).
Neither of these studies mentions drug-free controls. On
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
400
this basis the Palella-study found that the mortality of
initially asymptomatic, HIV-positive people, which are
treated with new anti-HIV drug cocktails, is 8⋅8% (“8⋅8
per 100 person-years”) and the Hogg-study found it is 6⋅7%.
But, in the absence of untreated control groups, the
effects of the new anti-HIV drugs on the morbidity and
mortality of HIV-positive recipients can not be deter-
mined scientifically from the results of these surveys.
However, the average annual AIDS mortality of all HIV-
positives on this planet [including the minority that is on
anti-HIV drugs (The Durban Declaration 2000)] can be
estimated for 2000, the year that falls in between the two
surveys, based on data provided by the WHO and the
Durban Declaration: The WHO and the Declaration report
in 2000 34⋅3 million “living with HIV”, and the WHO
reports 471,451 AIDS cases for 2000 (World Health
Organization 2001b) (obtained by subtracting the WHO’s
cumulative total of 1999 from that of 2000, see also table
4). Thus, even if we assume that all AIDS cases were
fatal in 2000, the resulting global mortality rate of HIV-
positives would only be 1⋅4% – and thus 4 to 6 times
lower than the 6⋅7–8⋅8% mortality rate of HIV-positives
treated with anti-HIV drugs in the US and Canada.
Therefore, the claims that anti-HIV drugs reduce the
mortality of, and delay progression to AIDS are at odds
with the AIDS facts reported by the Durban Declaration
and the WHO. Contrary to these claims, the controlled
trials and uncontrolled surveys listed above prove that
anti-HIV drugs (possibly in conjunction with recreational
drugs) increase the mortality of HIV positives 4- to 6-
fold. It would appear that anti-HIV drugs are prescrip-
tions for, rather than treatments of AIDS.
(iii) Skepticism about anti-HIV drugs in the medical
establishment: Even in the absence of scientifically con-
trolled studies proving the toxicity of the new anti-HIV
drugs, many AIDS doctors and researchers have warned
of the numerous toxic effects of these drugs – even the
Durban Declaration calls for drugs wich “have fewer side
effects”. For example, HIV co-discoverer Jay Levy wrote
in the Lancet, “Caution: should we be treating HIV infec-
tion early? . . . No cancer patient takes three or four che-
motherapeutic drugs for a lifetime. What is overlooked
. . . is that these drugs can be toxic and can be directly
detrimental to a natural immune response to HIV.” (Levy
1998). And retrovirus researcher Etienne De Harven des-
cribes the treatment of AIDS with DNA chain-termi-
nators as a “so-called therapy worse than the disease
itself!” (de Harven 1999).
Because of such concerns about the toxicity of anti-
HIV drugs AIDS doctors have recently introduced “struc-
tured treatment interruption” (Lori et al 2000) or “drug
holidays” (Christensen 2000), to allow the patients to
recover from the toxic effects of the DNA chain-ter-
minators, such as AZT, ddI, and d4T, and of the protease
inhibitors prescribed to kill HIV. In the words of Kendall
Smith from the New York Hospital-Cornell Medical Cen-
ter, “Right now, the disease is life-threatening (he did not
say HIV), on one hand, and the drugs that we have so far
have life-threatening toxicities, on the other hand. It puts us
between a rock and a hard place.” (Christensen 2000).
In view of this the US government has appointed a
panel of AIDS scientists to review the toxic effects of
antiviral medications and issued recommendations to re-
strict prescriptions of anti-HIV drugs that were published
by the New York Times (Altman 2001b):
“Altering a long-held policy, federal health officials
are now recommending that treatment for the AIDS
virus be delayed as long as possible for people with-
out symptoms because of increased concerns over toxic
effects of the therapies. . . . More recently, concern
has grown over nerve damage, weakened bones, unus-
ual accumulations of fat in the neck and abdomen,
diabetes and a number of other serious side effects of
therapy. Many people have developed dangerously
high levels of cholesterol and other lipids in the
blood, raising concern that H.I.V.-infected people
might face another epidemic–of heart disease. . . . Dr
Fauci, who is co-chairman of the panel, said in an in-
terview, ‘We are adopting a significantly more con-
servative recommendation profile’”. (According to
the panel), “Much remains to be learned about how
best to treat H.I.V.-infected individuals”.
However, it is hard to understand, why it should have
taken AIDS researchers 14 years since the introduction of
DNA chain-terminators as anti-HIV drugs (Kolata 1987)
to make these observations and issue warnings about the
“side effects” of these drugs.
In April 2001, the FDA followed up on these concerns
by “ordering drug makers to tone down their upbeat ads
for AIDS medications, calling them ‘misleading’ . . . be-
cause they imply greater efficacy than demonstrated by
substantial evidence, or minimize the risks associated with
HIV drugs” (Russell 2001) – again 14 years after approv-
ing these drugs for currently 450,000 American recipients.
Many other independent observers have since commen-
ted on the “U-turn” of AIDS researchers (Day 2000) from
“Hit HIV early and hard” in 1995 (Ho 1995) to reducing,
skipping and delaying treatments, and even recalling
some anti-HIV drugs (Altman 2001c; Associated Press
2001). Even conservative, nonscientific media such as
Mothering magazine now warn expecting mothers not to
use anti-viral drugs during pregnancy with heart-breaking
accounts of the clinical consequences for the babies, and
of the bewildering pressures by the medical and even
legal authorities on mothers to enforce compliance with
prescriptions of DNA chain-terminators for their babies
(Farber 1998; Gerhard 2001; Hodgkinson 2001).
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
401
But despite a preponderance of evidence against anti-
HIV drugs, these drugs have not been restricted or ban-
ned by any country except South Africa (Cherry 2000).
4.4 Prediction 3: AIDS diseases and epidemics
are not self-limiting via immunity
The drug hypothesis predicts that AIDS is not self-limit-
ing via immunity. Indeed twenty years into the AIDS
epidemics, there is no evidence of individual immunity
against AIDS, nor is there any evidence that any of the
AIDS epidemics is self-limiting (World Health Organiza-
tion 1999; The Durban Declaration 2000; Centers for
Disease Control and Prevention 2001), (see figure 1a, c).
According to the Durban Declaration, “there is no end in
sight”. Indeed the chronologies of the current AIDS epi-
demics conform exactly to the time courses of epidemics
of chemical diseases that are not self-limiting, such as the
American drug epidemic shown in figure 2, and the epi-
demics of smoking and of subsequent lung cancers in
England, shown in figure 3b.
4.5 Prediction 4: No AIDS in the absence of
anti-viral and recreational drugs, despite HIV
To test this prediction, HIV antibody-positive people,
who are not using drugs, must be identified who survive
the average hypothetical latent period from HIV to AIDS
of 5–10 years (§ 3, table 4). The following examples
meet this prediction.
In 2002 the San Francisco Chronicle described a small
group of drug-free and AIDS-free long-term survivors of
HIV. Among them is a healthy artist who is HIV-positive
for 23 years (based on frozen blood samples) and was
“chastised by his doctors when he refused to start taking
medication” (Hendrix 2002). Further, a 1-year old HIV-
positive, AZT-treated baby girl with severe muscle pain,
insomnia, nausea and failure to grow was taken off AZT
treatments in 1992 based on our hypothesis; as a result
the baby immediately recovered (Duesberg 1996b). Now,
at the age of 11, she is a completely normal, healthy kid,
and a leading player in her school’s soccer team (Sheryl
and Steve Nagel, personal communication). In addition,
People magazine just described a healthy woman who is
HIV-positive for an estimated 15 years, and “needs no
medication”. The woman has since founded a support
group, termed Center for Positive Connections, for HIV-
positive heterosexuals in Miami (Cheakalos and Rosza
2002). In Los Angeles, Christine Maggiore is HIV-posi-
tive since 1992, has given birth to two very healthy chil-
dren, ages 1 and 5, and has never taken anti-HIV drugs.
Maggiore, a former HIV-AIDS counselor, has since also
founded a support group, Alive & Well, and has written a
book, What if everything you thought you knew about
AIDS was wrong?, to instruct HIV-positives not to use
anti-HIV drugs (Maggiore 2000). An appendix of the book
features letters from 34 Maggiore-graduates, all living
over 10 years with HIV but without anti-HIV drugs, or
after having discontinued such drugs.
Even HIV-AIDS researchers have inadvertently confir-
med our prediction of no AIDS in drug-free HIV-positi-
ves. For example, David Ho, signatory of the Durban
Declaration, points out that in a group of “long-term
survivors” of HIV studied in his lab, “none had received
antiretroviral therapy” (Cao et al 1995). In a parallel pub-
lication, Pantaleo et al studying a group of long-term
“non-progressors” of HIV have made the same observation
(Pantaleo et al 1995). Ho et al recently attributed long-
term survival to some special human proteins, termed
“defensins” (Zhang et al 2002), but acknowledged perso-
nally that all long-term survivors had again abstained
from anti-HIV therapies (David Ho, personal communi-
cation). One wonders why any humans would ever get
sick from HIV, if the human genome encodes HIV defen-
sins! Munoz reported that none of the long-term survi-
vors of the largest, federally funded study of AIDS risk
factors of homosexual men, the MACS study, had used
AZT (Munoz 1995). Fahey et al observed that among
HIV-positive male homosexuals with less than 200 T-cells
per µl, “45% of the group who were AIDS-free > or = 3
years after CD4+ cells fell below 200 × 106/l had not
used these (anti-HIV) treatments.” (Hoover et al 1995).
According to a university magazine, AIDS researchers
Abrams and Levy from the University of California at
San Francisco have lectured in 1998 on drug-free long-
term survivors of HIV to their medical students (Tanaka
1996; Duesberg and Rasnick 1998). Levy also published
in 1998 in the Lancet, that “effective antiviral immune
response is characteristic of long-term survivors who
have been infected for over 20 years, have no symptoms,
and have not been on any therapy” (Levy 1998). In 1999,
Pitcher et al also described a group of 9 “long-term non-
progressors (with) untreated HIV-1 infection for 7–15
years”, compared to controls with a “decline of (T cells)
with antiretroviral therapy” (Pitcher et al 1999). An Aus-
tralian research team described a group of untreated HIV-
positives who were infected by blood transfusions but did
not develop AIDS 10 years later (Learmont et al 1992).
