Much Longer Can We Afford the AIDS Virus Monopoly?
To be published
in the Genetica monograph, "AIDS: Virus- or Drug-Induced?"
By Peter H.
AIDS science was open. Initially, the new epidemic of pneumonias
and Kaposi's sarcomas, since called AIDS, was considered a collection
of non-infectious "lifestyle" diseases. But the Centers
for Disease Control in Atlanta published that the pneumonias and
Kaposi's sarcomas of male homosexuals, who were addicted to recreational
drugs, were caused by a common infectious agent because patients
had been "linked" by sexual contacts. On the basis of
the CDC's sexual linkage study, the Secretary of Health and Human
Services announced in 1984 the hypothesis that the retrovirus HIV
is the cause of AIDS. The HIV-AIDS hypothesis currently holds a
monopoly on all AIDS research and treatment. However, the HIV hypothesis
is scientifically unproven. It has failed each of 15 testable predictions,
as for example that AIDS would explode via sexual transmission of
HIV into the general population. Moreover, HIV meets all classical
criteria of a harmless passenger virus: unpredictable intervals
between infection and any subsequent disease, and unpredictable
presence and activity of the virus during a disease. Since HIV is
rare in the US, it is a marker of real AIDS risks, frequent injection
of intravenous drugs, thousands of drug-mediated sexual contacts,
and transfusions. Indeed, AIDS does not meet even one of the classical
criteria of an infectious disease, as for example equal distribution
between the sexes, disease within days or weeks after infection,
and exponential spread of the disease in an un-immunized population
Far from being
beneficial, the HIV-AIDS hypothesis has become a threat to public
health in the last 10 years: It is the sole basis for (1) the daily
treatment of at least 200,000 HIV-positives with cytotoxic DNA chain
terminators originally designed to kill growing human cells for
chemotherapy, like AZT, that are now prescribed as anti-HIV drugs;
(2) the clean-needle programs that encourage intravenous drug use,
and the misinformation that HIV-infection is the only health risk
of recreational drug use. However, recreational drugs, such as heroin,
cocaine, amphetamines and nitrite inhalants, have long been known
to have immunotoxic, cytotoxic and/or carcinogenic effects; and
(3) the anxiety and the many restrictions of human rights associated
with a positive HIV-test.
Here it is
proposed that American and European AIDS is caused by the long-term
consumption of recreational and of anti-HIV drugs like AZT. The
drug-AIDS hypothesis correctly predicts American/European AIDS:
(1) AIDS is restricted to intravenous and oral users of recreational
drugs and AZT; (2) AIDS is 87% male, because males consume this
share of recreational drugs; (3) AIDS occurs in newborns, because
mothers use recreational drugs during pregnancy; (4) AIDS is new
in America, because AIDS is a consequence of the recreational drug
use epidemic that started in the 1960s, and of AZT prescriptions
that started in 1987; (5) AIDS occurs only in a small fraction of
recreational drug users, because only the highest life-time dose
of drugs causes irreversible AIDS-defining diseases - likewise only
the heaviest smokers get emphysema or lung cancer; (6) AIDS manifests
as specific diseases in specific risk groups, because each group
has specific drug habits. For example, pulmonary Kaposi's sarcoma
is exclusively diagnosed in male homosexuals who inhale carcinogenic
alkyl nitrites; (7) AIDS does not occur in millions of HIV-positive
non-drug users, and there are thousands of HIV-free AIDS cases,
because AIDS is not caused by HIV; (8) AIDS is stabilized, even
cured, if patients stop using recreational drugs or AZT - regardless
of the presence of HIV. The drug hypothesis predicts that AIDS is
an entirely preventable and in part curable disease. The solution
to AIDS could be as close as a very testable and affordable alternative
to the HIV hypothesis - the drug-AIDS hypothesis.
Table of Contents
the case for infectious AIDS
II. The HIV-AIDS
hypothesis proves to be unprovable
- a harmless passenger virus
IV. HIV -
a marker for AIDS risks
V. The myth
of infectious AIDS - unconfirmed
VI. The HIV-AIDS
hypothesis is costly, unproductive and harmful
drug-AIDS hypothesis predicts American/European AIDS - completely
IX. A possible
solution - at last
marched in the procession under the beautiful canopy, and all who
saw him in the street and out of the windows exclaimed: "Indeed,
the emperor's new suit is incomparable! What a long train he has!"
... "But he has nothing on at all," said a little child
at last.... "But he has nothing on at all," cried at last
the whole people. That made a deep impression upon the emperor,
for it seemed to him that they were right; but he thought to himself,
"Now I must bear up to the end." And the chamberlains
walked with still greater dignity, as if they carried the train
which did not exist.
Andersen, The Emperor's New Suit
the case for infectious AIDS
remembers that in its first three years, from 1981 to 1984, AIDS
science was open. The new epidemic of pneumonias and Kaposi's sarcomas,
that was called AIDS, was considered infectious by some, but many
independent investigators and even scientists from the Centers for
Disease Control (CDC) in Atlanta considered AIDS behavioral diseases.
Recreational drugs such as nitrite and ethylchloride inhalants,
cocaine, heroin, amphetamines, phenylcyclidine, LSD, and some others
were proposed by epidemiologists and toxicologists as the causes
of AIDS because in the early 1980s nearly all AIDS patients were
either male homosexuals who had used these drugs as aphrodisiacs
and psychoactive agents, or were heterosexual intravenous drug users
#(Goedert et al., 1982; Marmor et al., 1982; Jaffe
et al., 1983; Mathur-Wagh et al., 1984; Haverkos et
al., 1985; Newell et al., 1985a; Newell et al.,
1985b; Lauritsen and Wilson, 1986; Haverkos and Dougherty, 1988).
Drugs seemed to be the most plausible explanation for the restriction
of AIDS to these risk groups, because drug consumption was their
only specific common denominator-not shared with the general population.
This original drug-AIDS hypothesis was called the "lifestyle
hypothesis" #(Oppenheimer, 1992)#.
But in April
1984 the secretary of Health and Human Services and AIDS researcher
Robert Gallo from the National Institutes of Health (NIH) announced
at an international press conference in Washington that a virus
is the "probable cause of AIDS" #(Altman, 1984)#. This
"AIDS virus" #(Altman, 1984)# had been discovered a year
earlier in France, in a male homosexual without AIDS #(Barré-Sinoussi
et al., 1983)#. Within two years after that announcement
an international committee of retrovirologists had named this virus,
the Human Immunodeficiency Virus (HIV), to indicate that it was
the accepted cause of AIDS #(Coffin et al., 1986)#.
The road for
the ready acceptance of the "AIDS virus" by the scientific
community had been paved by epidemiologists from the CDC. By tracing
sexual contacts of male homosexual AIDS patients the CDC claimed
that it could "link patients," "who had sexual exposure
with other AIDS patients within five years of the onset of symptoms."
#(Auerbach et al., 1984)#. On that basis the CDC proposed
that AIDS "may be caused by an infectious agent that is transmissible
from person to person in a manner analogous to hepatitis B virus
infection: through sexual contacts; through parenteral exposure
by intravenous drug abusers...; through blood products; and, perhaps,
through mothers who are ... intravenous drug users to their infants."
#(Auerbach et al., 1984)#.
to hepatitis B or any other authentic infectious disease, the CDC's
case for infectious AIDS was bizarre with regard to the diversity
of the diseases linked. The CDC had "linked by sexual contact"
the Kaposi's sarcomas of some patients to the pneumonias of others
and vice versa. The uncritical acceptance by the scientific community
of a common infectious cause for such diametrically different diseases
as cancer and pneumonia allowed the CDC to fabricate infectious
AIDS. Since cancer, pneumonia, and by now about 30 different diseases
were all said to have the same cause, they would soon all be called
by the same new name, AIDS #(Institute of Medicine, 1988; Centers
for Disease Control and Prevention, 1992; National Institute of
Allergy and Infectious Diseases, 1994)#.
A second bizarre
element in the CDCs case for infectious AIDS was the assumption
of an average "latency period" from infection to AIDS
of 10 months #(Auerbach et al., 1984)#, now 10 years (see
below). The assumption of a microbe that only causes disease
after an average latency period of 10 months was without proven
precedent. It was necessary, because prospective patients "were
asymptomatic at the time of sexual exposure," and only developed
AIDS up to 5 years after a critical contact #(Auerbach et al.,
1984)#. Indeed, the carriers of the assumed infectious agent
had to be exceedingly healthy during the latency period, because
they had "large numbers" of "approximately 250 different
male sexual partners each year." In view of such large numbers
of sexual contacts and the long latency periods between infection
and AIDS, tracing the one contact that would cause a disease had
to be a masterpiece of epidemiological detective work. Therefore
the CDC's case for sexual transmission of AIDS was about as compelling
as the claim that one car had a flat tire at an intersection, because
another car had blown a head gasket at the same intersection in
the previous 5 years. Nevertheless, the sexual contact study was
accepted by the scientific community as proof for infectious AIDS
without further scrutiny.
The fact that
"linked patients" "have been frequent users of inhaled
amyl and butyl nitrite" and "of recreational drugs other
than nitrite" was not considered an AIDS risk by the CDC in
1984 #(Auerbach et al., 1984)#, although CDC scientists had
originally proposed recreational drugs as the cause of AIDS #(Oppenheimer,
In 1984, the
CDC also presented typical hemophilia diseases, like pneumonia and
candidiasis, as AIDS from parenteral infection via blood transfusions-in
support of its claim that AIDS was infectious #(Curran et al.,
1984; Evatt et al., 1984; Duesberg, 1995b)#. The paradox
that none of the CDC's hemophiliacs with AIDS would have developed
Kaposi's sarcoma from an infectious agent that presumably caused
Kaposi's sarcoma in homosexuals was effectively hidden because all
these entirely unrelated diseases had been named AIDS #(Duesberg,
1992; Duesberg, 1994a; Duesberg, 1995b)#.
CDC, originally established to fight infectious diseases, had grown
desperate for a new infectious disease, because ever since polio
had been eliminated by vaccines over 30 years ago, no new infectious
diseases had plagued the Western World. In the words of a Red Cross
official, "... the CDC increasingly needs a major epidemic
to justify its existence" #(Associated Press, 1994)#. Infectious
AIDS, but not the drug-AIDS hypothesis, offered such an opportunity.
A new infectious epidemic readily generates fear and funding. But
research on the toxicity of recreational drugs is trivial, not likely
to make headlines in the scientific literature. As a possible investment
in its future existence, the CDC has recently launched a new journal,
Emerging Infectious Diseases, to raise "public awareness
of exotic bugs." #(Kaiser, 1994)#. For example, in 1994 the
CDC promoted the Hanta virus -after it presumably killed some Indians
#(Denetclaw and Denetclaw, 1994a; Denetclaw and Denetclaw, 1994b)#-
into a threat to the nation, and in 1995 the Ebola virus, that had
apparently killed some Zairens, was promoted into a global "killer
virus" #(Associated Press, 1995a)#. The CDC claimed that 108
people may have been killed by the Ebola outbreak in Zaire in 1995
#(Centers for Disease Control, 1995)#. But it failed to mention
that 20% of the 55 million Zairens are Ebola virus antibody-positive,
having survived the virus without apparent disease #(Dietrich J.,
As AIDS claimed
ever more victims and gained ever more media attention, the CDC's
message that AIDS was a new infectious disease was enthusiastically
picked up by the stars of medical research, particularly the virologists.
A new infectious disease is a magnet for virologists, microbiologists
and immunologists because it holds the promise for a new microbial
pathogen and new vaccines. Since the discovery of pathogenic microbes
by Robert Koch and Louis Pasteur in the 1880s, the identification
of a new microbial pathogen has been the key for many brilliant
careers-like those of Walter Reed, John Enders, and Albert Sabin.
Stated the New York Times on the search for an AIDS virus
"... the greatest thrills for a scientist are in discovering
a new microbe, a new disease, cure and prevention ..." #(Altman,
of basic research in the War on Cancer, an army of highly sophisticated
virologists had failed to prove that viruses can cause cancer in
humans #(Greenberg, 1986; Booth, 1988)#. Among these were the current
leaders of AIDS research, Luc Montagnier from France, Robin Weiss
from the U.K., David Baltimore, Jay Levy, Robert Gallo and even
Peter Duesberg from the U.S. among others. Searching for other diseases
for their viruses, most cancer virologists welcomed AIDS as a new
frontier to apply their considerable skills #(Duesberg, 1987; Booth,
1988; Duesberg and Schwartz, 1992)#. With an AIDS virus, the
medical virologists could continue their familiar research, and
their companies could extend their markets from the narrow confines
of conventional virus tests and vaccines to the new multi-billion
dollar markets of HIV-antibody tests, HIV vaccines, and anti-HIV
drugs #(Weiss and Jaffe, 1990; Duesberg, 1992)#.
The AIDS virus
also proved to be the politically correct cause of AIDS. No AIDS
risk group could be blamed for being infected by a God-given egalitarian
virus. A virus could reach all of us. Nobody would be ostracized
since "We are all in this together." Not so with drugs:
The consumption of illicit psychoactive drugs implies individual
and social responsibilities that nobody wanted to face.
as the politically correct explanation of AIDS, the HIV hypothesis
has become the central investment for a whole generation of AIDS
scientists, AIDS companies, AIDS journalists, AIDS politicians and
danger of an AIDS virus decimating the general public also provided
the scientific and moral arguments for quick and unreflective action
and for the complete dismissal of the competing drug-AIDS hypothesis.