Further, Migueles et al (2000) reported that none of 13
long-term survivors had received “antiretroviral therapy”.
Carr et al (2001) observed even recovery from fatal
hypertension, liver failure and mitochondrial dysfunction
after discontinuation of antiviral drugs that had been pre-
scribed to a previously healthy HIV-positive man. Thus
HIV-AIDS researchers confirm our prediction that HIV-
positives, who do not use drugs, do not develop AIDS or
may even recover from it.
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
402
In an effort to obtain independent proof that abstaining
from anti-HIV drugs and recreational drugs is sufficient
to survive HIV-infection or even to recover from AIDS,
one of us, CK, in 1985 initiated a study of AIDS
patients from Kiel, Germany, who have volunteered to
abstain from anti-HIV treatments. Remarkably, only 8%
(3 of 36) of the patients not treated with anti-HIV drugs
have died since their HIV antibodies were first detected,
two of them 16 years and one 10 years after their first
diagnosis of antibodies against HIV (table 8). Most have
recovered from their initial AIDS-indicator symptoms.
By contrast, 63% of all German AIDS patients (11,700
out of 18,700) of which most were treated since 1987
with anti-HIV drugs have died (Robert Koch Institut
2000). Thus our relatively small sample supports the
hypothesis that without anti-HIV drugs and/or recrea-
tional drugs HIV fails to cause AIDS. Indeed without
drugs AIDS patients recover, despite the presence of HIV.
4.6 In sum, the chemical AIDS-hypothesis explains
the AIDS facts, and resolves all paradoxes
of the HIV-AIDS hypothesis
Our review shows that the chemical-AIDS hypothesis
explains all AIDS facts: the non-random distribution of
Table 8. Long-term HIV survivors not treated with antiviral drugs and abstaining from illicit,
psychoactive drugs from the Kiel-Koehnlein study begun in 1985.
Case
Date
HIV+
Age
Sex
Clinic
CD4
Illicit
drugs
Treatment
Death
1
1985
52 m-homo
Herpes zoster
256 ?
None
2
1985
45 f
Asymptomatic
None
3
1985–2001
43 m
PCP, TB
4 iv
Antibiotics
Heart failure
4
1985–2001
42 m-homo
Kaposi,
PCP
Nitrites
None
Kaposi
5
1985
35 m
Psoriasis
None
6
1985
38 f
Salmonella sepsis
28
Antibiotics
7
1985
31 m
Hemophilia, lymphadenopathy
low
8
1985
30 m
Hemophilia
325
None
9
1986
17 f (black)
Asymptomatic
450
None
10
1986
31 m
Asymptomatic
11
1988
32 f
Asymptomatic
None
12
1989
49 f
Candida, TB
28 iv
Antibiotics
13
1990
34 m-homo
Coli-Meningitis,
Hydrocephalus
85 Nitrites
Shunt
14
1991
6 m
Pneumonia
Antibiotics
15
1991
31 f
Asymptomatic
None
16
1991–2001
36 f
Toxoplasmosis
1993–94 AZT,
antibiotics
Toxoplasmosis
17
1992
33 f
Asymptomatic
460
None
18
1993
7 f
Asymptomatic
None
19
1996
52 m-homo
Facial paresis
540 Nitrites
None
20
1996
39 m-homo
Asymptomatic
485 Nitrites
None
21
1996
38 m
Pneumonia, Sinusitis
53
Antibiotics
22
1997
44 m-homo
Colitis
Nitrites
None
23
1997
37 m-homo
Asymptomatic
223 Nitrites
None
24
1997
37 m-homo
Thrombocytopenia
700 Nitrites
Cortisone
25
1997
34 m-homo
Asymptomatic
220 Nitrites
None
26
1997
33 m-homo
Lymphadenopathy
None
27
1997
31 m-homo
Thrombocytopenia
357 Nitrites
Cortisone
28
1997
3 m
Pneumonia
Antibiotics
29
1998
31 m-homo
Diarrhea
Nitrites
None
30
1998
40 m-homo
Condyloma, Candida
107 Nitrites
None
31
1998
39 m-homo
Diarrhea
187 Nitrites
None
32
1998
27 m-homo
TB of the bowel
18
Antibiotics
33
2000
35 m-homo
Asymptomatic
None
34
2000
31 m-homo
Lymphadenopathy, EBV
None
35
2000
30 m-homo
Asymptomatic
428
None
36
2000
27 f
Lymphadenopathy, EBV
107
None
m, Male; f, female; PCP, Pneumocystis carinii pneumonia; EBV, Epstein-Barr virus; AZT, azidothymidine; TB, tuberculosis. Evidence
for illicit drug use is self reported; iv, intravenous drug use.
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
403
drug-AIDS in the US and Europe, the risk-group-specific
AIDS diseases in the US and Europe as consequences of
risk-group-specific drugs, the random distribution of mal-
nutrition-AIDS in Africa, the non-contagiousness of chemi-
cal AIDS, the absence of natural immunity against
chemical AIDS, the lifestyle-dependent onset of AIDS
diseases – unrelated to, but typically long after infection
by HIV, and the time courses of the AIDS epidemics of
the US and Europe as consequences of the drug epidemics.
In addition chemical AIDS proves that HIV is not
necessary for even one AIDS-defining disease, because
(i) drugs and malnutrition cause drug- and malnutrition-
specific AIDS diseases regardless of the presence of
HIV, because (ii) in HIV antibody-positives and nega-
tives the risk of developing AIDS is proportional to the
degree or lifetime dosage of drug use, and (iii) because
all AIDS diseases have been diagnosed in HIV-free AIDS
risk groups by AIDS researchers (Duesberg 1993d) and
also long before the AIDS era (Stedman’s Medical Diction-
ary 1982). Thus HIV meets all criteria of a harmless pas-
senger virus, laid out in table 4 and described previously
(Duesberg 1994; Duesberg and Rasnick 1998). In this
way our proposal resolves the fundamental paradox of the
HIV-AIDS hypothesis: the paradox that a latent, non-
cytopathic and immunologically neutralized retrovirus,
that is only present in less than 1 out of 500 susceptible
T-cells and rarely expressed in a few of those, would
cause a plethora of fatal diseases in sexually active,
young men and women. And, that the plethora of diseases
attributed to this virus would not show up for 5–10 years
after infection.
The chemical AIDS hypothesis could be readily refu-
ted by any of the following experiments:
(i) Demonstrate that in two matched groups, differing
only with regard to HIV infection, HIV-positives develop
AIDS but HIV-negatives do not (above the low, long-
established risk of AIDS defining diseases in the general
population). HIV antibody-positive and negative recruits
from the US Army, which tests routinely for HIV, would
be ideal for this experiment since their health, lifestyles
and age are closely matched.
(ii) Demonstrate that in two matched groups of intrave-
nous drug users, differing only in the presence of HIV,
only the HIV-positives develop AIDS diseases.
(iii) Demonstrate that in two matched groups of HIV-
positive humans, differing only in the addiction to recrea-
tional drugs, both groups have the same incidence of
AIDS-defining diseases.
(iv) Demonstrate that in two matched groups of HIV-free
humans or animals, differing only with regard to the
addiction to or treatment with recreational drugs, neither
group would develop AIDS defining diseases over time.
(v) Demonstrate that in two matched groups of HIV-
positives, differing only in the treatment with anti-HIV
drugs, the untreated group develops AIDS long before the
treated group.
(vi) Demonstrate that in two matched groups of pregnant,
HIV-positive mothers, differing only in the now standard
treatment with AZT during the last two trimesters, those
treated with AZT are free of abortions and deliver
healthy babies, but those who are not treated either abort
spontaneously or deliver babies with AIDS.
(vii) Demonstrate that in two groups of HIV-positive
hemophiliacs matched for age and lifetime dosage of fac-
tor VIII, differing only in anti-HIV treatments, those who
are untreated have a higher mortality and a higher AIDS
risk than treated controls.
Although the controlled studies proposed here follow
classical, scientific standards, they are not available in
the huge AIDS literature. This is surprising in view of the
many AIDS advocacy groups or “activists” reviewing
AIDS research for flaws and for new clues. The lack of
adequately controlled studies of the long-term effects of
recreational drugs and anti-HIV drugs in animals is parti-
cularly surprising, because all of these drugs and research
funds for AIDS are abundant. Yet despite the scientific
intolerance of current AIDS science for alternative hypo-
theses (Weiss and Jaffe 1990; Cohen 1994; O’Brien and
Goedert 1996), the pathogenicity of most of the chemi-
cals proposed here to cause AIDS – illicit drugs, antiviral
drugs, and malnutrition – has de facto already been pro-
ved – even by HIV-AIDS researchers, despite their
efforts to the contrary [see above, tables 6 and 7 and
Duesberg and Rasnick (1998)].
Suppose the chemical-AIDS hypothesis were confir-
med and accepted: AIDS would be entirely preventable
by banning anti-HIV drugs, by publicizing that recreatio-
nal drugs cause AIDS and by adequate nutrition. More-
over, many AIDS patients could still be saved from fatal
damage by drug intoxication, if their AIDS-defining dis-
eases were treated with time-proven, disease-specific
medications. Such testable predictions are the hallmarks
of a good hypothesis.
So, why do current AIDS researchers not investigate
and not even consider the role of chemicals in AIDS
or study other non-HIV-AIDS theories to solve the AIDS
dilemma? The following is an attempt to answer this
question.
5. Epilogue
5.1 Why is AIDS research not free to investigate
non-HIV hypotheses?
The probable answer to the question, why HIV-AIDS
researchers do not study or fund non-HIV-AIDS theories,
lays in the structure of the large, government-sponsored
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
404
research programs that dominate academic research since
World War II (Duesberg 1996b). Such programs favour
individual investigators who contribute to the establish-
ment a maximum of data and a minimum of controversy.
However, if individual researchers move into new direc-
tions, that threaten the scientific and commercial invest-
ments of the establishment, the establishment can impose
various sanctions via the “peer review system”. The most
powerful of these are denial of funding and of publi-
cation.
The peer review system derives its power from the
little known practice of governments to deputize their
authority to distribute funds for research to committees of
“experts”. These experts are academic researchers distin-
guished by outstanding contributions to the current esta-
blishment. They alone review the merits of research
applications from their peers, and they have the right to
elect each other to review committees. Outwardly, this
“peer review system” appears to the unsuspecting govern-
ment and taxpayer as the equivalent of a jury system –
free of all conflicts of interest. But, in view of the many
professional and commercial investments in and benefits
from their expertise, and even of the rewards from their
universities and institutions for the corresponding over-
heads and partnerships – all legal in the US since presi-
dent Reagan – ”peer reviewers” do not fund applications
that challenge their own interests (Duesberg 1996b; Lang
1998; Zuger 2001). Since “peer review” is protected by
anonymity, does not allow the applicant personal repre-
sentation or an independent representative, nor a say or
even a veto in the selection of the “jury”, and does not
allow an appeal, its powers to defend the orthodoxy are
unlimited. The corporate equivalent of academia’s peer
review system” would be to give General Motors and
Ford the authority to review and veto all innovations by
less established carmakers competing for the consumer.
Even the professional journals and the science writers
of the public media comply with the interests of govern-
ment-funded majorities because they depend on their
monthly “scientific breakthroughs”, the lucrative adver-
tisements from their companies, and the opinion of their
subscribers. For example, an early precursor of this arti-
cle was written in response to an open invitation from a
pharmacology-journal over 3 years ago. But, after consi-
derable pressure on the journal from anonymous “AIDS
experts”, the editor requested a reduced article, which
was neither accepted nor rejected. Instead, the editor
simply dropped all further correspondence. Subsequently,
the editor of a prestigious German-based science journal
invited another precursor of this article 2 years ago,
which received two favourable reviews in short order.
But before the manuscript could be revised, the editor
informed us that the publisher was concerned about los-
ing subscribers if our paper were published and ceased all
further correspondence. It is this passive resistance that
can grind down even the most determined truth seeker.
However, the mere potential to resolve the agony of
AIDS by alternative hypotheses, such as ours, should be
sufficient reason to replace the medieval “peer review
system” by a modern jury system without conflicts of
interest and with rights for representation and appeals of
the applicant. If the current, unproductive AIDS estab-
lishment objects, because AIDS-science is too complex
to be understood by non-HIV-AIDS scientists, funding
should be withheld until the AIDS establishment finds
ways to explain the complexity and merits of its expertise
to other scientists.
Acknowledgements
We gratefully acknowledge critical and challenging
information from the presidential AIDS advisory panel
of South African president Thabo Mbeki, especially those
who joined us in publishing a rebuttal to the Durban
declaration (Stewart et al 2000). Harry Haverkos (CDC/
FDA, Rockville, MD), Phil Johnson (UC Berkeley),
Roland Scholz (Institut fuer Physiologische Chemie, Uni-
versity of Muenchen, Germany), David Steele (Attorney,
San Francisco), and Rudi Werner (University of Miami,
School of Medicine) are acknowledged for providing
critical comments and specific information. We also
appreciate expert technical assistance in preparing the
manuscript from Sigrid Duesberg, and the figures from
Ruhong Li (UC Berkeley). We thank philanthropists
Michael S Kennedy (Panama City, FL), Christopher
Morrill (San Anselmo, CA), Robert Leppo (San Francisco,
CA), an American foundation that prefers to be anony-
mous, the Abraham J and Phyllis Katz Foundation (New
York), and other private sources for support.
References
Abouya Y L, Beaumel A, Lucas S, Dago-Akribi A, Coulibaly
G, N’Dhatz M, Konan J B, Yapi A and De Cock K M 1992
Pneumocystis carinii pneumonia. An uncommon cause of
death in African patients with acquired immunodeficiency
syndrome; Am. Rev. Respir. Dis. 145 617–620
Achard C, Bernard H and Gagneux C 1909 Action de la mor-
phine sur les proprietes leucocytaires; leuco-diagnostic du
morphinisme; Bull. Mem. Soc. Med. Hopitaux Paris 28 3rd
Series 958–966
Adams J 1989 AIDS: The HIV myth (New York: St. Martin’s
Press)
Alcabes P, Schoenbaum E E and Klein R S 1993 Correlates of
the rate of decline of CD4+ lymphocytes among injection
drug users infected with the human immunodeficiency virus;
Am. J. Epidemiol. 137 989–1000
Altman L 2001a The AIDS questions that linger; New York
Times, New York, January 30, p. F1
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
405
Altman L 2001b US Panel seeks Changes in Treatment of
AIDS Virus; New York Times, New York, February 4, p. 16
Altman L 2001c US warns doctors to limit use of anti-HIV
drug; New York Times, New York, January 5, p. A12
Altman L K 1984 Researchers believe AIDS virus is found;
New York Times, New York, April 24, p. C1, C3
Altman L K 2002 Many Americans with HIV don’t know it or
don’t seek care study shows; New York Times, New York,
February 26, p. A20
Anand R, Reed C, Forlenza S, Siegal F, Cheung T and Moore J
1987 Non-cytocidal natural variants of human immunodefi-
ciency virus isolated from AIDS patients with neurological
disorders; Lancet 2 234–238
Anderson R M 1996 The spread of HIV and sexual mixing pat-
terns; in AIDS in the World II (Oxford: Oxford University
Press) pp 71–86
Anonymous 1999 Rapid disease progression in HIV-1 perina-
tally infected children born to mothers receiving zidovudine
monotherapy during pregnancy. The Italian register for HIV
Infection in Children; Aids 13 927–933
Archer C B, Spittle M F and Smith N P 1989 Kaposi’s sarcoma
in a homosexual – 10 years on; Clin. Exp. Dermatol. 14 233–
236
Archibald C P, Schechter M T, Le T N, Craib K J P, Montaner
J S G and O’Shaughnessy M V 1992 Evidence for a sexually
transmitted cofactor for AIDS-related Kaposi’s sarcoma in a
cohort of homosexual men; Epidemiology 3 203–209
Ascher M S, Sheppard H W, Winkelstein W Jr and Vittinghoff
E 1993a Does drug use cause AIDS?; Nature (London) 362
103–104
Ascher M S, Sheppard H W, Winkelstein W Jr and Vittinghoff
E 1993b Aetiology of AIDS; Lancet 341 1223
Ascher M S, Sheppard H W and Winkelstein W Jr 1995 AIDS-
associated Kaposi’s sarcoma (letter); Science 267 1080
Associated Press 2001 Delaying HIV drugs may be OK; New
York Times, New York, November 27
Ayers K M 1988 Preclinical Toxicology of Zidovudine; Am. J.
Med. (Suppl. 2A) 85 186–188
Bacellar H, Munoz A, Miller E N, Cohen B A, Besley D,
Selnes O A, Becker J T and McArthur J C 1994 Temporal
trends in the incidence of HIV-1-related neurologic diseases:
Multicenter AIDS Cohort Study 1985–1992; Neurology 44
1892–1900
Barre-Sinoussi F, Chermann J C, Rey F, Nugeyre M T, Cha-
maret S, Gruest C, Dauget C, Axler-Blin C, Vezinet-Brun F,
Rouzioux C, Rozenbaum W and Montagnier L 1983 Isolation
of a T-lymphotropic retrovirus from a patient at risk for
acquired immune deficiency syndrome (AIDS); Science 220
868–871
Bayley A C 1984 Aggressive Kaposi’s sarcoma in Zambia,
1983; Lancet 1 1318–1320
Beral V, Peterman T A, Berkelman R L and Jaffe H W 1990
Kaposi’s sarcoma among persons with AIDS: a sexually
transmitted infection?; Lancet 335 123–128
Blanche S, Rouzioux C, Moscato M L G, Veber F, Mayaux
M J, Jacomet C, Tricoire J, Deville A, Vial M, Firtion G, de
Crepy A, Douard D, Robin M, Courpotin C, Ciran-Vineron
N, Le Deist F, Griscelli C and the HIV Infection in New-
borns French Collaborative Study Group 1989 A prospective
study of infants born to women seropositive for human im-
munodeficiency virus type 1; N. Engl. J. Med. 320 1643–1648
Blanche S, Tardieu M, Rustin P, Slama A, Barret B, Firtion G,
Ciraru-Vigneron N, Lacroix C, Rouzioux C, Mandelbrot L,
Desguerre I, Rotig A, Mayaux M J and Delfraissy J F 1999
Persistent mitochondrial dysfunction and perinatal exposure to
antiretroviral nucleoside analogues; Lancet 354 1084–1089
Blattner W A, Gallo R C and Temin H M 1988 HIV causes
AIDS; Science 241 514–515
Botnick M R, Heath K V, Cornelisse P G, Strathdee S A,
Martindale S L and Hogg R S 2002 Correlates of suicide
attempts in an open cohort of young men who have sex with
men; Can. J. Public Health 93 59–62
Braeu N, Leaf H L, Wieczorck R L and Margolis D M 1997
Severe hepatitis in three AIDS patients treated with Indi-
navir; Lancet 349 924–925
Brandt A M 1988 AIDS in historical perspective: Four lessons
from the history of sexually transmitted diseases; Am. J. Pub-
lic Health 78 367–371
Bregman D J and Langmuir A D 1990 Farr’s law applied to
AIDS projections; J. Am. Med. Assoc. 263 50–57
Brinkman K, Smeitink J A, Romijn J A and Reiss P 1999 Mito-
chondrial toxicity induced by nucleoside-analogue reverse-
transcriptase inhibitors is a key factor in the pathogenesis of
antiretroviral-therapy-related lipodystrophy; Lancet 354
1112–1115
Bull S S, Piper P and Rietmeijer C 2002 Men who have sex
with men and also inject drugs-profiles of risk related to the
synergy of sex and drug injection behaviors; J. Homosex 42
31–51
Cairns J 1978 Cancer: science and society (San Francisco: W H
Freeman)
Cairns J 1997 Matters of life and death; perspectives on public
health, molecular biology, cancer and the prospects for the
human race (Princeton, New Jersey: Princeton University Press)
Cao Y, Quin L, Zhang L, Safrit J and Ho D D 1995 Virologic
and Immunologic Characterization of Long-Term Survivors
of Human Immunodeficiency Virus Type 1 Infection; N.