The fear of nature's presumably uncontrollable microbes created
an unscientific war-mentality that has since dominated the field
#(Christie, 1994)#. Scientists, health care workers, and journalists
would rather be safe and fast in protecting against HIV, than sorry
and slow in reflecting about the clinical and political consequences
of drug use #(Lang, 1994)#. The confrontation with man-made drugs,
after all, would have to take second place in urgency, as they would
not reach the innocent public.
priority, the virus-AIDS orthodoxy justifies intolerance, even censorship,
of all those who question infectious AIDS #(San Francisco Project
Inform, 1992; Maddox, 1993b; Maddox, 1993a; Cohen, 1994a; Lang,
1994; see Chapter 12)#. Epidemiologists from the CDC warn that to
"ignore this [HIV-AIDS] concept would result in an unconscionable
tragedy." #(Garza, Drotman and Jaffe, 1994)#. Virologists are
quick to call those who question the virus-AIDS hypothesis "irresponsible
and pernicious" #(Booth, 1988; Baltimore and Feinberg, 1989)#.
And the New York Times still calls all non-HIV science "cruelly
irresponsible anti-science" #(Lewis, 1994)#.
the "AIDS virus" won unprecedented popularity within a
short time after its announcement.
years later, in 1995, the virus-AIDS hypothesis has still failed
to produce any public health benefits in the war on AIDS. No vaccine,
no antiviral drug, no cure, not even an effective AIDS prevention
have been developed. It cannot even be predicted whether and when
an infected person will get ill. And it cannot predict which of
the about 30 AIDS diseases it will be #(Duesberg, 1992; Benditt
and Jasny, 1993; Cohen, 1994a; Cohen, 1994b; Wade, 1995)#. Moreover,
the very basis of the virus-AIDS hypothesis, the assumption that
AIDS is infectious, has since become questionable on several grounds.
you have believed AIDS is infectious 11 years ago, if you had known
that until now not even one of the doctors and health-care workers
who have treated the over 400,000 American AIDS patients since 1984
#(Centers for Disease Control and Prevention, 1994c)# is confirmed
to have contracted AIDS from a patient? Even if that would not have
changed your mind, would you still believe in infectious AIDS if
you had considered that the health care workers were neither protected
by an anti-HIV vaccine nor by an antiviral drug #(Duesberg, 1992)?
you have believed that a sexually transmitted virus was causing
AIDS if you had known that none of the wives of the 15,000 HIV-positive
American hemophiliacs has contracted AIDS from their husbands in
the last 10 years? Their risk of developing an AIDS-defining disease
is the normal background of these diseases in the U.S. #(Duesberg,
1992; Duesberg, 1995b)#.
you have believed that AIDS was contagious if you had known that
after a marriage of 10 years, neither the wife nor the 6-year old
daughter of the late tennis star and AIDS patient Arthur Ashe have
developed AIDS or even become HIV-positive #(Ashe and Rampersad,
1993)#; or that the long-term lover of the movie star Rock Hudson
has no AIDS symptoms, 10 years after Hudson died from AIDS in 1985?
Would you believe that AIDS was sexually transmitted if you had
known that, after a 13-year marriage and 2 children, the husband
of the late AIDS patient Elizabeth Glaser is healthy and HIV-free
you have believed in an AIDS virus if you had known that nobody
ever contracted Kaposi's sarcoma in the US from a blood donor with
Kaposi's sarcoma #(Haverkos, Drotman and Hanson, 1994)?
you have believed AIDS is a sexually transmitted disease in 1984
if you had known that 11 years later there is still no AIDS in American
heterosexuals, not even in prostitutes, unless they are drug addicts
you have believed in a sexually transmitted AIDS virus if you had
considered that such a virus would be incompatible with life? Because
sex is the only known source of human life, a sexually transmitted,
fatal virus would have exterminated itself together with its host
Have we lost
the war on AIDS because we have mistaken a harmless virus for its
HIV-AIDS hypothesis proves to be unprovable
hypothesis #(Institute of Medicine, 1988; National Institute of
Allergy and Infectious Diseases, 1994)# postulates that:
1. HIV causes
immunodeficiency by killing T-cells (lymphocytes);
occurs on average only 10 years after this virus has been neutralized
by antiviral immunity-a condition termed a "positive HIV test";
is the basis for about 30 previously known diseases, including pneumocystis
pneumonia, tuberculosis, candidiasis, Kaposi's sarcoma, dementia,
diarrhea, >10% weight loss, and many others (Table 1);
4. AIDS is
a sexually transmitted disease, because HIV is a sexually transmitted
Owing to the
immense popularity of this hypothesis, over 100,000 scientific papers
have been published on HIV since 1984. But not even one of these
has been able to explain how HIV causes AIDS. Worse yet,
not one paper exists that proves that HIV causes AIDS #(Duesberg,
1992; Dickson, 1994; Fields, 1994; Schoch, 1994; Thomas Jr., Mullis
and Johnson, 1994)#.
Definition of Aids
In view of
this proof-deficit, the HIV-AIDS establishment cites the "perfect"
correlation between HIV and AIDS as support for the hypothesis that
HIV causes AIDS #(Blattner, Gallo and Temin, 1988; Weiss and Jaffe,
1990; San Francisco Project Inform, 1992; Maddox, 1993b; Garza,
Drotman and Jaffe, 1994; National Institute of Allergy and Infectious
Diseases, 1994)#. However, this argument is inadequate as an element
of proof for three reasons:
to the HIV-AIDS hypothesis, the 30 AIDS-defining diseases are diagnosed
as AIDS only when antibody against HIV is present. In its absence
these diseases are called by their old name and caused by their
old causes. In other words, AIDS is defined entirely by its hypothetical
cause, HIV. Therefore, the perfect correlation is not a natural
coincidence but a perfect artifact of the definition of AIDS by
its hypothetical cause, HIV. It is one of the purest examples of
(2) The HIV
antibody-test for the detection of HIV is indirect, because it does
not assay for the virus. Moreover it is not reliable; up to 90%
false-positives are obtained, depending on the subjects tested and
on the tests used #(Duesberg, 1993f; Papadopulos-Eleopulos, Turner
and Papadimitriou, 1993)#.
(3) Even a
perfect correlation is not sufficient to prove causation. For example,
perfect correlations between yellow teeth and lung cancer, or between
hospitalization and death do not prove that one causes the other
#(Duesberg, 1989; Smith and Phillips, 1992; Duesberg, 1993d).
of the HIV Hypothesis
In the absence
of direct proof, the merit of a scientific hypothesis is determined
by the accuracy of its predictions. For example, there is no direct
proof for the hypothesis that smoking causes lung cancer and emphysema,
but the prediction that long-term smoking causes these diseases
has validated this hypothesis. In the following we will analyze
the predictions of the HIV-AIDS hypothesis #(Duesberg, 1994a)#:
persons will get AIDS, and otherwise matched HIV-negatives will
not. In the face of the relentless propaganda for the HIV
hypothesis, it comes as a big surprise to almost everybody that
there is not even one study to show that American, heterosexual
or homosexual men, who are HIV-positive but not drug users or hemophiliacs
ever get AIDS. More precisely, there is no study to show that such
men would get AIDS-defining diseases that exceed the long-established,
low background of these diseases in otherwise matched, HIV-free
counterparts #(Duesberg, 1995a, see Chapter 10)#. There is not a
single epidemiological study to support the most frightening slogan
of the HIV orthodoxy; that HIV-positives develop AIDS-defining diseases
because of HIV.
that claim HIV causes AIDS have instead analyzed the AIDS risks
of HIV-positive people who were recreational drug users, were treated
with AZT or other anti-viral drugs, had received transfusions, suffered
from congenital diseases, or were subject to exotic life styles
as in Africa. The AIDS risks of such groups were then determined
by comparisons, either with normal HIV-free people or with HIV-negative
people from risk groups who were not matched for drug use or other
AIDS risks #(Duesberg, 1992; Duesberg, 1993a; Duesberg, 1993c; Duesberg,
1993d, see Chapter 8)#. In other words, there is no epidemiological
evidence properly controlled for confounding factors that HIV is
a "deadly virus" or "the virus that causes AIDS."
In view of
the enormous experimental difficulties and costs in sorting out
the possible role HIV plays in AIDS from the roles that recreational
drugs, AZT, transfusions, congenital diseases and exotic life styles
play, it is surprising that the assumption that HIV causes AIDS
has never been studied in people who are free of confounding AIDS
risks. There can only be one plausible explanation for the absence
of an epidemiological study that shows that HIV causes AIDS in people
who are not in risk groups: HIV does not cause AIDS.
are 1 million HIV-positive Americans #(National Institute of Allergy
and Infectious Diseases, 1994)# and 17 million HIV-positive humans
#(Merson, 1993; World Health Organization, 1995)# who are healthy,
probably because they are not subject to real AIDS risks other than
the hypothetical AIDS risk HIV. Moreover, HIV-positives who stop
practicing risk behavior or stop being subjected to AIDS risks even
recover lost immunity-despite the presence of HIV (see below Section
VIII). For example, HIV-positive hemophiliacs treated for 3 years
with highly purified blood clotting factor regained lost immunity,
while controls treated with unpurified blood products continued
to lose immunity #(Seremetis et al., 1993; Duesberg, 1995b
and Chapter 11)#.
Thus HIV is
only ever deadly for people who are at risk for AIDS from toxic
drugs or who depend on long-term blood transfusions to treat underlying
deadly diseases #(Duesberg, 1992, see Chapter 6)#.
AIDS is new, because HIV is new in America. However, in
America HIV is a long-established retrovirus #(Duesberg, 1992, see
Chapter 6)#. Ever since the virus could be detected in 1984, an
unchanging 1 million Americans are HIV-positive (Fig 1A) #(Curran
et al., 1985; National Institute of Allergy and Infectious
Diseases, 1994, Farber, 1995b)#. By contrast, a new microbe/virus
spreads exponentially in a susceptible population (see V). Thus
the non-spread of HIV establishes it as an old virus in America
is active and abundant in persons with AIDS, and inactive and rare
in healthy virus carriers. All microbes cause diseases
by killing or alterating a larger number of target cells than the
host can spare or regenerate during the course of an infection.
Thus HIV would have to infect and kill at least 50% of all human
T-cells to cause AIDS.
AIDS patients HIV is found hibernating in only 0.1% of T-cells,
and biochemically active in less than 0.01% of T-cells #(Duesberg,
1992; Duesberg, 1993e; Piatak et al., 1993)#. Indeed, there
are healthy HIV-positive people with 30- to 40-times more infected
T-cells than in AIDS patients #(Simmonds et al., 1990; Bagasra
et al., 1992; Duesberg, 1992)#. The fact that the vast majority
of susceptible T-cells remain uninfected, even in people dying from
AIDS, is the definitive evidence that there is no active HIV in
HIV-antibody-positive persons. HIV is neutralized by antiviral immunity,
even in AIDS patients. If there were un-neutralized HIV, all T-cells
would be infected.
problem for the HIV-hypothesis is not just how HIV works, but how
it causes fatal diseases when it does not work at all. Since there
is no rational explanation for how HIV could cause AIDS, HIV researchers
now postulate a multiplicity of indirect mechanisms of pathogenesis
#(Blattner, Gallo and Temin, 1988; Booth, 1988; Gallo, 1991; Maddox,
1991; Weiss et al., 1992; Maddox, 1993b; Maddox, 1995; Wade,
1995; Wain-Hobson, 1995)#.
causes AIDS by killing T-cells. However, viruses that integrate
their genomes with that of the host, like HIV, cannot kill the host
cell. Since the genes of such viruses are part of the host's genes,
integrated viruses can only replicate as long as the host survives
integration and remains able to express integrated viral genes.
All integrated viruses survive from passive, and some retroviruses
also from active replication with the host. This strategy only works
if the host survives integration. If the virus were to kill the
cell as it is integrated, integration would be a useless exercise
and it would be undetectable. Indeed, HIV is mass-produced for the
"HIV test" in immortal T-cell lines in cell culture
at titers of 106 infectious units per ml #(Rubinstein, 1990; Karpas
et al., 1992)#. Luc Montagnier, the discoverer of HIV, and
many other researchers have confirmed that HIV does not kill T-cells
#(Lemaitre et al., 1990; Duesberg, 1992)#.
the generation time of HIV is two days, HIV will cause AIDS two
weeks after infection. The HIV-hypothesis predicts AIDS
within 2 weeks after infection, because HIV, like all other retroviruses,
replicates within two days. During that time one infected cell produces
at least 100 new viruses #(Weiss et al., 1985)#. In the absence
of antiviral immunity, these 100 viruses would in turn infect 100
cells producing 100 x 100 viruses, or 104 infected cells within
4 days after infection. Within 14 days of such exponential growth,
1014 cells -the equivalent of a human body- would be infected. This
is the typical latent period of proven pathogenic retroviruses,
like Rous sarcoma virus, and of pathogenic human viruses like flu,
measels, mumps, chicken pox, and herpes, which all have generation
times like HIV #(Fenner et al., 1974; Mims and White, 1984)#.
dated from the time of HIV infection, AIDS occurs at totally unpredictable
times. The latent period between infection and AIDS was estimated
to average 10 months in 1984 #(Auerbach et al., 1984)#, 10
years in 1988 #(Institute of Medicine, 1988)# and over 20 years
in HIV-positive hemophiliacs in 1994 #(Phillips et al., 1994)#.