Engl. J. Med. 332 201–208
Carr A, Miller J, Law M and Cooper D A 2000 A syndrome of
lipoatrophy, lactic acidaemia and liver failure dysfunction
with HIV nucleoside analogue therapy: contribution to pro-
tease inhibitor-associated lipodystrophy syndrome; Aids 14
F25–F32
Carr A, Morey A, Mallon P, Williams D and Thorburn D R
2001 Fatal portal hypertension, liver failure, and mitochon-
drial dysfunction after HIV-1 nucleoside analogue-induced
hepatitis and lactic acidaemia; Lancet 357 1412–1414
Centers for Disease Control 1981a Koposi's sarcoma and Pneu-
mocystis pneumonia among homosexual men – New York city
and California; Morb. Mortal. Weekly Rep. 30 305–308
Centers for Disease Control 1981b Update on Acquired Immune
Deficiency Syndrome (AIDS); Morb. Mortal. Weekly Rep. 31
507–514
Centers for Disease Control 1985 Revision of the case defini-
tion of AIDS for national reporting – United States; Morb.
Mortal. Weekly Rep. 34 373–375
Centers for Disease Control (ed.) 1986 Reports on AIDS pub-
lished in the Morbidity and Mortality Weekly Report, June
1981 through February 1986 (US Dept. of Health and
Human Services, National Technical Information Service,
Springfield, VA)
Centers for Disease Control 1987 Revision of the CDC sur-
veillance case definition for acquired immunodeficiency syn-
drome; Jama 258 1143–1154
Centers for Disease Control 1992 1993 revised classification
system for HIV infection and expanded surveillance case
definition for AIDS among adolescents and adults; Morb.
Mortal. Weekly Rep. 41 (No. RR17) 1–19
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
406
Centers for Disease Control and Prevention 1997 US HIV and
AIDS cases reported through December 1997; Year-end
Edition 9 1–43
Centers for Disease Control and Prevention 2001 US HIV and
AIDS cases reported through December 2001; HIV/AIDS
Surveillance Rep. 13 1–44
Cheakalos C and Rosza L 2002 Positive Approach; People, 4
March, 95–96
Cherry M 2000 Mbeki gives AIDS scientists the cold shoulder;
Nature (London) 406 113
Christensen D 2000 Taking a break; Can interrupting their
treatment benefit HIV-infected people?; Sci. News 157 248–
249
Clark S J, Saag M S, Decker W D, Campbell-Hill S, Roberson
J L, Veldkamp P J, Kappes J C, Hahn B H and Shaw G M
1991 High titers of cytopathic virus in plasma of patients
with symptomatic primary HIV-infection; N. Engl. J. Med.
324 954–960
Clinton W and The White House 1996 The National Drug
Control Strategy (Washington DC: The White House)
Coffin J, Haase A, Levy J A, Montagnier L, Oroszlan S, Teich
N, Temin H, Varmus H, Vogt P and Weiss R 1986 Human
immunodeficiency viruses; Science 232 697
Cohen J 1993 HHS: Gallo guilty of misconduct; Science 259
168–170
Cohen J 1994 The Duesberg Phenomenon; Science 266 1642–
1649
Cohen J 2003 HIV/AIDS. Vaccine results lose significance
under scrutiny; Science 299 1495
Cohen S S 1987 Antiretroviral therapy for AIDS; N. Engl. J.
Med. 317 629
Colebunders R, Mann J, Francis H, Bila K, Izaley L, Kakonde
N, Kabasele K, Ifoto L, Nzilambi N, Quinn T, van der Groen
G, Curran J, Vercauten B and Piot P 1987 Evaluation of
a clinical case definition of Acquired Immunodeficiency
Syndrome in Africa; Lancet 1 492–494
Colfax G N, Mansergh G, Guzman R, Vittinghoff E, Marks G,
Rader M and Buchbinder S 2001 Drug use and sexual risk
behavior among gay and bisexual men who attend circuit
parties: a venue-based comparison; J. Acquir. Immune. Defic.
Syndr. 28 373–379
Connor E M, Sperling R S, Gelber R, Kiselev P, Scott G,
O’Sullivan M J, VanDyke R, Bey M, Shearer W, Jacobson
R L, Jimenez E, O’Neill E, Bazin B, Delfraissy J-F, Culnane
M, Coombs R, Elkins M, Moye J, Stratton P, Balsley J and
Pediatric AIDS Clinical Trials Group Protocol 076 Study
Group 1994 Reduction of Maternal-Infant Transmission of
Human Immunodeficiency Virus Type 1 With Zidovudine
Treatment; N. Engl. J. Med. 331 1173–1180
Costello R B (ed.) 1995 Webster’s College Dictionary (New
York: Random House)
Craib K J, Weber A C, Cornelisse P G, Martindale S L, Miller
M L, Schechter M T, Strathdee S A, Schilder A and Hogg
R S 2000 Comparison of sexual behaviors unprotected sex
and substance use between two independent cohorts of gay
and bisexual men; Aids 14 303–311
Cronkite E P and Bullis J 1990 In vivo toxicity of 3′-azido-2′,
3′-dideoxythymindine (AZT) on CBA/Ca mice; Int. J. Cell
Cloning 8 332–345
Curran J, Lawrence D N, Jaffe H, Kaplan J E, Zyla L D, Cham-
berland M, Weinstein R, Lui K-J, Schonberger L B, Spira
T J, Alexander W J, Swinger G, Ammann A, Solomon S,
Auerbach D, Mildvan D, Stoneburner R, Jason J M, Haver-
kos H W and Evatt B L 1984 Acquired immunodeficiency
syndrome (AIDS) associated with transfusions; N. Engl. J.
Med. 310 69–75
Curran J W, Morgan M W, Hardy A M, Jaffe H W, Darrow
W W and Dowdle W R 1985 The epidemiology of AIDS:
current status and future prospects; Science 229 1352–1357
Daar E S, Moudgil T, Meyer R D and Ho D D 1991 Transient
high levels of viremia in patients with primary human immu-
nodeficiency virus type 1 infection; N. Engl. J. Med. 324
961–964
Dalakas M C, Illa I, Pezeshkpour G H, Laukaitis J P, Cohen B
and Griffin J L 1990 Mitochondrial myopathy caused by long-
term zidovudine therapy; N. Engl. J. Med. 322 1098–1105
Darby S C, Ewart D W, Giangrande P L F, Dolin P J, Spooner
R J D, Rizza C R and on behalf of the UK Haemophilia
Centre Directors’ Organisation 1995 Mortality before and
after HIV infection in the complete UK population of hae-
mophiliacs (letter); Nature (London) 377 79–82
Darrow W W, Echenberg D F, Jaffe H W, O’Malley P M,
Byers R H, Getchell J P and Curran J W 1987 Risk factors
for human immunodeficiency virus (HIV) infections in
homosexual men; Am. J. Publ. Health 77 479–483
Day M 2000 No more cocktails; New Scientist, 16 December, p. 7
de Harven E 1999 Viral etiology of human cancer: a historical
perspective; Haematologica 84 385–389
de Souza R S, Gomez-Marin O, Scott G B, Guasti S,
O’Sullivan M J, Oliveira R H and Mitchell C D 2000 Effect
of prenatal zidovudine on disease progression in perinatally
HIV-1-infected infants; J. Acquir. Immune Defic. Syndr. 24
154–161
Deeks S G, Smith M, Holodniy M and Kahn J O 1997 HIV-1
protease inhibitors. A review for clinicians; Jama 277 145–
153
Diamond C, Thiede H, Perdue T, MacKellar D, Valleroy L A
and Corey L 2001 Seroepidemiology of human herpesvirus 8
among young men who have sex with men; Sex Transm. Dis.
28 176–183
Dournon E, Matheron S, Rozenbaum W, Gharakhanian S,
Michon C, Girard P M, Perrone C, Salmon D, DeTruchis P,
Leport C and the Claude Bernard Hospital AZT Study Group
1988 Effects of zidovudine in 365 consecutive patients with
AIDS or AIDS-related complex; Lancet 2 1297–1302
Downs A M, Ancelle R A, Jager H J and Brunet J B 1987 AIDS
in Europe: current trends and short-term predictions estimated
from surveillance data, January 1981–June 1986; Aids 1 53–
57
Duesberg P and Bialy H 1996 Duesberg and the Right of Reply
According to Maddox – Nature; in AIDS: Virus- or drug in-
duced? (ed.) P H Duesberg (Dordrecht: Kluwer) pp 111–125
Duesberg P H 1987 Retroviruses as carcinogens and pathogens:
expectations and reality; Cancer Res. 47 1199–1220
Duesberg P H 1988 HIV is not the cause of AIDS; Science 241
514–516
Duesberg P H 1992 AIDS acquired by drug consumption and
other noncontagious risk factors; Pharmacol. Therapeutics
55 201–277
Duesberg P H 1993a Aetiology of AIDS; Lancet 341 1544
Duesberg P H 1993b HIV and AIDS; Science 260 1705–1706
Duesberg P H 1993c HIV and the aetiology of AIDS; Lancet
341 957–958
Duesberg P H 1993d The HIV gap in national AIDS statistics;
Biotechnology 11 955–956
Duesberg P H 1994 Infectious AIDS – stretching the germ theory
beyond its limits; Int. Arch. Allergy Immunol. 103 131–142
Duesberg P H 1995a AIDS Data; Science 268 350–351
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
407
Duesberg P H 1995b “The Duesberg-Phenomenon”: Duesberg
and Other Voices (letter); Science 267 313–314
Duesberg P H 1995c Foreign-protein-mediated immunodefi-
ciency in hemophiliacs with and without HIV; Genetica 95
51–70
Duesberg P H 1995d Is HIV the cause of AIDS? (letter); Lancet
346 1371–1372
Duesberg P H 1996a Commentary: non-HIV hypotheses must
be studied more carefully; Br. Med. J. 312 210–211
Duesberg P H 1996b Inventing the AIDS Virus (Washington:
Regnery Publishing Inc.)