A Berkeley mathematician recently has determined the most accurate
formula for the latent period of HIV, by subtracting 1984, the year
when HIV was proposed to cause AIDS, from the current calendar year.
But blaming AIDS on a HIV infection that occured 10 years earlier
is the logical equivalent of blaming today's broken leg on stumbling
over a crack in the sidewalk 10 years ago.
AIDS will spread exponentially ("explode"). The
AIDS orthodoxy has predicted that according to Farr's law #(Bregman
and Langmuir, 1990)#, AIDS would spread exponentially ("explode")
into the general, unimmunized population #(Duesberg, 1992)#-just
like all other new infectious diseases.
in America and Europe remained confined to the original risk groups,
i.e. male homosexuals practicing risk behaviour and intravenous
drug users #(National Commission on AIDS, 1991; Centers for Disease
Control and Prevention, 1994b)#. Instead of growing exponentially,
AIDS in America (and Europe) has increased slowly, over 15 years,
far from reaching saturation of the susceptible population of over
100 million sexually active adults (Fig. 1A). AIDS behaved just
like an occupational disease.
spread of AIDS will follow the dissemination of HIV. However,
there is no correlation between the spreads of AIDS and HIV in America.
In the last 10 years, AIDS increased in America from a few hundred
to about 100,000 cases annually (Fig. 1A) #(Centers for Disease
Control and Prevention, 1994c)#. (The burst of AIDS cases in 1993
is largely an artifact of the most recent redefinition of AIDS,
which nearly doubled the AIDS cases in one year #(Centers for Disease
Control and Prevention, 1994c)#.)
those same 10 years HIV did not spread at all (Fig. 1A). Ever since
HIV became detectable in 1985, an unchanging one million Americans
have been HIV-positive up to 1994 (Fig. 1A) #(Duesberg, 1992; Duesberg,
1994a; National Institute of Allergy and Infectious Diseases, 1994)#.
To hide this discrepancy, a latency period of 10 years has been
postulated between HIV and AIDS.
all other sexually transmitted diseases, AIDS in America will equilibrate
between the sexes. However, since 1981, AIDS has remained
in the original risk groups in America, i.e. male homosexuals, intravenous
drug users of which over 75% are males #(Duesberg, 1992)#, and hemophiliacs
which are nearly all males. Since 1981, 347,767 out of 401,749,
or 87% of all American AIDS cases, have been males #(Centers for
Disease Control and Prevention, 1994c)#.
is a sexually transmitted virus. However, HIV could never
survive in evolution from sexual transmission. Based on studies
of discordant couples, e.g. hemophiliacs with HIV and spouses without,
conducted by the CDC and others, it takes on average 1000 unprotected
sexual contacts to transmit HIV #(Hearst and Hulley, 1988; Peterman
et al., 1988; Rosenberg and Weiner, 1988; Lawrence et
al., 1990; Blattner, 1991)#. According to Rosenberg and Weiner,
"HIV infection in non-drug using prostitutes tends to be low
or absent, implying that sexual activity alone does not place them
at high risk." The efficiency of transmission in homosexual
contacts is also estimated at 1 in 1000 contacts #(Jacquez et
10 to 30 sexual contacts are required to generate a child, but 30
contacts are required to transmit HIV, HIV could never survive natural
selection on the basis of sexual transmission, because the host
would outgrow the parasite. Conventional venereal microbes, like
syphilis and gonorrhea, survive because they are transmitted by
about two sexual contacts #(Freeman, 1979)#. HIV also could not
survive from transmission to newborns if it were fatally pathogenic
to babies, as is claimed by the proponents of the HIV hypothesis
#(Blattner, Gallo and Temin, 1988; Institute of Medicine, 1988)#.
low efficiency of sexual transmission of HIV also predicts that
the safe-sex-campaigns conducted by the HIV orthodoxy will be of
very limited value. Only those would benefit who either have on
average 1,000 sexual contacts with HIV positives or those who have
on average 250,000 contacts with average Americans, of which only
1 million in 250 million is HIV positive (Fig. 1A) #(Duesberg, 1992;
National Institute of Allergy and Infectious Diseases, 1994)#.
will be restricted by controlling sexual transmission of HIV via
"safe sex," and parenteral transmission of HIV via "clean
needles." But AIDS continues to increase steadily
despite the "safe sex" and "clean needle" programs
#(Centers for Disease Control and Prevention, 1994c)# (see Fig. 1A).
workers will contract AIDS from their patients, scientists from
propagating virus, and prostitutes from their clients. Not
a single confirmed case exists in the scientific literature of a
health-care worker who contracted AIDS #(Duesberg, 1992; Duesberg,
1994a)# from one of the over 400,000 American AIDS patients #(Centers
for Disease Control and Prevention, 1994c)#. None of the tens of
thousands of HIV researchers have developed AIDS from propagating
HIV. And no prostitutes picked up AIDS from their clients-despite
the absence of antiviral vaccines or effective anti-HIV drugs #(Duesberg,
1992; Duesberg, 1994a)#.
A few unpublished
cases have been claimed, but each of these seemed to have been treated
with the cytotoxic drug AZT that is sufficient to cause immunodeficiency
(see below) #(Cohen, 1994a)#.
inoculated with HIV will develop AIDS, and the 15,000 American hemophiliacs
who were infected by transfusions before 1984 will die from AIDS. Not
one of the 150 chimpanzees inoculated with HIV since 1983 has developed
AIDS #(Duesberg, 1992)#. Contrary to prediction, the median life
of American hemophiliacs has increased 2.5-fold from 11 to 27 years
between 1972 and 1987 #(Institute of Medicine, 1988; Stehr-Green
et al., 1989)#, although 75% (15,000) were infected with
HIV by transfusions received before 1984 #(Duesberg, 1992)#. However,
in 1987 the median life of HIV-positive hemophiliacs started to
decrease again #(Chorba et al., 1994)# because since then
they have been treated with the cytotoxic AZT #(Duesberg, 1995b,
See Chapter 11)# (see below).
or vaccine-induced anti-HIV immunity will cure AIDS or protect against
future AIDS. Natural antiviral immunity, a positive HIV-test,
is observed in many AIDS patients, but does not protect against
AIDS. Paradoxically, anti-HIV immunity is by HIV-AIDS definition
the only criterion to predict who gets AIDS. With all other viruses
and microbes -there is no exception- immunity is the only criterion
to predict who does not get a disease. It is for this reason that
antiviral/microbial immunity is artificially induced by vaccination.
It is also for this reason that the HIV-AIDS establishment has called
for an HIV vaccine since 1984.
AIDS diseases are consequences of HIV-mediated T-cell deficiency. Indeed,
up to 1992 about 61% of all American AIDS diseases, the microbial
diseases such as Pneumocystis carinii, candida, tuberculosis,
etc. were consequences of Acquired ImmunoDeficiency (Table 1) #(Centers
for Disease Control, 1993)#.
were neither caused by, nor consistently associated with, immunodeficiency.
These include Kaposi's sarcoma, lymphoma, >10% weight loss, and
dementia (Table 1). Accordingly, Kaposi's sarcoma and dementia have
been diagnosed in male homosexuals whose immune systems were normal
#(Murray et al., 1988; Spornraft et al., 1988; Gill
et al., 1989; Friedman-Kien et al., 1990; Duesberg,
1992; Kaldor et al., 1993; Bacellar et al., 1994)#.
the CDC introduced, once more, a new AIDS definition #(Centers for
Disease Control and Prevention, 1992)#. This has shifted the balance
of immunodeficiency to non-immunodeficiency AIDS diseases significantly
in favour of immunodeficiency diseases, i.e. from 61% to 80% (Table
1) #(Centers for Disease Control and Prevention, 1994a)#. The critical
innovation of this new definition was that a healthy person with
less than 200 T-cells, but with no clinical disease, would now be
registered as an AIDS patient. The new AIDS definition nearly doubled
the new AIDS cases, thus adding new life to the sagging curves of
the American AIDS statistics (Fig. 1A). However, if one substracts
from the 1993 statistics the new AIDS cases with less than 200 T-cells,
the ratio of the remaining real immunodeficiency diseases to the
non-immunodeficiency diseases is almost the same as in 1992.
rationalizations an unprejudiced virologist, who is aware of the
heterogeneity of AIDS-defining diseases, must make to accommodate
an AIDS virus. Ever since Koch and Pasteur, microbiologists and
virologists were taught that a specific microbe or virus would cause
a specific disease-e.g. polio, flu, measels, chicken pox, hepatitis,
etc.-just like a particular musical instrument would make specific
the AIDS virus, the concept of a specific microbe causing a specific
disease had to be abandoned for the following bewildering scenario:
By picking up the AIDS virus from a diarrhea patient, a person would
get Kaposi's sarcoma. The Kaposi patient would then be able to cause
dementia or pneumonia in others by passing on the diarrhea virus,
just as the CDC's sexual contact study had claimed in 1984 #(Auerbach
et al., 1984)#. As of 1993, any one of these patients could
have also caused a clinically undetectable depletion of T-cells
in others, again by passing on their diarrhea, dementia, Kaposi's
sarcoma and pneumonia virus.
the unprejudiced virologist would have to reconcile this bewildering
pathogenic potential of HIV with the fact that HIV is one of the
most primitive viruses in terms of genetic information that exist,
carrying only 9,000 nucleotides. This is the viral equivalent of
a musical instrument that is said to sound like an orchestra, although
it only has the repertoire of a bell.
HIV is the cause of AIDS, the percent incidence of AIDS diseases
will be the same in all risk groups. However, the percent
incidence of AIDS-defining diseases is very different in different
risk groups. For example, Kaposi's sarcoma in America and Europe
is almost exclusively observed in male homosexuals #(Beral et
al., 1990)#. Intravenous drug users have a proclivity for tuberculosis,
weight loss, and pneumonia #(Duesberg, 1992)# and a very high mortality
dying at 30 years #(Lockemann et al., 1995)#. Pneumonia and
candidiasis are virtually the only AIDS diseases ever diagnosed
in hemophiliacs #(Duesberg, 1992; Duesberg, 1995b)#. And bacterial
infections other than tuberculosis are almost exclusively diagnosed
in babies with AIDS #(Centers for Disease Control, 1987; Centers
for Disease Control and Prevention, 1992; Duesberg, 1992, see Chapter
6)#. Thus the percent incidence of an AIDS diseases is very different
in different AIDS risk groups.
In view of
this, some AIDS researchers cite co-factors of HIV, such as recreational
drugs and immunosuppressive transfusions, as explanations for risk
group-specific diseases #(Evans, 1989; Duesberg, 1992; Ludlam, 1992;
Root-Bernstein, 1995a)#. However, they fail to provide evidence
that such cofactors depend on the cofactor HIV to be pathogenic.
The CDC and
other mainstream AIDS researchers insist that recreational drugs
and transfusions solely enhance the risk to get infected by HIV,
rather than playing causative roles in AIDS #(Cohen, 1994a)#. It
is for this reason that the CDC refers to drug- or transfusion-risk
groups as "exposure categories" #(Centers for Disease
Control and Prevention, 1994a)#. In fact, the CDC obscures the existence
of risk-group-specific AIDS diseases by reporting only the percent
incidence of AIDS diseases in all risk groups combined #(Centers
for Disease Control and Prevention, 1994a)#.
It is evident
that the HIV-AIDS hypothesis is unable to make even one verifiable
prediction-the hallmark of a failed hypothesis.
Even if a
hypothesis fails to make valid predictions in terms of established
scientific criteria, it could by chance lead to a valid prevention
or treatment. But the HIV-AIDS hypothesis has not lead to any public
health benefit. Instead it has harmed not only AIDS patients but
also healthy persons who are at risk for AIDS or just antibody-positive
harmless passenger virus
with the evidence that the HIV-AIDS hypothesis has failed to make
valid predictions and failed to lead to public health benefits,
many agree that HIV may not cause AIDS. But then, they wonder: What
does HIV do?
viruses are generally assumed to be pathogenic by an unsuspecting
public, because a few of them actually are. Likewise, a whole nation
is often stereotyped by the characteristics of a minority. For example
the French are considered great lovers and the Italians great singers,
because a few of them are great lovers and singers. The same is
true for viruses.
most viruses cause no disease at all. Viruses are not here to kill
their hosts, not even to cause disease. Instead, viruses are here
for exactly the same reasons we are, to continue their species.
This goal can only be achieved by keeping the host species alive,
and it is achieved best if every host survives the infection. That
is the reason that most viruses never cause a disease in their host.
Therefore they are called passenger viruses. Passenger viruses
are those that take a ride on the host, but demand no more from
the host than a passenger demands from an airplane (see Chapter
is not the cause of AIDS, the simplest and most plausible HIV hypothesis
postulates that HIV is just a passenger virus #(Duesberg, 1994a)#.
A passenger virus is defined as follows:
(1) The time
of infection is irrelevant to the onset of any disease.
(2) The passenger
virus can be either active or passive, either rare or abundant during
(3) The passenger
virus can be entirely absent during any disease.
(4) If the
passenger virus is de-repressed by a failing immune system, as for
example during a disease, the passenger virus may or may not contribute
to the disease. For example HHV-6 #(Cone et al., 1994)# or
cytomegalovirus may contribute their specific pathogenic properties
to an immunodeficient patient.
all these criteria with regard to its relation to AIDS:
(1) HIV infects
at totally unpredictable times prior to or even after the onset
of AIDS (see VIII below) or not at all #(Duesberg, 1992; Phair et
al., 1992; Duesberg, 1993f)#.