Duesberg P H and Rasnick D 1998 The AIDS dilemma: drug
diseases blamed on a passenger virus; Genetica 104 85–
132
Dukers N H, Renwick N, Prins M, Geskus R B, Schulz T F,
Weverling G J, Coutinho R A and Goudsmit J 2000 Risk fac-
tors for human herpesvirus 8 seropositivity and seroconver-
sion in a cohort of homosexual men; Am. J. Epidemiol. 151
213–224
Durack D T 1981 Opportunistic infections and Kaposi’s sar-
coma in homosexual men; N. Engl. J. Med. 305 1465–1467
Eggers H J and Weyer J J 1991 Linkage and independence of
AIDS Kaposi disease: The interaction of human immuno-
deficiency virus and some coagents; Infection 19 115–122
Ellison B J, Downey A B and Duesberg P H. 1996 HIV as a
surrogate marker for drug-use: a re-analysis of the San Fran-
cisco Men’s Health Study. in AIDS: virus- or drug induced?
(ed.) P H Duesberg (Dordrecht, The Netherlands: Kluwer
Academic Publishers) pp 97–104
Enserink M 2001 Old guard urges virologists to go back to
basics; Science 293 24–25
European Collaborative Study 1991 Children born to women
with HIV-1 infection: natural history and risk of transmis-
sion; Lancet 337 253–260
Farber C 1998 AZT Roulette; Mothering 90 52–65
Fellay J, Boubaker K, Ledergerber B, Bernasconi E, Furrer H,
Battegay M, Hirschel B, Vernazza P, Francioli P, Greub G,
Flepp M and Telenti A 2001 Prevalence of adverse events
associated with potent antiretroviral treatment: Swiss HIV
Cohort Study; Lancet 358 1322–1327
Fenner F, McAuslan B R, Mims C A, Sambrook J and White
D O 1974 The biology of animal viruses (New York: Acade-
mic Press)
Fiala C 1998 AIDS in Africa: dirty tricks; NewAfrican April, pp
36–38
Fiala C, de Harven E, Herxheimer A, Kohnlein C, Mhlongo
S and Stewart G T 2002 HIV/AIDS data in South Africa;
Lancet 359 1782
Fields B 2001 Field’s virology (Philadelphia: Lippincott Wil-
liams & Wilkins)
Fischl M A, Richman D D, Grieco M H, Gottlieb M S,
Volberding P A, Laskin O L, Leedon J M, Groopman J E,
Mildvan D, Schooley R T, Jackson G G, Durack D T, King D
and the AZT Collaborative Working Group 1987 The effi-
cacy of azidothymidine (AZT) in the treatment of patients
with AIDS and AIDS-related complex; N. Engl. J. Med. 317
185–191
Fischl M A, Richman D D, Causey D M, Grieco M H, Bryson
Y, Mildvan D, Laskin O L, Groopman J E, Volberding P A,
Schooley R T, Jackson G G, Durack D T, Andrews J C,
Nusinoff-Lehrman S, Barry D W and the AZT Collaborative
working Group 1989 Prolonged zidovudine therapy in
patients with AIDS and advanced AIDS-related complex;
Jama 262 2405–2410
Fischl M A, Stanley K, Collier A C, Arduino J M, Stein D S,
Feinberg J E, Allan J D, Goldsmith J C and Powderly W G
1995 Combination and monotherapy with zidovudine and
zalcitabine in patients with advanced HIV disease. The
NIAID AIDS Clinical Trials Group; Ann. Int. Med. 122 24–
32
Fogelman I, Lim L, Bassett R, Volberding P, Fischl M A,
Stanley K, Cotton D J for the AIDS Clinical Trials Group
1994 Prevalence and patterns of use of concomitant medica-
tions among participants in three multicenter human immu-
nodeficiency virus type 1 clinical trials; J. Aquir.
Immune Defic. Syndr. 7 1057–1063
France D 2001 The angry prophet is dying: Controversial
author Larry Kramer is a one-man history of the AIDS strug-
gle, from early activism to the fading hope of medical sal-
vation; Newsweek June, pp 42–46
Francis D P, Curran J W and Essex M 1983 Epidemic acquired
immune deficiency syndrome: Epidemiologic evidence for a
transmissible agent; J. Natl. Cancer Inst. 71 1–4
Fujimura J 1996 Crafting science; a sociohistory of the quest
for the genetics of cancer (Cambridge, MA: Harvard Univer-
sity Press)
Gallo R C, Salahuddin S Z, Popovic M, Shearer G M, Kaplan
M, Haynes B F, Palker T J, Redfield R, Oleske J, Safai B,
White G, Foster P and Markham P D 1984 Frequent detec-
tion and isolation of cytopathic retrovirus (HTLV-III) from
patients with AIDS and at risk for AIDS; Science 224 500–503
Gellman B 2000 S. African President Escalates AIDS Feud;
Washington Post, April 19, p. A01
Gerhard S 2001 Safe and sound underground: HIV-positive
women birthing outside the system; Mothering September/
October, pp 42–57
Gerschenson M, Erhart S W, Paik C Y, St Claire M C, Naga-
shima K, Skopets B, Harbaugh S W, Harbaugh J W, Quan W
and Poirier M C 2000 Fetal mitochondrial heart and skeletal
muscle damage in Erythrocebus patas monkeys exposed in
utero to 3′-azido-3′-deoxythymidine; AIDS Res. Hum. Retro-
viruses 16 635–644
Gibbons J 1996 Drugs & Us; Gay Times (London), September,
pp 17–37
Gill P S, Rarick M, Byrnes R K, Causey D, Loureiro C and
Levine A M 1987 Azidothymidine associated with bone mar-
row failure in the acquired immunodeficiency syndrome
(AIDS); Ann. Int. Med. 107 502–505
Gisselquist D, Rothenberg R, Potterat J and Drucker E 2002
HIV infections in sub-Saharan Africa not explained by sex-
ual or vertical transmission; Int. J. STD AIDS 13 657–666
Goedert J J, Cohen A R, Kessler C M, Eichinger S, Seremetis
S V, Rabkin C S, Yellin F J, Rosenberg P S and Aledort L M
1994 Risks of immunodeficiency, AIDS, and death related to
purity of factor VIII concentrate; Lancet 344 791–792
Goedert J J, Neuland C Y, Wallen W C, Greene M H, Mann
D L, Murray C, Strong D M, Fraumeni J F Jr and Blattner
W A 1982 Amyl nitrite may alter T lymphocytes in homo-
sexual men; Lancet 1 412–416
Goodgame R W 1990 AIDS in Uganda-clinical and social fea-
tures; N. Engl. J. Med. 323 383–389
Gottlieb M S, Schroff R, Schanker H M, Weisman J D, Fan
P T, Wolf R A and Saxon A 1981 Pneumocystis carinii
pneumonia and mucosal candidiasis in previously healthy
homosexual men: evidence of a new acquired cellular immu-
nodeficiency; N. Engl. J. Med. 305 1425–1431
Grossman S J, Reinfoed N, Eydelloth R S, Alberts D W, Smith
P F and Patrick D H 1997 Hepatotoxicity of an HIV protease
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
408
inhibitor in dogs and rats; Toxicol. Appl. Pharmacol. 146
40–52
Hall C T 1996 AIDS advances boost drugmaker; San Francisco
Chronicle, August 1, pp E1–E2
Harper M E, Marselle L M, Gallo R C and Wong-Staal F 1986
Detection of lymphocytes expressing human T-lymphotropic
virus type III in lymph nodes and peripheral blood from
infected individuals by in situ hybridization; Proc. Natl.
Acad. Sci. USA 83 772–776
Haverkos H 1988 Epidemiologic studies – Kaposi’s sarcoma
vs. opportunistic infections among homosexual men with
AIDS; in Health hazards of nitrite inhalants (eds) H W
Haverkos and J A Doughertry (Rockville, MD: US Depart-
ment of Health and Human Services, National Institute on
Drug Abuse) pp 96–105
Haverkos H W 1996 Is Kaposi sarcoma caused by new herpes-
virus?; Biomed. Pharmacother. 50 318–319
Haverkos H W and Dougherty J A (eds) 1988 Health hazards
of nitrite inhalants (83 NIDA Research Monograph, US
Department of Health and Human Services, Washington DC)
Haverkos H W and Drotman D P 1995 Measuring inhalant
nitrite exposure in gay men: implications for elucidating the
etiology of AIDS-related Kaposi’s sarcoma; Genetica 95
157–164
Haverkos H W and Drotman D P 1996 NIDA technical review:
nitrite inhalants; Biomed. Pharmacother. 50 228–230
Haverkos H W, Drotman D P and Hanson D 1994 Surveillance
for AIDS-related Kaposi's sarcoma (KS): update; NIDA/
CDC, Rockville, MD/Atlanta, GA May
Haverkos H W, Pinsky P F, Drotman D P and Bregman D J
1985 Disease manifestation among homosexual men with
acquired immunodeficiency syndrome: a possible role of
nitrites in Kaposi’s sarcoma; J. Sex. Trans. Dis. 12 203–
208
Hazenberg M D, Hamann D, Schuitemaker H and Miedema F
2000 T cell depletion in HIV-1 infection: how CD4+ T cells
go out of stock; Nature Immunol. 1 285–289
Hearst N and Hulley S 1988 Preventing the heterosexual spread
of AIDS: Are we giving our patients the best advice?; Jama
259 2428–2432
Hendrix A 2002 Artist’s perception stroked by his longtime
HIV status; San Francisco Chronicle, March 20
Heredia C 2003a Dance of death, first of three parts: crystal meth
fuels HIV; San Francisco Chronicle, May 4, p. A1
Heredia C 2003b Ph D Takes fall to addiction; San Franscisco
Chronicle, May 5, p. A1
Heresi G P, Caceres E, Atkins J T, Rueben J and Doyle M 1997
Pneumocystis carinii pneumonia in infants who were expo-
sed to human immunodeficiency virus but were not infected:
an exception to the AIDS Surveillance case definition; Clin.
Infect. Dis. 25 739–740
Hitchcock M J M 1991 Review: Antiviral portrait series Num-
ber 1; 2′,3′-Didehydro-2′,3′-dideoxythymidine (D4T), an
anti-HIV agent; Antiviral Chem. Chemother. 2 125–132
Ho D D 1995 Time to hit HIV, early and hard; N. Engl. J. Med.
333 450–451
Ho D D, Neumann A U, Perelson A S, Chen W, Leonard J M
and Markowitz M 1995 Rapid Turnover of Plasma Virions
and CD4 Lymphocytes in HIV-1 Infection: Nature (London)
373 123–126
Hodgkinson N 1996 AIDS: the failure of contemporary science
(London: Fourth Estate)
Hodgkinson N 2001 Molecular miscarriage: Is the HIV theory a
tragic mistake?; Mothering September/October, pp 58–73
Hogg R S, Yip B, Chan K J, Wood E, Craib K J,
O’Shaughnessy M V and Montaner J S 2001 Rates of Dis-
ease Progression by Baseline CD4 Cell Count and Viral Load
After Initiating Triple-Drug Therapy; Jama 286 2568–2577
Hoots K and Canty D 1998 Clotting factor concentrates and
immune function in haemophilic patients; Haemophilia 4
704–713
Hoover D R, Rinaldo C, He Y, Phair J, Fahey J and Graham
N M 1995 Long-term survival without clinical AIDS after
CD4+ cell counts fall below 200 × 10(6)/1; Aids 9 145–152
Horton R 1995 Will Duesberg now concede defeat?; Lancet
346 656
Horwitz J P, Chua J and Noel M 1964 Nucleosides. V. The
monomesylates of 1-(2′-deoxy-beta-D-lyxofuranosyl) thymi-
dine; J. Org. Chem. 29 2076
Hoxie J A, Haggarty B S, Rakowski J L, Pillsbury N and Levy
J A 1985 Persistent noncytopathic infection of normal human
T lymphocytes with AIDS-associated retrovirus; Science 229
1400–1402
Inoue T, Cronkite E P, Hirabayashi Y, Bullis J E Jr, Mitsui H
and Umemura T 1997 Lifetime treatment of mice with azido-
thymidine (AZT) produces myelodysplasia; Leukemia
(Suppl. 3) 11 123–127
Institute of Medicine and National Academy of Sciences 1986
Confronting AIDS (Washington DC: National Academy Press)
Institute of Medicine and National Academy of Sciences 1988
Confronting AIDS–Update 1988 (Washington DC: National
Academy Press)
Jacobson M A, de Miranda P, Gordon S M, Blum M R,
Volberding P and Mills J 1988 Prolonged pancytopenia due
to combined ganciclovir and zidovuduine therapy; J. Infect.
Dis. 158 489–490
Jacquez J A, Koopman J S, Simon C P and Longini Jr I M 1994
Role of the primary infection in epidemics of HIV infection
in gay cohorts; J. Acquir. Immune Defic. Syndr. 7 1169–
1184
Jaffe H W, Choi K, Thomas P A, Haverkos H W, Auerbach
D M, Guinan M E, Rogers M F, Spira T J, Darrow W W,
Kramer M A, Friedman S M, Monroe J M, Friedman-Kien
A E, Laubenstein L J, Marmor M, Safai B, Dritz S K, Crispi
S J, Fannin S L, Orkwis J P, Kelter A, Rushing W R,
Thacker S B and Curran J W 1983 National case-control
study of Kaposi’s sarcoma and Pneumocystis carinii pneu-
monia in homosexual men: Part 1, Epidemiologic results;
Ann. Int. Med. 99 145–151
Johnson J A 2000 AIDS Funding for Federal Government Pro-
grams: FY1981-FY2001 (Congressional Research Ser-
vice/The Library of Congress)
Kaslow R A, Blackwelder W C, Ostrow D G, Yerg D,
Palenicek J, Coulson A H and Valdiserri R O 1989 No evi-
dence for a role of alcohol or other psychoactive drugs in
accelerating immunodeficiency in HIV-1-positive indivi-
duals; Jama 261 3424–3429
Kline M W, Van Dyke R B, Lindsey J C, Gwynne M, Culnane
M, McKinney R E, Nichols S, Mitchell W G, Yogev R,
Hutcheon N and the AIDS Clinical Trials Group 240 Team
1998 A randomized comparative trial of stavudine (d4T) ver-
sus zidovudine (ZDU, AZT) in children with human immu-
nodeficiency virus infection; Pediatrics 101 214–220
Kolata G 1987 Imminent marketing of AZT raises problems;
Marrow suppression hampers AZT use in AIDS victims; Sci-
ence 235 1462–1463
Konotey-Ahulu F I D 1987a AIDS in Africa: Misinformation
and disinformation; Lancet 2 206–207
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
409
Konotey-Ahulu F I D 1987b Clinical epidemiology, not sero-
epidemiology, is the answer to Africa’s AIDS problem; Br.
Med. J. 294 1593–1594
Konotey-Ahulu F I D 1989 What is AIDS? (Watford, England:
Tetteh-A’Domenco)
Kuhn L, Abrams E J, Weedon J, Lambert G, Schoenbaum E E,
Nesheim S R, Palumbo P, Vink P E and Bulterys M 2000
Disease progression and early viral dynamics in human
immunodeficiency virus-infected children exposed to zido-
vudine during prenatal and perinatal periods; J. Infect. Dis.
182 104–111
Kumar R M, Hughes P F and Khurranna A 1994 Zidovudine
use in pregnancy: a report on 104 cases and the occurence of
birth defects; J. Acquir. Immune Defic. Syndr. 7 1034–1039
Lang S 1998 Challenges (New York: Springer)
Langhoff E, McElrath J, Bos H J, Pruett J, Granelli-Piperno A,
Cohn Z A and Steinman R M 1989 Most CD4+ T cells from
human immunodeficiency virus-1 infected patients can un-
dergo prolonged clonal expansion; J. Clin. Invest. 84 1637–
1643
Lauritsen J 1994 NIH reconsiders nitrites’ link to AIDS; Bio-
technology 12 762–763
Lauritsen J and Wilson H 1986 Death rush, poppers and AIDS
(New York: Pagan Press)
Learmont J, Tindall B, Evans L, Cunningham A, Cunningham
P, Wells J, Penny R, Kaldor J and Cooper D A 1992 Long-
term symptomless HIV-1 infection in recipients of blood
products from a single donor; Lancet 340 863–867
Lerner W D 1989 Cocaine abuse and acquired immunodefi-
ciency syndrome: tale of two epidemics; Am. J. Med. 87
661–663
Levy J A 1998 Caution: should we be treating HIV infection
early?; Lancet 352 982–983
Levy J A, Hoffman A D, Kramer S M, Landis J A and Shima-
bukuro J M 1984 Isolation of lymphocytopathic retroviruses
from San Francisco patients with AIDS; Science 225 840–
842
Lifson A R, Darrow W W, Hessol N A, O’Malley P M, Barn-
hart J L, Jaffe H W and Rutherford G W 1990 Kaposi’s
sarcoma in a cohort of homosexual and bisexual men: epi-
demiology and analysis for cofactors; Am. J. Epidemiol. 131
221–231
Lori F, Maserati R, Foli A, Seminari E, Timpone J and
Lisziewicz J 2000 Structured treatment interruptions to con-
trol HIV-1 infection; Lancet 355 287–288
Los Angeles Times 1998 Clinton to announce new drug plan;
San Francisco Chronicle, February 13, p. A17
Maddox J 1993 Has Duesberg a right of reply?; Nature (Lon-
don) 363 109
Maddox J 1995 More conviction on HIV and AIDS; Nature
(London) 377 1
Maggiore C 2000 What if everything you thought you knew
about AIDS was wrong? (Los Angeles: The American Foun-
dation for AIDS Alternatives)
Malan R 2001 AIDS in Africa in search of the truth; Rolling
Stone, 22 November, pp 70–72, 74–78, 80, 82, 100, 102
Mansergh G, Colfax G N, Marks G, Rader M, Guzman R and
Buchbinder S 2001 The Circuit Party Men’s Health Survey:
findings and implications for gay and bisexual men; Am. J.
Public Health 91 953–958
Marmor M, Friedman-Kien A E, Laubenstein L, Byrum R D,
William D C, D’Onofrio S and Dubin N 1982 Risk factors
for Kaposi’s sarcoma in homosexual men; Lancet 1 1083–
1087
Marx J 1984 Strong new candidate for AIDS agent; Science
224 475–477
Mathur-Wagh U, Enlow R W, Spigland I, Winchester R J,
Sacks H S, Rorat E, Yancovitz S R, Klein M J, William D C
and Mildvan D 1984 Longitudinal study of persistent gener-
alized lymphadenopathy in homosexual men: Relation to
acquired immunodeficiency syndrome; Lancet 1 1033–1038
Mattison A M, Ross M W, Wolfson T and Franklin D 2001
Circuit party attendance, club drug use, and unsafe sex in gay
men; J. Subst. Abuse 13 119–126
McCune J M 2001 The dynamics of CD4+ T-cell depletion in
HIV disease; Nature (London) 410 974–979
McKallip R J, Nagarkatti M and Nagarkatti P S 1995 Immu-
notoxicity of AZT: Inhibitory Effect on Thymocyte Differen-
tiation and Peripheral T Cell Responsiveness to gp120 of
Human Immunodeficiency Virus; Toxicol. Appl. Pharmacol.
131 53–62
McManus T J, Starrett L A and Harris J R W 1982 Amyl Nitrite
Use by Homosexuals; Lancet 1 503
McNall M and Remafedi G 1999 Relationship of amphetamine
and other substance use to unprotected intercourse among
young men who have sex with men; Arch. Pediatr. Adolesc.