(2) HIV is
typically passive and rare during AIDS-hence the notorious difficulties
of leading AIDS researchers in isolating HIV from AIDS patients
#(Duesberg, 1992, see Chapter 6)#.
are thousands of HIV-free AIDS cases, e.g. HIV-free homosexuals
with Kaposi's sarcoma and HIV-free intravenous drug users with tuberculosis
#(Duesberg, 1993f, see Chapter 7)#.
is no report in the literature that AIDS patients are clinically
distinguishable from each other because HIV is active or passive
or not present at all #(Duesberg, 1993b; Duesberg, 1994a)#. Thus
HIV is a harmless passenger virus, even when it is active in some
rare immunodeficient persons #(Duesberg, 1993e)#.
If this is
true, there should be many more HIV carriers than AIDS patients.
Indeed, there are 1 million healthy HIV-positive Americans #(Duesberg,
1992; Duesberg, 1994a)# and there are 17 million healthy HIV-positive
humans #(Merson, 1993; National Institute of Allergy and Infectious
Diseases, 1994; World Health Organization, 1995)#.
there is some tenuous evidence that HIV can function as an autonomous
pathogen, causing a mild flu-like or mononucleosis-like condition,
prior to antiviral immunity #(Albert et al., 1987; Duesberg,
1987; Kessler et al., 1987; Gaines et al., 1988; Marcus
and the CDC Cooperative Needlestick Surveillance Group, 1988; Tindall
et al., 1988; Pedersen et al., 1990; Duesberg, 1992;
Niu, Stein and Schnittmann, 1993, see Chapters 1, 6)#. However,
in millions of HIV-positives HIV infection has gone unnoticed, because
they do not experience a characteristic HIV-disease prior to antiviral
immunity-like measles, mumps or flu which all occur prior to immunity
against these viral infections.
The rare cases
in which HIV infections, prior to antiviral immunity, have been
linked with mononucleosis or flu-like symptoms are restricted to
prospective studies of male homosexuals at risk for AIDS. These
cases could either be coincidences with a common cold or with intoxications
from recreational drug use (see below) #(Gaines et al., 1988;
Tindall et al., 1988; Pedersen et al., 1990)# rather
than evidence for HIV disease.
marker for AIDS risks
who understand all virological arguments against HIV as the cause
of AIDS, and for HIV as a passenger virus, have misgivings about
dismissing the HIV-AIDS hypothesis, because HIV is more common in
AIDS patients than in the healthy population. This sounds like an
ominous connection, but only if it is taken out of its trivial microbiological
context is that AIDS risk behavior is synonymous with collecting
microbes. The common denominator of all AIDS risk groups in
America and Europe is that they collect microbes either from unsterile
drugs injected with unsterile equipment, or from the thousands of
drug-mediated sexual contacts, that are required to transmit HIV
sexually, or from transfusions received for the treatment of illnesses
#(Jaffe et al., 1983; Auerbach et al., 1984; Lauritsen
and Wilson, 1986; Haverkos and Dougherty, 1988; Rappoport, 1988;
Adams, 1989; Callen, 1990; Lifson et al., 1990; Archibald
et al., 1992; Duesberg, 1992; Jones, 1994; Mullis, 1995)#.
This is the reason that numerous uncommon microbes are common not
only in AIDS patients but also in healthy persons from AIDS risk
groups. For example, the bacteria that cause syphilis, gonorrhea,
and tuberculosis, the hepatitis virus, rare strains of herpes virus,
putative leukemia virus, genital papilloma virus, and even HIV are
all common in AIDS risk groups and AIDS patients but uncommon in
the general population #(Duesberg, 1992, see Chapter 6)#. Thus HIV
is just one of many microbial markers of AIDS risk behavior. Since
AIDS is defined as one of 30 diseases in the presence of HIV, rather
than any other microbial or viral marker, the correlation between
HIV and AIDS is in theory 100%.
myth of infectious AIDS-unconfirmed
If a hypothesis
is unproductive, and unable to make verifiable predictions, the
scientific method calls for alternative hypotheses. To find the
correct AIDS hypothesis, we need to decide first whether to look
for other viruses and microbes or for drugs as causes of AIDS. In
other words, we need to know whether AIDS is infectious or not.
five classic criteria to define an infectious disease.
(1) The causative
microbe/virus is abundant and very active in target tissues during
the course of the disease.
(2) The disease
follows within days or weeks after infection, because microbes/viruses
multiply exponentially with generation times of 0.5 to 48 hrs, unless
they are stopped by immunity (see above).
(3) The disease
spreads, according to Farr's law, exponentially in an un-immunized
population within weeks or months, and subsequently fades away as
antiviral immunity builds up #(Bregman and Langmuir, 1990)#. The
bell shaped curve of a seasonal flu epidemic is the model.
diseases are equally distributed between the sexes.
diseases are most commonly observed in those under 20 and over 60
years of age. This is because after birth the immune system builds
up a wide repertoire of antimicrobial resistances that is nearly
complete at 20, and over 60 the system begins to decline.
AIDS does not fit one of these criteria:
is no abundant microbe common to all American AIDS cases. If HIV
is present, it is typically rare and hibernating.
(2) If dated
from the time of HIV infection, AIDS occurs at entirely unpredictable
times ranging from less than 1 year to over 10 years or never. It
has now been 10 years since 1 million Americans were found to be
HIV-infected. Most of these and 17 million healthy, HIV-positive
non-Americans are still waiting for HIV to cause AIDS.
AIDS has slowly increased over 10 years. Although AIDS affects annually
only a small fraction of susceptible persons-less than 100,000 out
of a susceptible pool of 250 million Americans-it has has now almost
plateaued for 4 years [after adjusting for new additions of diseases
to the AIDS definition] #(Centers for Disease Control and Prevention,
1994b)#. Thus AIDS in America has increased steadily over years,
just like an occupational disease, as for example lung cancer from
smoking. There is no evidence for immunity and no evidence for a
bell shaped AIDS curve.
AIDS is 87% male #(Centers for Disease Control and Prevention, 1994c)#,
which is epidemiologically as far from equality between the sexes
as the sun is from the earth. A similar sexual bias has been observed
early in the epidemic of smoking-related diseases in the 1960s,
before women picked up smoking at the same rate as men.
(5) 98% of
all American AIDS cases are over 20 and under 60 #(Centers for Disease
Control and Prevention, 1994c)#. Only 1% each are under 20 and over
60! Such an age bias is typical of occupational diseases, like bullet
wounds for soldiers.
in America and Europe #(Duesberg, 1992)# does not meet even one
of the criteria of infectious disease.
proponents of the HIV-AIDS hypothesis, such as Jaap Goudsmit from
the University of Amsterdam, grant that "AIDS does not have
the characteristics of an ordinary infectious disease. This view
is incontrovertible" #(Goudsmit, 1992)#. The AIDS epidemiologists
Eggers and Weyer from the University of Cologne state that "the
spread of AIDS does not behave like the spread of a disease that
is caused by a single sexually transmitted agent" #(Eggers
and Weyer, 1991)#. To reconcile AIDS with infectious disease they
"simulated a cofactor [that] cannot be identified with any
known infectious agent." The epidemiologists Anderson and May
from the University of London had to invent "assortative scenarios"
for different AIDS risk groups to match AIDS with infectious disease
#(Anderson and May, 1992)#.
Until we have
scientific evidence, infectious AIDS is just a myth-and, in view
of the facts, a very implausible myth indeed.
VI. The HIV-AIDS
hypothesis is costly,
unproductive and harmful
For 11 years
now the world has fought the war on AIDS united by the HIV-AIDS
hypothesis. But despite its enormous popularity, the virus-AIDS
hypothesis has been a complete failure in terms of public health
benefits: no vaccine has been developed that prevents AIDS, no drug
that cures AIDS, no policy that stops the spread of AIDS #(Benditt
and Jasny, 1993; Fields, 1994; Swinbanks, 1994; Wade, 1995)#.
reasons are for the complete failure of the HIV-AIDS hypothesis
to produce public health benefits, one thing is clear: it was not
for lack of trying. The passionate complaint of Shilts' 1987 book,
And the Band Played On, that indifference was the only obstacle
against a solution of AIDS #(Shilts, 1987)# has long become profoundly
obsolete. Since 1984, an unprecedented $35 billion has been paid
by the US taxpayer alone in support of HIV-AIDS research and treatment-more
than for all other viral and microbial diseases combined #(AIDS
Weekly, 1995; Gutknecht, 1995; Henry, 1995; Stone and Cohen, 1995)#.
With all this spending, more research has been done on HIV than
on any other virus in history, but absolutely no progress has been
made against AIDS. Time, at least, has voted against the HIV-hypothesis.
Traditionally, such complete failures are the consequences of a
But the HIV-AIDS
establishment does not only cost dearly and fails to produce positive
results, it also causes irreparable (1) clinical, (2) educational,
and (3) psychological damage:
damage. Worldwide about 200,000 HIV antibody-positive persons
are prescribed, every six hours, the highly toxic DNA chain terminator
AZT or equivalents like ddI, ddC, and d4T as anti-HIV drugs #(Duesberg,
1992; Thomas, 1995)#. Most of these, ie. 200,000 minus the 50,000
to 80,000 annual AIDS patients in America and Europe, are healthy
HIV-positives given AZT to prevent AIDS. Recently these include
even unborn American and French children and their HIV-positive
mothers, although the risk of such children to pick up HIV from
their mothers is only about 25% #(The Lancet, 1994; Farber, 1995a)#.
AZT was designed
30 years ago to kill growing human cells for cancer chemotherapy
#(Horwitz, Chua and Noel, 1964; Duesberg, 1992)#. In view of its
inevitable toxicity, AZT was approved as an anti-HIV drug only tentatively
in 1987 #(Kolata, 1987)#. See the warnings of a non-medical manufacturer,
Sigma, on the label of an AZT bottle (Fig. 2). The label points
out, with skull and cross bones, AZTs toxicity to the bone marrow,
the source of T-cells.
therapy of HIV appears harmful and irrational. Since HIV is postulated
to cause AIDS by killing T-cells (see above), it is irrational to
kill the same HIV-infected cells twice-once with HIV and again with
AZT. Moreover, it is harmful to kill numerous uninfected cells with
AZT collaterally #(Kolata, 1987; Lauritsen, 1990; Nussbaum, 1990;
AZT has failed to cure even one AIDS patient or to prevent AIDS
in HIV-infected persons #(Duesberg, 1992; Oddone et al.,
1993; Tokars et al., 1993; Bacellar et al., 1994;
Goedert et al., 1994; Lenderking et al., 1994; Seligmann
et al., 1994, Volberding, 1995, Ho, 1995)#. Instead, evidence
is growing that AZT causes AIDS-defining and other diseases as expected
from a chain terminator of DNA synthesis (see below) #(Mir and Costello,
1988; Lauritsen, 1990; Duesberg, 1992; Lauritsen, 1992; Bacellar
et al., 1994; Cohen, 1994a; Duesberg, 1994a; Goedert et
al., 1994; Lewis-Thorton, 1994)#. Yet this evidence is either
denied or belittled by the AIDS establishment as the following examples
(i) The observation
that "HIV dementia among those reporting any antiretroviral
use (AZT, ddI, ddC, or d4T) was 97% higher than among those not
using this antiretroviral therapy" is interpreted by its authors
with little concern for percentages: "This effect was not statistically
significant" #(Bacellar et al., 1994)#.
al., explain their stunning results-that HIV-positive hemophiliacs
on AZT have 4.5-times more AIDS and have a 2.4-times higher mortality
than untreated HIV-positive hemophiliacs-by saying this happened
"probably because zidovudine was administered first to those
whom clinicians considered to be at highest risk" #(Goedert
et al., 1994)#.
et al. explain their observation that male homosexuals on AZT have
a two- to four-fold higher risk of Pneumocystis pneumonia than untreated
controls as follows: "Zidovudine was no longer significant
after T-helper lymphocyte count was considered, primarily because
nonusers had higher cell counts..." #(Saah et al., 1995)#.
The fact that an inhibitor of DNA synthesis designed to kill human
cells would inhibit lymphocyte growth was not mentioned.
blunt result that AZT prophylaxis reduced survival from 3 to 2 years,
and caused "wasting syndrome, cryptosporidiosis, and cytomegalovirus
infection ... almost exclusively" in AZT-treated AIDS patients,
was interpreted like this: "The study of patients who progress
from primary HIV infection to AIDS without receiving medical intervention
gives insights into the effects of medical intervention on presentation
and survival after developing an AIDS defining illness." But
the nature of these "insights" was not revealed by the
authors #(Poznansky et al., 1995)#.
(iv) The largest
test of AIDS prophylaxis with AZT of its kind, the Concorde trial,
found a 25% higher mortality in AZT recipients than in untreated
controls. In view of this Seligmann et al., reached the conservative
conclusion: "The results of Concorde do not encourage the early
use of zidovudine [AZT] in symptom-free HIV-infected adults"
#(Seligmann et al., 1994)#.
(v) Five years
after introducing AZT prophylaxis to several hundred thousands of
healthy HIV-positives, Paul Volberding of the University of California
at San Francisco, Anthony Fauci of the National Institute of Allergy
and Infectious Diseases and over 100 scientific collaborators now
publish in the New England Journal of Medicine: "Zidovudine
... does not significantly prolong either AIDS-free or overall survival.