Med. 153 1130–1135
Merriam-Webster (ed.) 1965 Webster’s Third International
Dictionary (Springfield, MA: G & C Merriam)
Migueles S A, Sabbaghian M S, Shupert W L, Bettinotti M P,
Marincola F M, Martino L, Hallahan C W, Selig S M,
Schwartz D, Sullivan J and Connors M 2000 HLA B*5701 is
highly associated with restriction of virus replication in a
subgroup of HIV-infected long term nonprogressors; Proc.
Natl. Acad. Sci. USA 97 2709–2714
Mims C and White D O 1984 Viral pathogenesis and immunol-
ogy (Oxford: Blackwell)
Mir N and Costello C 1988 Zidovudine and bone marrow;
Lancet 2 1195–1196
Mocroft A, Kirk O, Barton S E, Dietrich M, Proenca R, Cole-
bunders R, Pradier C, dArminio Monforte A, Ledergerber B
and Lundgren J D 1999 Anaemia is an independent predic-
tive marker for clinical prognosis in HIV-infected patients
from across Europe. EuroSIDA study group; Aids 13 943–
950
Moss A R 1987 AIDS and intravenous drug use: the real hete-
rosexual epidemic; Br. Med. J. 294 389–390
Moye J, Rich K C, Kalish L A, Sheon A R, Diaz C, Cooper E R,
Pitt J, Handelsman E and for the Women and Infants Trans-
mission Study Group 1996 Natural history of somatic growth
in infants born to women infected by human immunodefi-
ciency virus; J. Pediatr. 128 58–67
Munoz A 1995 Disease progression; 15 percent of HIV-infec-
ted men will be long-term survivors; AIDS Weekly (News
Report) May 15 and 29, 5–6, 3–4
Namango N and World Food Program of the United Nations
2001 AIDS und Hunger haengen zusammen; Frankfurter
Rundschau, July 20
National Institute of Allergy and Infectious Diseases and Natio-
nal Institutes of Health 2001 The evidence that HIV causes
AIDS (US government web site: www.niaid.nih.gov/fact-
sheets/evidhiv)
Newell G R, Adamas S C, Mansell P W A and Hersh E M 1984
Toxicity, immunosupprressive effects, and carcinogenic
potential of volatile nitrites: possible relationship to Kaposi’s
sarcoma; Pharmacotherapy 4 284–291
Newell G R, Mansell P W A, Spitz M R, Reuben J M and
Hersh E M 1985 Volatile nitrites: Use and adverse effects
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
410
related to the current epidemic of the acquired immune defi-
ciency syndrome; Am. J. Med. 78 811–816
Newell G R, Spitz M R and Wilson M B 1988 Nitrite inhalants:
Historical perspective; in Health hazards of nitrite inhalants
(eds) H W Haverkos and J A Dougherty (Rockville, MD:
National Institue of Drug Abuse) pp 1–14
Newschaffer C J, Zhang D, Hauck W W, Fanning T and Turner
B J 1999 Effect of enhanced prenatal and HIV-focused servi-
ces for pregnant women who are infected by human immu-
nodeficiency virus on emergency department use; Med. Care
37 1308–1319
Novick B E and Rubinstein A 1987 AIDS–The paediatric pers-
pective; Aids 1 3–7
Nussbaum B 1990 Good intentions: How big business politics
and medicine are corrupting the fight against AIDS (New
York: Atlantic Monthly Press)
O'Brien S J 1997 The HIV-AIDS debate is over; HIV Newsline
4 3–9
O'Brien S J and Goedert J J 1996 HIV causes AIDS: Koch's
postulates fulfilled; Curr. Opin. Immunol. 8 613–618
Oliver R T D 2000 Though HIV is the main cause of AIDS,
other factors play a role; Nature (London) 406 673
Olivero O A, Anderson L M, Diwan B A, Haines D C, Har-
baugh S W, Moskal T J, Jones A B, Rice J M, Riggs C W,
Logsdon D, Yuspa S H and Poirier M C 1997 Transplacental
effects of 3′-azido-2′,3′-dideoxythymidine (AZT): tumori-
genicity in mice and genotoxicity in mice and monkeys; J.
Natl. Cancer Inst. 89 1602–1608
Omar R F, Gourde P, Desormeaux A, Tremblay M, Beauchamp
D and Bergeron M G 1996 In vivo toxicity of foscarnet and
zidovudine given alone or in combination; Toxicol Appl.
Pharmacol. 139 324–332
Oppenheimer G M 1992 Causes, cases, and cohorts: The role of
epidemiology in the historical construction of AIDS; in
AIDS: The making of a chronic disease (eds) E Fee and D M
Fox (Berkeley: University of California Press) pp 49–83
Ostrow D G, Beltran E D, Joseph J G, DiFranceisco W, Wesch
J and Chmiel J S 1993 Recreational drugs and sexual beha-
viour in the Chicago MACS/CCS cohort of homosexually
active men; J. Substance Abuse 5 311–325
Ostrow D G, Van Raden M J, Fox R, Kingsley L A, Dudley J,
Kaslow R A and the Multicenter AIDS Cohort Study
(MACS) 1990 Recreational drug use and sexual behaviour
change in a cohort of homosexual men; Aids 4 759–765
Padian N S, Shiboski S C, Glass S O and Vittinghoff E 1997
Heterosexual transmission of human immunodeficiency virus
(HIV) in Northern California: results from a ten-year study;
Am. J. Epidemiol. 146 350–357
Palella F J Jr, Delaney K M, Moorman A C, Loveless M O,
Fuhrer J, Satten G A, Aschman D J and Holmberg S D 1998
Declining morbidity and mortality among patients with
advanced human immunodeficiency virus infection. HIV out-
patient Study Investigators; N. Engl. J. Med. 338 853–860
Pallangyo K J, Mbaga I M, Mugusi F, Mbena E, Mhalu F S,
Bredberg U and Biberfeld G 1987 Clinical case definition of
AIDS in African adults; Lancet 2 972
Pantaleo G, Menzo S, Vaccarezza M, Graziosi C, Cohen O J,
Demarest J F, Montefiori D, Orenstein J M, Fox C, Schrager
L K, Margolick J B, Buchbinder S, Giorgi J V and Fauci A S
1995 Studies in subjects with long-term nonprogressive
human immunodeficiency virus infection; N. Engl. J. Med.
332 209–216
Pauk J, Huang M L, Brodie S J, Wald A, Koelle D M, Schacker
T, Celum C, Selke S and Corey L 2000 Mucosal shedding of
human herpesvirus 8 in men; N. Engl. J. Med. 343 1369–
1377
Phillips A N, Staszewski S, Weber R, Kirk O, Francioli P,
Miller V, Vernazza P, Lundgren J D and Ledergerber B 2001
HIV Viral Load Response to Antiretroviral Therapy Accord-
ing to the Baseline CD4 Cell Count and Viral Load; Jama
286 2560–2567
Piot P, Quinn T C, Taelman H, Feinsod F M, Minlangu K B,
Wobin O, Mbendi N, Mazebo P, Ndangi K, Stevens W et al
1984 Acquired immunodeficiency syndrome in a hetero-
sexual population in Zaire; Lancet 2 65–69
Pitcher C J, Quittner C, Peterson D M, Connors M, Koup R A,
Maino V C and Picker L J 1999 HIV-1-specific CD4+ T cells
are detectable in most individuals with active HIV-1 infec-
tion but decline with prolonged viral suppression; Nat. Med.
5 518–525
Pluda J M, Yarchoan R, Jaffe E S, Feuerstein I M, Solomon D,
Steinberg S, Wyvill K M, Raubitschek A, Katz D and Broder
S 1990 Development of non-Hodgkin lymphoma in a cohort
of patients with severe human immunodeficiency virus (HIV)
infection on long-term antiretroviral therapy; Ann. Int. Med.
113 276–282
Poznansky M C, Coker R, Skinner C, Hill A, Bailey S,
Whitaker L, Renton A and Weber J 1995 HIV positive
patients first presenting with an AIDS defining illness: cha-
racteristics and survival; Br. Med. J. 311 156–158
Quinn T C, Mann J M, Curran J W and Piot P 1986 AIDS in
Africa: an epidemiological paradigm; Science 234 955–963
Quinn T C, Piot P, McCormick J B, Feinsod F M, Taelman H,
Kapita B, Stevens W and Fauci A S 1987 Serologic and
immunologic studies in patients with AIDS in North America
and Africa: the potential role of infectious agents as cofac-
tors in human immunodeficiency virus infection; Jama 257
2617–2621
Race E M, Adelson-Mitty J, Kriegel G R, Barlam T F, Reimann
K A, Letvin N L and Japour A J 1998 Focal mycobacterial
lymphadenitis following initiation of protease-inhibitor the-
rapy in patients with advanced HIV-1 disease; Lancet 351
252–255
Rappoport J 1988 AIDS INC (San Bruno, CA: Human Energy
Press)
Rasnick D 1997 Kinetics analysis of consecutive HIV pro-
teolytic cleavages of the Gag-Pol polyprotein; J. Biol. Chem.
272 6348–6353
Richman D D, Fischl M A, Grieco M H, Gottlieb M S, Vol-
berding P A, Laskin O L, Leedom J M, Groopman J E, Mild-
van D, Hirsch M S, Jackson G G, Durack D T, Nusinoff-
Lehrman S and the AZT Collaborative Working Group 1987
The toxicity of azidothymidine (AZT) in the treatment of
patients with AIDS and AIDS-related complex; N. Engl. J.