These results do not encourage the routine use of Zidovudine"
(Volberding et al., 1995). In an accompanying editorial "Time
to hit HIV, early and hard" the "Journal" makes the
forward recommendation to treat HIV infection with AZT and other
experimental drugs before antiviral immunity restricts the virus
to chronic latency (Ho, 1995). The article suggests that current
AZT prophylaxis is too little too late. This is said although the
ineffectiveness of the proposed "early and hard" treatment
is known since 1993 (Tokars et al., 1993).
(vi) The occurence
of 8 serious birth defects, 8 spontaneous abortions and 8 therapeutic
abortions among 104 pregnancies treated with AZT is interpreted
as "not proving safety, thus lending tenous support to the
use of this drug." #(Kumar, Hughes and Khurranna, 1994)#.
AZT must be
considered the most toxic among legal public health threats available
to healthy persons, much more toxic than alcohol and tobacco. For
this reason I have termed AZT AIDS by prescription #(Duesberg,
1992, see Chapter 6)#. Even Burroughs Wellcome, the manufacturer
of AZT, makes that same assessment, but expresses it in different
words: "It was often difficult to distinguish adverse events
possibly associated with zidovudine [AZT] administration from underlying
signs of HIV disease..." #(Physicians' Desk Reference, 1994)#.
damage. Since HIV, but not drugs, is thought to cause AIDS,
the HIV-AIDS establishment educates the public to use "clean
needles" for the injection of unsterile (!) street drugs and
to wear condoms for sex under the influence of aphrodisiac drugs
#(Institute of Medicine, 1988; San Francisco Project Inform, 1992;
Benditt and Jasny, 1993; National Institute of Allergy and Infectious
Diseases, 1994)#. However, the disregard, in fact explicit dismissal,
of drug toxicity by the AIDS establishment #(Weiss and Jaffe, 1990;
Ascher et al., 1993; Duesberg, 1993d; Maddox, 1993a; Schechter
et al., 1993b; Schechter et al., 1993c; Cohen, 1994a)#
encourages recreational drug use because it eliminates the fear
of drug toxicity. A popular joke illustrates this point: "Two
junkies are reminded by a friend not to share a syringe full of
cocaine. Their response: 'We wear condoms and use a clean needle'."
use of recreational drugs, including cocaine, heroin, amyl- and
isobutyl nitrite inhalants, amphetamines, and others has been documented
in numerous studies to cause exactly the same diseases that are
now blamed on HIV #(Haverkos and Dougherty, 1988; Stoneburner et
al., 1988; Lerner, 1989; Duesberg, 1992, see Chapter 6)#. The
list of drug-induced diseases, established long before the discovery
of HIV, reads like a catalogue of AIDS-defining diseases: weight
loss, fever, dementia, tuberculosis, oral thrush, pneumonia, diarrhea,
mouth infections, night sweats, and many others (see below) #(Lerner,
1989; Duesberg, 1992)#.
damage. According to the HIV-AIDS establishment, nearly all
HIV-infected, healthy persons are claimed to die from AIDS on average
10 years after infection by HIV #(Institute of Medicine, 1988; Garza,
Drotman and Jaffe, 1994; National Institute of Allergy and Infectious
Diseases, 1994; Thomas Jr., Mullis and Johnson, 1994). In view of
this, one million HIV-positive but healthy Americans, and 17 million
HIV-positive but healthy humans on this planet #(Merson, 1993; National
Institute of Allergy and Infectious Diseases, 1994; World Health
Organization, 1995)#, are subjected to a multiplicity of psychological
and sociological pressures #(Anonymous, 1992; Duesberg, 1992; Schmalz,
1992b; Schmalz, 1992a; Miami Herald, 1994; Yarbo, 1994)#.
They are given
a death sentence by the medical establishment for being HIV-positive;
they are denied coverage by health insurance companies; they lose
their jobs and social status; they are denied entrance visas to
many countries including the U.S.; they are denied employment by
the US Army; and worst of all they are pressured to accept the toxic
AZT therapy-all of this, only because they have made antibodies
against a virus that is presumed to cause AIDS. If they refuse to
submit to these pressures, they are charged with denial (of
the HIV-AIDS hypothesis) by the AIDS establishment #(Moss, Osmond
and Bacchetti, 1988; San Francisco Project Inform, 1992)#.
In sum, the
public health record of the HIV-AIDS hypothesis in America adds
up to a staggering deficit: for $35 billion #(Duesberg, 1994b; AIDS
Weekly, 1995; Gutknecht, 1995)# there is no cure, no vaccine, no
effective prevention, hundreds of thousands are subjected to psychological
pressures resulting from positive HIV-tests, and several million
American drug addicts are denied available information that recreational
drugs cause AIDS-defining and other diseases #(Drug Strategies,
1995)#, and about 150,000 are subjected annually to AZT poisoning-many
just for being HIV-positive, not for having AIDS #(Duesberg, 1992).
Given no evidence
for infectious AIDS, the reasons for the original "lifestyle
hypothesis," and the logic of Sherlock Holmes-that "when
you have eliminated the impossible, whatever remains however improbable
must be the truth"-AIDS must be non-infectious.
In view of
this I propose that:
diseases in America and Europe that exceed their long-established,
normal backgrounds are caused by the long-term consumption of recreational
drugs and by AZT and its analogs.
transfusion-AIDS, and the extremely rare AIDS cases of the general
population reflect the normal incidence plus the AZT-induced incidence
of these diseases under a new name.
AIDS is a new name for old diseases caused by malnutrition, parasitic
infections and poor sanitation #(Duesberg, 1991; Duesberg, 1992;
Duesberg, 1994a, see Chapters 6 and 9).
recreational drug use epidemics, that started in America and Europe
during the Vietnam war, are the only new health risk of the Western
World since World War II. Since its beginnings the drug use and
AIDS epidemics in the US and Europe have coincided both epidemiologically
and chronologically #(Duesberg, 1992)#. About 33% of all American
AIDS patients, nearly all heterosexual AIDS patients, are intravenous
drug users #(Centers for Disease Control and Prevention, 1994b)#.
Over 60% are male homosexuals who have used psychoactive and aphrodisiac
drugs orally such as nitrite inhalants, amphetamines, cocaine and
phenylcyclidine (Table 2). Many of these recreational drug users
and most of the few AIDS patients who have not used recreational
drugs have used AZT and cytotoxic DNA chain terminators as anti-HIV
drugs (see below) #(Duesberg, 1992; Duesberg, 1994a)#. Allowing
a "latent period of 10 years" for chronic recreational
drug use to cause AIDS, the beginning of the American drug use epidemics
in the late 1960s and 1970s predicts exactly the origin of AIDS
in the 1980s.
virus-AIDS hypothesis, the drug hypothesis has a plausible chemical
and experimentally testable basis. The recreational drugs postulated
to cause AIDS have strong biochemical and psychoactive effects every
time they are taken-the reason for their popularity (see Chapter
6). By contrast, HIV is latent, and neither chemically nor clinically
detectable in "HIV antibody-positives" with and without
AIDS. Despite 11 years of unprecedented research efforts no biochemical
evidence has been found in support of the HIV-AIDS hypothesis (Cohen
toxicity and dosages of recreational and medical drugs used by American
and European AIDS risk groups can explain all AIDS diseases #(Duesberg,
1992)#. AIDS drugs are either indirectly toxic, or cytotoxic, or
genotoxic and cytotoxic.
toxic. Cocaine, amphetamines and heroin are indirectly immunotoxic.
All three function as catalysts in the human body. Cocaine and heroin
are natural compounds and amphetamines are synthetic adrenalins
first developed in Germany during World War II to suppress fatigue
and anxiety in pilots and tank commanders #(Weil and Rosen, 1983)#.
is the result of malnutrition and insomnia which in turn are consequences
of drug-induced suppression of appetite and fatigue #(Layon et
al., 1984; Lerner, 1989; Pillai, Nair and Watson, 1991; Duesberg,
1992; Larrat and Zierler, 1993; Mientjes et al., 1993; Sadownick,
1994)#. These problems are compounded by poverty due to the enormous
costs of illicit drugs. Direct, long-term pathogenic effects of
cocaine and heroin have not been studied owing to the general disregard
of drug toxicity #(Duesberg, 1992)#.
and genotoxic. Nitrite inhalants are cytotoxic, and thus are
immunotoxic in animals and humans #(Goedert et al., 1982;
Haverkos and Dougherty, 1988)#. A recreational dose of 1 ml per
day #(Haverkos and Dougherty, 1988; Duesberg, 1992)# corresponds
to about 15 ppm in a 75 kg-person, and corresponds to 107 nitrite
molecules for everyone of the 1014 cells in the human body. The
cytotoxicity of nitrites on the epithelial tissues of the lung are
enhanced by the toxins of cigarette smoke, which also suppresses
the immunesystem #(Nieman et al., 1993).
nitrite inhalants are among the best established mutagens and carcinogens
#(National Research Council, 1982; Lewis, 1989; Winter, 1989; Mirvish
et al., 1993)#. In view of the toxicity of nitrite inhalants,
a prescription requirement was instated by the US Food and Drug
Administration in 1969 #(Newell et al., 1985a)#, and because
of an "AIDS link" #(Cox, 1986)# the sale of nitrites was
banned by the U.S. Congress in 1988 (Public Law 100-690) #(Haverkos,
1990)# and by the "Crime Control Act of 1990" #(Duesberg,
1992)#. Moreover, the US Food and Drug Administration limits nitrites
as food preservatives to less than 200 ppm, because of direct toxicity
and because "they have been implicated in an increased incidence
of cancer" #(Lewis, 1989, National Research Council, 1982)#.
AZT, ddI and other DNA chain terminators are directly toxic
by killing all growing cells, in particular the fastest growing
ones-the hematopoietic and epithelial cells (Fig. 2), #(Merck Research
Laboratories, 1992; Chiu and Duesberg, 1995)#. In addition, AZT
prevents mitochondrial DNA synthesis in non-growing cells, such
as neurons or muscles, and can be carcinogenic by mutating cells
#(Pluda et al., 1990; Duesberg, 1992; Parker and Cheng, 1994)#.
The key to
the drug hypothesis is that only long-term consumption causes irreversible
AIDS-defining diseases. Occasional or short-term recreational drug
use causes reversible diseases or no diseases at all. With drugs,
the dose is the poison. Yet, most studies investigating the
effects of recreational drugs are concerned with their short-term
psychoactive rather with their long-term clinical effects #(Duesberg,
1992). For example, it takes 20 years of smoking to acquire irreversible
lung cancer or emphysema, and 20 years of drinking to acquire
irreversible liver cirrhosis. In contrast to drugs, infectious
agents are self-replicating toxins. By multiplying exponentially
in the body infectious agents may generate sufficient doses of toxic
substances to cause diseases within days or weeks.
no experiments are being done in America to test the drug hypothesis,
I have evaluated the drug-AIDS hypothesis on the basis of its predictions.
In contrast to the HIV-AIDS hypothesis, the drug hypothesis can
predict all parameters of American/European AIDS.
drug-hypothesis predicts the American/European AIDS epidemic-completely
is restricted to intravenous and oral users of recreational drugs
and of AZT, because drugs cause AIDS.
94% of all American AIDS cases have been from risk groups who had
used such drugs #(Centers for Disease Control and Prevention, 1994c)#.
About one-third of these were intravenous drug users #(Centers for
Disease Control, 1993)# and two-thirds were male homosexuals #(Centers
for Disease Control and Prevention, 1994c; Centers for Disease Control
and Prevention, 1994a)# who had used oral recreational drugs and
AZT #(Duesberg, 1992; Ascher et al., 1993; Duesberg, 1993c;
Duesberg, 1993a; Duesberg, 1993d; Parke, 1993; Schechter et al.,
1993b)#. HIV-positive hemophiliacs and transfusion recipients
also receive AZT as an antiviral drug #(Duesberg, 1992; Duesberg,
1995b)#. (However, a small percentage of hemophiliacs annually develop
a specific subset of AIDS-defining immunodeficiency diseases, mostly
pneumonia and candidiasis, only from the long-term transfusion of
foreign proteins that contaminate commercial factor VIII #(Duesberg,
1992; Duesberg, 1995b, see Chapter 11#). European AIDS also correlates
with drug consumption #(Duesberg, 1992, see Chapter 6)#.
AIDS predominantly affects adult males, because they are the predominant
users of recreational drugs and AZT.
The CDC reports
that 87% of all American AIDS patients are males #(Centers for Disease
Control and Prevention, 1994c)#. This number is the sum of the following
constituents: The National Institute on Drug Abuse and the Bureau
of Justice Statistics report that over 75% of hard, recreational
drugs are consumed intravenously by males #(Duesberg, 1992, see
to the federally supported Drug Strategies program "women account
for the fastest-growing population in jails and prisons, in large
part because of drug offenses" #(Drug Strategies, 1995)#. Therefore
the CDC reports that women are now the fastest growing AIDS risk
group #(Centers for Disease Control, 1994; Centers for Disease Control
and Prevention, 1994a)#.
The CDC and
independent investigators report that nearly all male homosexuals
with AIDS and at risk for AIDS are long-term users of oral drugs
such as nitrite inhalants, ethylchloride inhalants, amphetamines,
cocaine, and others to facilitate sexual contacts, particularly
anal intercourse #(Lifson et al., 1990; Duesberg, 1992; Ascher
et al., 1993; Duesberg, 1993d; Schechter et al., 1993a;
Schechter et al., 1993c)#. The drug use of male homosexuals
with AIDS or at risk for AIDS reported by the CDC #(Jaffe et
al., 1983; Darrow et al., 1987; Lifson et al.,
1990)# and others #(Ascher et al., 1993; Duesberg, 1993d;
Schechter et al., 1993c; Ellison, Downey and Duesberg, 1995)#
as of 1983 is listed in Table 2. Ostrow reported that nitrite inhalant
use in a cohort of over 5000 male homosexuals from Chicago, Baltimore,
Los Angeles and Pittsburgh showed a "consistent and strong
cross-sectional association with ... anal sex" #(Ostrow, 1994)#.
In addition, many HIV-positive homosexuals are prescribed AZT as
an antiviral drug #(Duesberg, 1992; Duesberg, 1993d; Ellison, Downey
and Duesberg, 1995)#.
drug users, who are 75% male, make up one-third of all AIDS patients,
and male homosexuals make up almost two-thirds of all American AIDS
patients, the drug hypothesis explains why 87% of all American AIDS
patients are males.
AIDS coccurs because of maternal drug addiction.
80% of pediatric AIDS cases in America and Europe are children born
to mothers who were intravenous drug users during pregnancy (see
below (5) and (8)), #(Mok et al., 1987; European Collaborative Study,
1991; Duesberg, 1992)#. The remainder reflects the normal low incidence
of AIDS-defining diseases among newborns.
AIDS is new and increasing steadily, because the American drug epidemic
is new and increasing steadily.
In the U.S.
recreational drug use is epidemiologically new, as it has increased
over the last decades from statistically undetectable levels to
epidemic levels at about the same rate as AIDS #(Duesberg, 1992)#.
cocaine consumption increased 200-fold from 1980 to 1990, based
on cocaine seizures that increased from 500 kg in 1980 to 100,000
kg in 1990 #(Duesberg, 1992, see Chapter 6)#. During the same time
cocaine-related hospital emergencies increased from 3,296 cases
in 1981, to 80,355 cases in 1990, and to 119,843 in 1992 and to
over 120,000 in 1993 #(Duesberg, 1992; Meddis, 1994; Drug Strategies,
1995)# (Fig. 1B).
In the last
three years, the increase of cocaine consumption has slowed down
at the expense of increases in heroin consumption, which were accompanied
by increases in heroin-related hospital emergencies #(Gettman, 1994;
Meddis, 1994; Drug Strategies, 1995)#. Heroin-related hospital emergencies
doubled, from over 30,000 in 1990 to over 60,000 in 1993 (Fig. 1B)#(Drug
consumption has increased 100-fold from 1980 to 1990 #(Bureau of
Justice Statistics, 1991)#. Non-scientific reports describe new
upsurges in the consumption of amphetamines (Sadownick, 1994) and
the "gay drug" (nitrite inhalants) (Mirken, 1995) among
male homosexuals. According to a recent report from the National
Institute on Drug Abuse and the CDC, "nitrite use has increased
in the 1990s in gay men in Chicago and San Francisco" after
a decline in the 1980s #(Haverkos and Drotman, 1995)#.
are now the "largest and fastest-growing category in the Federal
prisons population, accounting for 61% of the total, compared with
38% in 1986." The number of Federal drug offenders increased
from about 5,000 in 1980 to about 55,000 in 1993. In 1993, between
60 and 80% of the 12 million prisoners in the US had been on illicit
drugs #(Drug Strategies, 1995)#.
"Rauschgiftbilanz" reports an 11.2% increase in the consumption
of illicit recreational drugs in 1994 compared to 1993 #(Rauschgiftbilanz
grace period of about 10 years to achieve the dosage needed to cause
irreversible disease, and you can date the origin of AIDS in 1981
as a consequence of the drug use epidemic that started in America
in the late 1960s during the Vietnam War. Indeed, AIDS increased
from a few dozen cases annually in 1981 to about 100,000 in 1993
(Fig. 1A) #(Centers for Disease Control and Prevention, 1994c)#.
Note the parallelisms between the spread of AIDS and the spread
of cocaine and cocaine-related hospital emergencies since 1981 (Fig.
1A and B), and the contrast with the non-spread of HIV, the hypothetical
cause of AIDS, since 1984 (Fig. 1A). Thus both, the newness and
the increase of the AIDS epidemic are predictable by the drug-AIDS
of the epidemic has been accelerated by AZT. Since its introduction
in 1987, AZT is now prescribed to about 200,000 HIV-positives worldwide
#(Duesberg, 1992; Thomas, 1995)#.
a small fraction of drug users develop AIDS, because only the highest
cumulative drug doses cause irreversible diseases.
total of 401,749 American AIDS cases since 1981 that were reported
in June 1994 #(Centers for Disease Control and Prevention, 1994c)#
have been recruited from a much larger reservoir of drug users.
There are currently between 3 #(Drug Strategies, 1995)# and 8 million
cocaine addicts #(Duesberg, 1992)# and 0.6 million heroin addicts
in the US #(Drug Strategies, 1995)#. In 1980, 5 million Americans
had used nitrite inhalants. In 1989, 100 million doses of amphetamines
were consumed in the U.S. #(Duesberg, 1992)#.
to a 1994-survey of the National Institute on Drug Abuse, "more
than 5 percent (221,000) of the 4 million women who give birth each
year use illicit drugs during their pregnancy." #(Drug Strategies,
1995)#. These mothers are the reservoir from which most of the 1017
pediatric AIDS cases reported in the US in 1994 were recruited #(Centers
for Disease Control and Prevention, 1994b)# (see 10).
scientific documentation of recreational drug use is extremely sporadic
and inaccessible, not only because these drugs are illegal, but
more importantly because the medical-scientific community is totally
uninterested in drugs as a cause of AIDS (see above).
about 150,000 HIV-positive Americans were on AZT between 1992 and
#1995 (Duesberg, 1992; Thomas, 1995)#. Probably because drug toxicity
is generally ignored, there are also no national statistics available
on how many HIV-positive Americans are on AZT and other anti-HIV
drugs, that, like AZT, are designed to kill human cells #(Duesberg,
percentage of AIDS patients among the many American drug users reflects
the highest lifetime dose of drug use, just like the lung cancer
and emphysema patients reflect the highest lifetime tobacco dose
among the 50 million smokers in the U.S. The long "latent period
of HIV" is a euphemism for the time needed to accumulate the
drug dosage that is sufficient for AIDS. Indeed it takes about 10
years of injecting heroin and cocaine to develop weight loss, tuberculosis,
bronchitis, pneumonia and other drug-induced diseases #(Layon et
al., 1984; Schuster, 1984; Savona et al., 1985; Donahoe
et al., 1987; Espinoza et al., 1987; Weber et al.,
The time lag
from initiating a habit of inhaling nitrites to acquire Kaposi's
sarcoma has been determined to be 7 to 10 years #(Newell et al.,
1985a; Beral et al., 1990; Lifson et al., 1990; Duesberg,
1992)#. Blaming Kaposi's sarcoma on HIV after inhaling carcinogenic
nitrites for 10 years is like blaming lung cancer and emphysema
on a "slow" virus after smoking two packs of cigarettes
a day for 20 years.
AZT, at the
currently prescribed high doses of 0.5 to 1.5 grams per person per
day, causes many of the above described AZT-specific diseases faster
than recreational drugs, i.e. within weeks or months after administration
#(Duesberg, 1992; Lewis-Thorton, 1994)#.
group-specific AIDS diseases occur, because of risk group-specific
drug use explains the following risk-group-specific AIDS diseases:
sarcoma specific for male homosexuals. Kaposi's sarcoma as an
AIDS diagnosis is 20 times more common among homosexuals who use
nitrite inhalants than among AIDS patients who are intravenous drug
users, or hemophiliacs #(Haverkos and Dougherty, 1988; Beral et
al., 1990)#. Due to the carcinogenic potential, nitrites were
originally proposed as causes of Kaposi's sarcoma #(Marmor et
al., 1982; Haverkos et al., 1985)#. "Aggressive
and life-threatening" Kaposi's sarcoma particularly pulmonary
Kaposi's sarcoma, is exclusively observed in male homosexuals (Sloand,
Kumar and Pierce, 1993; Meduri et al., 1986; Garay et
al., 1987; Gill et al., 1989). Since the lungs are the
primary site of exposure to nitrite inhalants, the evidence that
up to 32% of Kaposi's sarcomas of homosexual men can be diagnosed
as pulmonary Kaposi's sarcoma #(Gill et al., 1989; Irwin
and Kaplan, 1993)#, lends additional support to the nitrite-Kaposi's
sarcoma hypothesis. Pulmonary Kaposi's sarcoma has never been described
by Moritz Kaposi, nor anywhere else prior to the AIDS epidemic #(Kaposi,
that the nitrite-induced AIDS Kaposi's sarcoma and the classic Kaposi's
sarcomas are entirely different cancers under the same name. The
"HIV-associated" Kaposi's sarcomas observed in male homosexuals
are "aggressive and life-threatening" #(Sloand, Kumar
and Pierce, 1993)#, fatal within 8-10 months after diagnosis, and
often located in the lung #(Meduri et al., 1986; Garay et
al., 1987; Gill et al., 1989; Irwin and Kaplan, 1993)#.
The classic "indolent and chronic" Kaposi's sarcomas are
diagnosed on the skin of the lower extremities and hardly progress
over many years #(Meduri et al., 1986; Drotman and Haverkos,
1992; Cohen, 1994a)#. Meduri et al. point out that the "pulmonary
involvement by the neoplasma has been an unusual clinical finding"
in the Kaposi's sarcomas of male homosexuals compared to all "classic"
Kaposi's sarcomas #(Meduri et al., 1986)#. Nevertheless,
the distinction between classic and AIDS Kaposi's sarcoma is hardly
ever emphasized and may have escaped many observers due to the "difficulty
in pre-mortem diagnosis," because "pulmonary Kaposi's
sarcoma was indistinguishable from opportunistic pneumonia ..."
#(Garay et al., 1987)#.
and cytotoxicity of nitrites also explains the proclivity of male
homosexual nitrite users for pneumonia, which is the most common
AIDS disease in the U.S. and Europe #(Haverkos and Dougherty, 1988;
Duesberg, 1992)# (Table 1) (Chapter 6). Moreover the immunotoxins
and cytotoxins of cigarette smoke explain, why in two groups of
otherwise matched HIV-positive male homosexuals cigarette smokers
developed pneumonia twice as often as non-smokers over a period
of 9 months #(Nieman et al., 1993)#.
mortality of intravenous drug users. Intravenous drug users
suffer from long-term malnutrition and insomnia, which are primary
causes of immunodeficiency worldwide #(Seligmann et al.,
1984)#. This explains the tuberculosis, pneumonia, and weight loss
that are typical of these risk groups #(Layon et al., 1984;
Stoneburner et al., 1988; Pillai, Nair and Watson, 1991;
Duesberg, 1992; Mientjes et al., 1993)#. Injection of unsterile
drugs combined with immunodeficiency also cause septicemia and endocarditis
that are common in AIDS patients who are intravenous drug users
#(Duesberg, 1992)#. As a result, intravenous drug users only achieve
a very low average age. A German study found the average age at
death to 29.6 years for HIV-free and 31.5 years for HIV-positive
addicts #(Lockemann et al., 1995)#; and an American study
showed that both HIV-positive and negative intravenous drug users
died from the same diseases #(Stoneburner et al., 1988)#.
birth weight and mental retardation of AIDS babies. 80%
of American/European babies with AIDS are born to mothers who were
intravenous drug users during pregnancy; they acquire low birth
weight, mental retardation and immunodeficiency through maternal
drug use #(Duesberg, 1992; Drug Strategies, 1995)#. The B-cell deficiencies
and certain bacterial infections-that are both only considered AIDS-defining
in children-are also specific expressions of their acquired immunodeficiency
#(Centers for Disease Control, 1987; Centers for Disease Control
and Prevention, 1992; Duesberg, 1992)#.
and wasting of AZT recipients. Anemia, leukopenia, pancytopenia,
diarrhea, weight loss, hair loss, impotence #(Duesberg, 1992), hepatitis
#(Freiman et al., 1993)#, and pneumocystis pneumonia #(Saah
et al., 1995)# that are observed in recipients of AZT and
other DNA chain terminators, are predictable consequences of the
cytotoxicity of these drugs (see Chapter 6). In addition, non-renewal
of mitochondrial DNA causes muscle atrophy, hepatitis, and dementia;
and carcinogenic activity causes cancers such as lymphoma in AZT
recipients #(Pluda et al., 1990; Duesberg, 1992; McLeod and
Hammer, 1992; Freiman et al., 1993; Bacellar et al.,
1994; Parker and Cheng, 1994; Physicians' Desk Reference, 1994)#.