Med. 317 192–197
Robert Koch Institut 2000 HIV/AIDS-Halbjahresbericht I/2000;
Epidemiol. Bulletin 15 September, pp 1–16
Rogers M F, Ou C-Y, Rayfield M, Thomas P A, Schoenbaum
E E, Abrams E, Krasinski K, Selwyn P A, Moore J, Kaul A,
Grimm K T, Bamji M, Schochetman G and the New York
City Collaborative Study of Maternal HIV Transmission and
Montefiori Medical Center HIV Perinatal Transmission
Study Group 1989 Use of the polymerase chain reaction for
early detection of the proviral sequences of human immuno-
deficiency virus in infants born to seropositive mothers;
N. Engl. J. Med. 320 1649–1654
Root-Bernstein R 1993 Rethinking AIDS; The tragic cost of
premature consensus (New York: Free Press)
J. Biosci. | Vol. 28 | No. 4 | June 2003
The chemical bases of the various AIDS epidemics
411
Rosenberg M J and Weiner J M 1988 Prostitutes and AIDS: A
health department priority?; Am. J. Public Health 78 418–
423
Ross E 2003 Sub-Saharan Africa, Kenya and the Malthusian
paradigm in contemporary development thinking; in Reclai-
ming knowledge for diversity (ed.) M Pimbert (Earthscan) (in
press)
Russell S 2001 Deceptive AIDS ads must stop, FDA says; San
Francisco Chronicle, 28 April, p. A1, A13
Sabin C A, Phillips A N and Lee C A 1996 Response: argu-
ments contradict the “foreign protein-zidovudine” hypothe-
sis; Br. Med. J. 312 211–212
Sadownick D 1994 Kneeling at the Crystal Cathedral; Genre
December/January, pp 40–45, 86–90
Saftig P, Hetman M, Schmahl W, Weber K, Heine L,
Mossmann H, Koster A, Hess B, Evers M, von Figura K et al
1995 Mice deficient for the lysosomal proteinase cathepsin D
exhibit progressive atrophy of the intestinal mucosa and pro-
found destruction of lymphoid cells; EMBO J. 14 3599–3608
Sande M A 1986 Transmission of AIDS. The case against
casual contagion; N. Engl. J. Med. 314 380–382
Saves M, Vandentorren S, Daucourt V, Marimoutou C, Dupon
M, Couzigou P, Bernard N, Mercie P and Dabis F 1999
Severe hepatic cytolysis: incidence and risk factors in
patients treated by antiretroviral combinations. Aquitaine
Cohort, France, 1996–1998. Groupe dEpidemiologie Clini-
que de Sida en Aquitaine (GECSA); Aids 13 F115–121
Scalfaro P, Chesaux J J, Buchwalder P A, Biollaz J and Micheli
J L 1998 Severe transient neonatal lactic acidosis during
prophylactic zidovudine treatment; Intensive Care Med. 24
247–250
Schechter M T, Craib K J P, Gelmon K A, Montaner J S G,
Le T N and O’Shaughnessy M V 1993 HIV-1 and the aetio-
logy of AIDS; Lancet 341 658–659
Schnittman S M, Psallidopoulos M C, Lane H C, Thompson L,
Baseler M, Massari F, Fox C H, Salzman N P and Fauci A
1989 The reservoir for HIV-1 in human peripheral blood is a
T cell that maintains expression of CD4; Science 245 305–308
Seligmann M, Chess L, Fahey J L, Fauci A S, Lachmann P J,
L’Age-Stehr J, Ngu J, Pinching A J, Rosen F S, Spira T J and
Wybran J 1984 AIDS–an immunologic reevaluation; N. Engl.
J. Med. 311 1286–1292
Seligmann M, Warrell D A, Aboulker J-P, Carbon C, Darby-
shire J H, Dormont J, Eschwege E, Girling D J, James D R,
Levy J-P, Peto P T A, Schwarz D, Stone A B, Weller I V D,
Withnall R, Gelmon K, Lafon E, Swart A M, Aber V R,
Babiker A G, Lhoro S, Nunn A J and Vray M 1994 Con-
corde: MRC/ANRS randomised double-blind controlled trial
of immediate and deferred zidovudine in symptom-free HIV
infection; Lancet 343 871–881
Selik R M, Starcher E T and Curran J W 1987 Opportunistic
diseases reported in AIDS patients: frequencies, associations,
and trends; Aids 1 175–182
Shenton J 1998 Positively False: exposing the myths around
HIV and AIDS (London/New York: IB Tauris)
Shilts R 1987 And the band played on (New York: St. Martin’s
Press)
Simmonds P, Balfe P, Peutherer J F, Ludlam C A, Bishop J O
and Leigh-Brown A J 1990 Human immunodeficiency virus-
infected individuals contain provirus in small numbers of
peripheral mononuclear cells and at low copy numbers; J.
Virol. 64 864–872
Smothers K 1991 Pharmacology and toxicology of AIDS thera-
pies; AIDS Reader 1 29–35
Stedman's Medical Dictionary 1982 (Baltimore: Wiliams &
Wilkins)
Stewart G T, Mhlongo S, de Harven E, Fiala C, Koehnlein C,
Herxheimer A, Duesberg P, Rasnick D, Giraldo R, Kothari
M, Bialy H and Geshekter C 2000 The Durban Declaration is
not accepted by all; Nature (London) 407 286
Stolberg S 2001 In AIDS war, new weapons and new victims;
New York Times, June 3, p. 1
Stoneburner R L, Des Jarlais D C, Benezra D, Gorelkin L,
Sotheran J L, Friedman S R, Schultz S, Marmor M, Mildvan
D and Maslansky R 1988 A larger spectrum of severe HIV-I-
related disease in intravenous drug users in New York City;
Science 242 916–919
Szasz T 2001 The Therapeutic State: The Tyranny of Pharma-
cracy; The Independent Review, Spring, pp 485–501
Tanaka M 1996 Abrams cautious on use of new AIDS drugs;
Synapse (University of California San Francisco) October
10, p. 1, 5
The Durban Declaration 2000 The Durban Declaration; Nature
(London) 406 15–16
Thompson M B, Dunnick J K, Sutphin M E, Giles H D,
Irwin R D and Prejean J D 1991 Hematologic toxicity of
AZT and ddC administered as single agents and in combina-
tion to rats and mice; Fundamental Appl. Toxicol. 17 159–176
Till M and MacDonnell K B 1990 Myopathy with human
immunodeficiency virus type 1 (HIV-1) infection: HIV-1 or
zidovudine?; Ann. Int. Med. 113 492–494
Toltzis P, Mourton T and Magnuson T 1993 Effect of zidovu-
dine on preimplantation murine embryos; Antimicrob. Agents
Chemother. 37 1610–1613
Toufexis A 1991 Innocent victims; Time May 13, pp 56–60
US Bureau of the Census International Data Base 2001 World
population by region and development category: 1950–2025
(US Department of Commerce, Bureau of the Census)
Van de Perre P, Rouvroy D, Lepage P, Bogaerts J, Kestelyn P,
Kayihigi J, Hekker A C, Butzler J P and Clumeck N 1984
Acquired immunodeficiency syndrome in Rwanda; Lancet 2
62–65
Veugelers P J, Page K A, Tindall B, Schechter M T, Moss A R,
Winkelstein W W, Cooper D A, Craib K J P, Charlebois E,
Coutinho R A and Van Griensven G J P 1994 Determinants
of HIV disease progression among homsexual men registered
in the tricontinental seroconverter study; Am. J. Epidemiol.
140 747–758
Volberding P A, Lagakos S W, Koch M A, Pettinelli C, Myers
M W, Booth D K, Balfour H H Jr, Reichman R C, Bartlett J
A, Hirsch M S, Murphy R L, Hardy W D, Soeiro R, Fischl
M A, Bartlett J G, Merigan T C, Hyslop N E, Richman D D,
Valentine F T, Corey L and the AIDS Clinical Trial Group of
the National Insitute of Allergy and Infectious Disease 1990
Zidovudine in asymptomatic human immunodeficiency virus
infection: A controlled trial in persons with fewer than 500
CD4-positive cells per cubic millimeter; N. Engl. J. Med. 322
941–949
Ward J W, Bush T J, Perkins H A, Lieb L E, Allen J R, Goldfinger
D, Samson S M, Pepkowitz S H, Fernando L P, Holland P V,
Kleinman S H, Grindon A J, Garner J L, Rutherford G W and
Holmberg S D 1989 The natural history of trasfusion-associated
infection with human immunodeficiency virus; N. Engl. J. Med.
321 947–952
Wei X, Ghosh S K, Taylor M E, Johnson V A, Emini E A, Deutsch
P, Lifson J D, Bonhoeffer S, Nowak M A, Hahn B H, Saag M S
and Shaw G M 1995 Viral dynamics in human immunodefi-
ciency virus type 1 infection; Nature (London) 373 117–122
J. Biosci. | Vol. 28 | No. 4 | June 2003
Peter Duesberg, Claus Koehnlein and David Rasnick
412
Weiss R 1991 Provenance of HIV strains; Nature (London) 349
374
Weiss R and Jaffe H 1990 Duesberg HIV and AIDS; Nature
(London) 345 659–660
White House Office of National Drug Control Policy 1998 Fact
Sheet: Drug data summary (DHSS, The White House)
Woody G E, VanEtten-Lee M L, McKirnan D, Donnell D,
Metzger D, Seage G III and Gross M 2001 Substance use among
men who have sex with men: comparison with a national house-
hold survey; J. Acquir. Immune Defic. Syndr. 27 86–90
World Health Organization 1986 Provisional WHO clinical
case definition for AIDS; Weekly Epidemiological Records,
March 7, 10 72–73
World Health Organization 1999 Global AIDS surveillance,
Part II; Weekly Epidemiological Records 74 (3 December)
409–411
World Health Organization 2000 Global AIDS surveillance,
Part I; Weekly Epidemiological Records 75 (26 November)
379–383
World Health Organization 2001a Global AIDS surveillance,
Part II; Weekly Epidemiological Records 76 (50) 390–
396
World Health Organization 2001b Global situation of the
HIV/AIDS pandemic, end 2001 Part I; Weekly Epidemiologi-
cal Records 76 (49) 381–384
Zhang L, Yu W, He T, Yu J, Caffrey R E, Dalmasso E A, Fu S,
Pham T, Mei J, Ho J J, Zhang W, Lopez P and Ho D D 2002
Contribution of Human {alpha}-Defensin-1, -2 and -3 to the
Anti-HIV-1 Activity of CD8 Antiviral Factor; Science 298
995–2000
Zuger A 2001 A molecular offspring, off to join the AIDS
wars; New York Times, 20 March, p. D7
MS received 22 January 2003; accepted 8 April 2003
Corresponding editor: ATHEL CORNISH-BOWDEN
0%
 
10%
 
20%
 
30%
 
40%
 
50%
 
60%
 
70%
 
80%
 
90%
 
100%