Compared to untreated controls AZT recipients die 2.4-times more
often #(Goedert et al., 1994)#, 25% more often #(Seligmann
et al., 1994)#, or live only 2 years instead of 3 years with
AIDS #(Poznansky et al., 1995)#.
between HIV and AIDS, because drugs, not HIV, cause AIDS.
survivors or "non-progressors." Persons infected by
HIV for more than the 10-year-latent-period-from-HIV-to-AIDS who
are studied by HIV researchers are termed long-term survivors and
more recently "non-progressors" #(Scolaro, Durham and
Pieczenik, 1991; Learmont et al., 1992; Cao et al.,
1995)#. David Ho et al. recently gave a key to long-term survival,
"none had received antiretroviral therapy" #(Cao et
al., 1995)#. Likewise Alvaro Munoz reported that not one of
the long-term survivors of the largest federally funded study of
male homosexuals at risk for AIDS, the MACS study, had used AZT
#(Munoz, 1995)#. And several survey studies document that in addition
to abstaining from antiviral drugs long-term survivors are those
who have given up or never taken recreational drugs #(Wells, 1993;
Gavzer, 1995; Root-Bernstein, 1995b)#.
vast majority of HIV-positives are long-term survivors! Worldwide,
they number 17 million, including 1 million HIV-positive but healthy
Americans and 0.5 million HIV-positive but healthy Europeans #(Merson,
1993; World Health Organization, 1995)#. Most of these have been
HIV-positive for at least 10 years now, because their numbers have
not changed since the time between 1984 to 1988, when the epidemic
of HIV-testing began in the respective countries #(Duesberg, 1992)#.
6% (or 1,025,073) of these 17 million HIV-positives have developed
AIDS diseases since AIDS statistics are kept #(World Health Organization,
1995)#. Since no more than 6% of HIV-carriers worldwide have developed
AIDS in 7 to 10 years, the annual AIDS risk of an HIV-carrier is
less than 1% per year. However, even this low figure is not corrected
for the normal occurence of the 29 AIDS-defining diseases in HIV-free
controls. There is no evidence that HIV-positive people who are
not drug users have a higher morbidity or mortality than HIV-free
controls #(Duesberg, 1995a, see Chapter 10).
drug users and male homosexuals losing their T-cells prior to HIV
infection. Prospective studies of male homosexuals using psychoactive
and sexual stimulants have demonstrated that their T-cells may decline
prior to infection with HIV. For example, the T-cells of 37 homosexual
men from San Francisco declined steadily prior to HIV infection
for 1.5 years from over 1200 to below 800 per µl #(Lang et
al., 1989)#. In fact, some had fewer than 500 T-cells 1.5 years
before seroconversion #(Lang et al., 1987)#. Although recreational
drug use was not mentioned in these articles, other studies of the
same cohort of homosexual men from San Francisco described extensive
use of recreational drugs including nitrites #(Darrow et al.,
1987; Moss, 1987; Ascher et al., 1993; Duesberg, 1993d; Ellison,
Downey and Duesberg, 1995)#. Likewise 33 HIV-free male homosexuals
from Vancouver, Canada, had "acquired" immunodeficiency
prior to HIV infection #(Marion et al., 1989)#. Again this
study did not mention drug use, but in other articles the authors
reported that all men of this cohort had used nitrites, cocaine
and amphetamines #(Archibald et al., 1992; Duesberg, 1993f;
Schechter et al., 1993c)#.
study of its kind reported that about 450 (16% of 2795) HIV-free,
homosexual American men of the MACS cohort from Chicago, Baltimore,
Pittsburgh and Los Angeles had acquired immunodeficiency, having
less than 600 T-cells per µl, prior to HIV infection #(Kaslow
et al., 1989)#. Many HIV-positive and -negative men of this
cohort had essentially the same degree of lymphadenopathy: "Although
seropositive men had a significantly higher mean number of involved
lymph node groups than seronegative men (5.7 compared to 4.5 nodes,
p0.005), the numerical difference in the means is not striking"
#(Kaslow et al., 1987)#. According to previous studies on
this cohort 71% of these men had used nitrite inhalants, in addition
to other drugs #(Kaslow et al., 1987)#; 83% had used one
drug, and 60% had used two or more drugs during sex in the previous
six months #(Ostrow et al., 1990)#.
of the same cohort observed that the risk of developing AIDS correlated
with the frequency of receptive anal intercourse prior to and after
HIV infection #(Phair et al., 1992)#. Other studies have
shown that receptive anal intercourse correlates directly with the
use of nitrite vasodilaters #(Haverkos and Dougherty, 1988; Duesberg,
1992; Parke, 1993)#.
Thus in male
homosexuals at risk for AIDS, AIDS often precedes infection by HIV,
not vice versa. Since the cause must precede the consequence, drug
use remains the only group-specific choice to explain "acquired"
immunodeficiencies prior to HIV. If male homosexuality were to cause
immunodeficiency, about 10% of the adult American male population
should have AIDS #(Duesberg, 1992; Seidman and Rieder, 1994)#.
studies of intravenous drug users also document T-cell losses prior
to infection by HIV. For example, among intravenous drug users in
New York "The relative risk for seroconversion among subjects
with one or more CD4 [T-cell] count <500 cells/µl compared
with HIV-negative subjects with all counts >500 cells/µl
was 4.53." #(Des Jarlais et al., 1993)#. A similar study
from Italy showed that a low number of T-cells was the highest risk
factor for HIV infection #(Nicolosi et al., 1990)#. Again,
a decrease in T-cells is a risk factor for HIV infection, and not
the hypothesis that HIV is a marker of drug consumption, rather
than the cause of AIDS (see IV): the more drugs are consumed intravenously
or for sex, the higher is the risk of HIV infection #(Duesberg,
AIDS. One summary of the AIDS literature describes over 4,621
clinically diagnosed AIDS cases who were not infected by HIV #(Duesberg,
1993f, see Chapter 7)#. Additional cases are described that were
not in this summary #(Kaslow et al., 1987; Lang et al.,
1987; European Collaborative Study, 1991; Weiss et al., 1992;
Ellison, Downey and Duesberg, 1995; Moore and Chang, 1995)#. They
include intravenous drug users, male homosexuals using aphrodisiac
drugs like nitrite inhalants, and hemophiliacs developing immune
suppression from long-term transfusion of foreign proteins contaminating
factor VIII #(Duesberg, 1993f; Duesberg, 1995b)#.
Each of these
non-correlations between HIV and AIDS are predicted by the hypothesis
that recreational drugs and other non-contagious risk factors cause
of drug use either stabilizes or cures AIDS and other diseases-even
Ten out of 11 HIV-positive, AZT-treated AIDS patients recovered
cellular immunity after discontinuing AZT in favor of an experimental
vaccine #(Scolaro, Durham and Pieczenik, 1991)#. Two weeks after
discontinuing AZT, 4 out of 5 AIDS patients recovered from myopathy
#(Till and MacDonnell, 1990)#. Three of four AIDS patients recovered
from severe pancytopenia and bone marrow aplasia 4-5 weeks after
AZT was discontinued #(Gill et al., 1987)#.
The incidence of AIDS diseases among HIV-positive intravenous
drug users over 16 months was 19% (23/124) and only 5% (5/93) among
those who stopped injecting drugs #(Weber et al., 1990).
The T-cell counts of HIV-positive intravenous drug users from New
York dropped 35% over 9 months, compared to HIV-positive controls
who had stopped injecting #(Des Jarlais et al., 1987)#.
drugs and AZT. The health of male homosexuals is stabilized
or even improved by avoiding recreational drugs. For example in
August 1993 there was no mortality during 1.25 years in a group
of 918 British HIV-positive homosexuals who had "avoided the
experimental medications on offer" and chose to "abstain
from or significantly reduce their use of recreational drugs, including
alcohol" #(Wells, 1993)#. Assuming an average 10-year latent
period from HIV to AIDS, the virus-AIDS hypothesis would have predicted
at least 58 (918/10 x 1.25 x 50%) AIDS cases among 918 HIV-positives
over 1.25 years. Indeed, the absence of mortality in this group
over 1.25 years corresponds to a minimal latent period from HIV
to AIDS of over 1,148 (918 x 1.25) years. On July 1, 1994 there
was still not a single AIDS case in this group of 918 HIV-positive
homosexuals (J. Wells, London, personal communication).
of 29% of 1,020 HIV-positive male homosexuals and intravenous drug
users in a clinical trial even increased over 2 years #(Hughes et
al., 1994)#. These HIV-positives belonged to the placebo arm
of an AZT trial for AIDS prevention and thus were not treated by
AZT. It is probable that under clinical surveillance the 29% whose
T-cells increased, despite HIV, have given up or reduced immunosuppressive
recreational drug use in the hope that AZT would prevent AIDS.
babies, born to drug-addicted mothers, recover after birth. HIV-positive
babies, born to mothers who were intravenous drug users during pregnancy,
provide the best examples for the prediction that termination of
drug use prevents, or cures AIDS-despite the presence of HIV. For
example, Blanche et al. have observed for three years 71
HIV-positive newborns who had shared intravenous drugs with their
mothers prior to birth. Ten of these children developed encephalopathy
and AIDS-defining diseases of which 9 died during their first 18
months of life. The study points out that the risk of a newborn
to develop AIDS was related "directly with the severity of
the disease in the mother at the time of delivery." Based on
the severity of their symptoms about 60% of the children were treated
prophylactically, but apparently briefly with AZT "for at least
one month," and 50% were treated with sulfa-drugs #(Blanche
et al., 1994)#. Despite HIV, 61 of the 71 HIV-positive children
either developed only "intermittent" diseases from which
they recovered during their first 18 months or developed no disease
at all during the 3 years of observation. The T-cells of these children
increased after birth from low to normal levels-despite the presence
A very similar
picture emerges from a collaborative European study of HIV-positive
newborns #(The European Collaborative Study, 1994)#. The study reports
that about 20% of the HIV-positive children had died or developed
long-term AIDS during the first year after birth, and another 20%
during the second and third year. About 10% of the children were
"treated with zidovudine [AZT]" before 6 months of age
and 40% by 4 years #(The European Collaborative Study, 1994)#. But
over 60% of congenitally-infected children proved to be healthy
up to 6 years after birth-despite the presence of HIV. Most of these
had experienced transient AIDS diseases, such as pneumonia, bacterial
infections, candidiasis and cryptosporidial infection during the
first year after birth.
study does not even mention the health and health risks of the mothers,
previous reports from the European Collaborative Study group have
documented that "nearly all children were born to mothers who
are intravenous drug users" #(Mok et al., 1987; Duesberg,
1992)#. In 1991, the European Collaborative Study group reported
that 80% of the children with pediatric AIDS were born to mothers
who were intravenous drug users #(European Collaborative Study,
1991)#. The 1991-study further points out that "children with
drug withdrawal symptoms" were most likely to develop diseases,
and that children with no withdrawal symptoms but "whose mothers
had used recreational drugs in the final 6 months of pregnancy were
intermediate" in their risk to develop diseases #(European
Collaborative Study, 1991)#.
to the HIV hypothesis every infected baby should have developed
AIDS and progressively lost T-cells, and according to an HIV plus
cofactor hypothesis, at least all those with intermittent diseases
should have progressed to AIDS. This was not observed.
to the drug hypothesis, the AIDS risk of the children is a function
of the drugs consumed. Those who received the highest doses of drugs
before birth would have acquired irreversible diseases and those
who acquired diseases from sublethal thresholds would be able to
recover after cessation of maternally administered drugs. Indeed,
both, the European Collaborative Study group and Blanche et al.
show that the majority of children gained T-cells and recovered
from transient diseases after discontinuation of maternal drug input-despite
the presence of HIV. The childrens risk for AIDS was related "directly
with the severity of the disease in the mother" #(Blanche et
al., 1994)#, which is an expression for the extent of drug consumption
by the mother.
the harm of maternal drug consumption to sick babies was compounded
after birth, because "prophylactic treatment [with] ... sulfamethoxazale
and zidovudine [AZT] was started earlier and was more frequent among
the 16 children born to mothers with class IV disease (AIDS)"
#(Blanche et al., 1994)#. (The Blanche study did include
mothers with AIDS who were not intravenous drug users). The European
Collaborative Study group reports that 10 to 40% of HIV-positive
children were treated with AZT.
that discontinuation of recreational and antiretroviral drug use
stabilizes and even cures AIDS in HIV-positive persons.
T-cells of HIV-positive hemophiliacs increase after removal of immunosuppressive
foreign proteins from their factor VIII therapy (Duesberg, 1995,
see Chapter 11), and the T-cells of African HIV-positive tuberculosis
patients increase after "standard anti-TB treatment" and
improved nutrition (Martin et al., 1995).
In sum, the
drug-AIDS hypothesis correctly predicts all aspects of American/European
AIDS, while the HIV-hypothesis predicts none.
X. A possible
solution at last
drug hypothesis should have a very high priority in AIDS research,
because this hypothesis makes verifiable predictions #(Cohen, 1994a;
DeNoon, 1995)#. Drug toxicity could be tested experimentally in
animals, and in human cells in tissue culture. In addition, drug
toxicity could be tested epidemiologically in humans who are addicted
to recreational drugs or are prescribed AZT. Such tests could be
conducted at a fraction of the cost that is now invested in the
If the drug
hypothesis proved to be correct, AIDS would be an entirely preventable
disease. Here is how:
(1) AZT use
would be banned immediately.
(2) AIDS from
illicit recreational drugs would be reduced or prevented by education
against drug use. (Hemophilia AIDS would be prevented by the use
of pure factor VIII (Chapter 10)).
(3) AIDS therapy
would be achieved by termination of recreational drug use and treating
AIDS diseases for their specific causes, e.g. tuberculosis with
antibiotics, Kaposi's sarcoma with conventional cancer therapy,
and weight loss with good nutrition-rather than treating each of
these unrelated diseases with the same cell-killer AZT.
to saving about 100,000 lives per year from AIDS, the drug hypothesis
could save the American tax payer up to $20 billion annually. Currently
the federal government spends annually $7.5 billion on AIDS treatment,
research and education #(AIDS Weekly, 1995; Gutknecht, 1995)#. And
the Federal drug budget currently costs $13 billion, mainly for
supply control, interdiction, methadone treatment and "education"
#(Drug Strategies, 1995)#.
AIDS education nor drug education ever target the health effects
of long-term drug use. They focus on the legal and social consequences
of drug use and on the effects of drug use on transmission of HIV
via unsafe sex and without "clean needles." Instead of
studying the unknown, and warning against the known health hazards
of recreational drugs, the medical establishment turns a blind eye
to drug toxicity in its single-minded pursuit of HIV with safe sex
and clean needles #(Project Inform, 1992; Ascher et al.,
1993; Cohen, 1994a)#. The clean-needle program of the AIDS-establishment
would appear to encourage rather than discourage intravenous drug
use. Reflecting this state of mind, Science recently rejected
the drug-AIDS hypothesis, quoting a drug researcher that "Heroin
is a blessedly untoxic drug" #(Cohen, 1994a)# and described
nitrite inhalant-AIDS links as another "hatched" theory
to warn against the health risks of drug addiction is certainly
one of the reasons that "drug use among young people has risen
substantially for the first time in more than a decade" #(Drug
Strategies, 1995)#. Nitrite use continues to remain popular and
has even increased recently, particulary among male homosexuals
#(Ascher et al., 1993; Duesberg, 1993d; Mansfield and Owen,
1993; Parke, 1993; Schechter et al., 1993b; Schechter et
al., 1993c; Bethell, 1994; Gorman, 1994; Hodgkinson, 1994; Lauritsen,
1994; Sadownick, 1994; Vollbrechtshausen, 1994; Brandley, 1995;
Haverkos and Drotman, 1995, Mirken, 1995). There is no report that
nitrite bans are ever enforced or that nitrite warnings are taken
seriously #(Bethell, 1994, Mirken, 1995)#. And the number of intravenous
drug-AIDS patients has increased steadily for years in America #(Centers
for Disease Control and Prevention, 1994b; Drug Strategies, 1995)#-probably
because drug control in America is "primarily focused on supply
control efforts" #(Drug Strategies, 1995)#.
AIDS and drug education were based on the health consequences of
long-term drug use, it would be as successful as the federal anti-smoking
program. Based on education that smoking causes lung cancer, emphysema
and heart disease, smoking has dropped in the US from 42% of the
adult population in 1965 to 25% in 1995 #(Associated Press, 1995b)#.
of AIDS could be as close as a very testable, very affordable, and
very practicable alternative hypothesis.
Ruhong Li for searching the AIDS literature and assistance with
computer programs, Prof. Phil Johnson, School of Law UC Berkeley,
for many references and critical commentary, Russell Schoch for
critical review of the manuscript, and Siggi Sachs for preparation
of, and review of the manuscript, and Claus Koehnlein (Kiel, Germany)
and Colman Jones (Toronto, Canada) for critical information. This
investigation was supported in part by the Council for Tobacco Research,
USA, and private donations from Thomas Boulger (Redondo Beach, Calif.,
USA), Glenn Braswell (Los Angeles, Calif., USA), Dr. Richard Fischer
(Annandale, Va., USA), Dr. Peter Paschen (Hamburg, Germany), Ruth
Sackman, president of the Foundation for the Advancement in Cancer
Therapy (New York, USA).
1989. AIDS: The HIV Myth. St. Martin's Press, New York.
1995. Government Congressman questions funding for AIDS research.
AIDS Weekly (electronic version) May 22.
H. Gaines, A. Sönnerborg, G. Nyström, P. O. Pehrson, F.
Chiodi, M. von Sydow, L. Moberg, K. Lidman, B. Christensson, B.
Åsjö and E. M. Fenyö, 1987. Isolation of human immunodeficiency
virus (HIV) from plasma during primary HIV infection. J. Med.
Virol. 23: 67-73.
K., 1984. Researchers believe AIDS virus is found. New York Times,
April 24, p C1, C3.
K., 1992. Working in public to explain AIDS-like ills. New York
Times, Aug. 18, p B6.
R. M. and R. M. May, 1992. Understanding the AIDS pandemic. Sci.
Am. 266: 20-26.
1992. Patient accuses Kaiser. Oakland Tribune December 1.
C. P., M. T. Schechter, T. N. Le, K. J. P. Craib, J. S. G. Montaner
and M. V. O'Shaughnessy, 1992. Evidence for a sexually transmitted
cofactor for AIDS-related Kaposi's sarcoma in a cohort of homosexual
men. Epidemiology 3: 203-209.
S., H. W. Sheppard, W. Winkelstein Jr and E. Vittinghoff, 1993.
Does drug use cause AIDS? Nature (London) 362: 103-104.
Ashe, A. and
A. Rampersad, 1993. Days of Grace. Alfred A. Knopf, New York.
Press, 1994. Red Cross knew of AIDS blood threat. San Francisco
Chronicle, May, 16, p A3.
Press, 1995a. Signs that Ebola Virus is Fading Away. San Francisco
Chronicle, May 24, p A6.
Press, 1995b. Study Finds Ex-Smokers Still Risk Lung Cancer. San
Francisco Chronicle, May 23, p A5.
D. M., W. W. Darrow, H. W. Jaffe and J. W. Curran, 1984. Cluster
of cases of the Acquired Immune Deficiency Syndrome patients linked
by sexual contact. Am. J. Med. 76: 487-492.
H., A. Munoz, E. N. Miller, B. A. Cohen, D. Besley, O. A. Selnes,
J. T. Becker and J. C. McArthur, 1994. Temporal trends in the incidence
of HIV-1-related neurologic diseases: Multicenter AIDS Cohort Study,
1985-1992. Neurology 44: 1892-1900.
S. P. Hauptman, H. W. Lischner, M. Sachs and R. J. Pomerantz, 1992.
Detection of human immunodeficiency virus type 1 provirus in mononuclear
cells by in situ polymerase chain reaction. N. Engl. J. Med.
D. and M. B. Feinberg, 1989. HIV revealed, toward a natural history
of the infection. N. Engl. J. Med. 321: 1673-1675.
F., J. C. Chermann, F. Rey, M. T. Nugeyre, S. Chamaret, C. Gruest,
C. Dauget, C. Axler-Blin, F. Vezinet-Brun, C. Rouzioux, W. Rozenbaum
and L. Montagnier, 1983. Isolation of a T-lymphotropic retrovirus
from a patient at risk for acquired immune deficiency syndrome (AIDS).
Science 220: 868-871.
and B. Jasny, 1993. AIDS the unanswered questions. Science
260: 1219, 1253-1293.
T. A. Peterman, R. L. Berkelman and H. W. Jaffe, 1990. Kaposi's
sarcoma among persons with AIDS: a sexually transmitted infection?
Lancet 335: 123-128.
1994. Do "poppers" hold the secret to one of the great
mysteries of AIDS? Spin 10: 87-89, 116.
M.-J. Mayaux, C. Rouzioux, J.-P. Teglas, G. Firtion, F. Monpoux,
N. Ciraru-Vigneron, F. Meier, J. Tricoire, C. Courpotin, E. Vilmer,
C. Griscelli, J.-F. Delfraissy and The French Pediatric HIV Infection
Study Group, 1994. Relation of the Course of HIV Infection in Children
to the Severity of the Disease in their Mothers at Delivery.
N. Engl. J. Med. 330: 308-312.
W. A., 1991. HIV epidemiology: past, present, and future. FASEB
J. 5: 2340-2348.
W. A., R. C. Gallo and H. M. Temin, 1988. HIV causes AIDS. Science
1988. A rebel without a cause for AIDS. Science 239: 1485-1488.
K., 1995. Crystal Symposium Next Thursday. Bay Area Reporter,
J. and A. D. Langmuir, 1990. Farr's law applied to AIDS projections.
J. Am. Med. Assoc. 263: 50-57.
Justice Statistics, 1991. Catalog of Federal Publications on
Illegal Drug and Alcohol Abuse. U.S. Department of Justice,
1990. Surviving AIDS. HarperPerennial, New York.
Cao, Y., L.
Quin, L. Zhang, J. Safrit and D. D. Ho, 1995. Virologic and Immunologic
Characterization of Long-Term Survivors of Human Immunodeficiency
Virus Type 1 Infection. N. Engl J. Med 332: 201-208.
Disease Control, 1987. Revision of the CDC surveillance case definition
for acquired immunodeficiency syndrome. J. Am. Med. Assoc.
Disease Control, 1993. U.S. AIDS cases reported through December
1992; year-end edition. HIV/AIDS Surveillance year-end edition:
Disease Control, 1994. Hetereosexually acquired AIDS-United States,
1993. Morb. Mortal. Weekly Reports 43: 155-160.
Disease Control, 1995. Update: Outbreak of Ebola viral hemorrhagic
fever-Zaire, 1995. Morb. Mort. Weekly Reports 44: 399.
Disease Control and Prevention, 1992. 1993 revised classification
system for HIV infection and expanded surveillance case definition
for AIDS among adolescents and adults. Morb Mort Weekly Rep 41(No.
Disease Control and Prevention, 1994a. U.S. HIV and AIDS cases reported
through December 1993; Year-end Edition. HIV/AIDS Surveillance
Disease Control and Prevention, 1994b. U.S. HIV and AIDS cases reported
through December 1994. HIV/AIDS Surveillance Report 6: 1-39.
Disease Control and Prevention, 1994c. U.S. HIV and AIDS cases reported
through June 1994, Mid-Year Edition. HIV/AIDS Surveillance Report
J., 1994. Mother of courage. Daily Mail, December 5, p 41.
Chiu, D. and
P. Duesberg, 1995. The Toxicity of Azidothymidine (AZT) on Human
and Animal Cells in Culture at Concentrations Used for Antiviral
Therapy. Genetica 95: 103-109.
L., R. C. Holman, T. W. Strine, M. J. Clarke and B. L. Evatt, 1994.
Changes in longevity and causes of death among persons with hemophilia
A. Am. J. Hematol. 45: 112-121.
H., 1994. Paradigms Lost. Continuum, Nov-Jan, p11-13, 27-28,
A. Haase, J. A. Levy, L. Montagnier, S. Oroszlan, N. Teich, H. Temin,
H. Varmus, P. Vogt and R. Weiss, 1986. Human immunodeficiency viruses.
Science 232: 697.
1994a. The Duesberg Phenomenon. Science 266: 1642-1649.
1994b. Is a new virus the cause of KS? Science 266: 1803-1804.
1995. Researchers air alternative views on how HIV kills cells.
Science 269: 1044-1045.
Cone, R. W.,
R. C. Hackman, M.-L. W. Huang, R. A. Bowden, J. D. Meyers, M. Metcalf,
J. Zeh, R. Ashley and L. Corey, 1994. Human herpes virus 6 in lung
tissue from patients with pneumonia after bone marrow transplantation.
N. Engl. J. Med. 329: 156-161.
Cox, G. D.,
1986. County health panel urges 'poppers' ban, cites AIDS link.
The Los Angeles Daily Journal, Mar. 24, p Section II, p.1.
M., 1995. HIV: Science by press conference. In: AIDS: Virus-
or Drug-Induced?, (eds.) Kluwer, Dordrecht, The Netherlands,
D. N. Lawrence, H. Jaffe, J. E. Kaplan, L. D. Zyla, M. Chamberland,
R. Weinstein, K.-J. Lui, L. B. Schonberger, T. J. Spira, W. J. Alexander,
G. Swinger, A. Ammann, S. Solomon, D. Auerbach, D. Mildvan, R. Stoneburner,
J. M. Jason, H. W. Haverkos and B. L. Evatt, 1984. Acquired immunodeficiency
syndrome (AIDS) associated with transfusions. N. Engl. J. Med.
W., M. W. Morgan, A. M. Hardy, H. W. Jaffe, W. W. Darrow and W.
R. Dowdle, 1985. The epidemiology of AIDS: current status and future
prospects. Science 229: 1352-1357.
W., D. F. Echenberg, H. W. Jaffe, P. M. O'Malley, R. H. Byers, J.
P. Getchell and J. W. Curran, 1987. Risk factors for human immunodeficiency
virus (HIV) infections in homosexual men. Am. J. Publ. Health
T. H. and W. F. J. Denetclaw, 1994a. Hantavirus pulmonary syndrome
in New England and Europe. N. Engl. J. Med. 331: 546-548.
W. F. and T. H. Denetclaw, 1994b. Is "south-west US mystery
disease" caused by Hantavirus? Lancet 343: 53-54.
J., 1995. Duesberg Redux (Commentary). AIDS Weekly, January
D., S. Friedman, M. Marmor, H. Cohen, D. Mildvan, S. Yancovitz,
U. Mathur, W. El-Sadr, T. J. Spira and J. Garber, 1987. Development
of AIDS, HIV seroconversion, and potential cofactors for T4 cell
loss in a cohort of intravenous drug users. AIDS 1: 105-111.
D. C., S. R. Friedman, M. Marmor, D. Mildvan, S. Yancovitz, J. L.
Sotheran, J. Wenston and S. Beatrice, 1993. CD4 Lymphocytopenia
among injecting drug users in New York City. J. Acquir. Immune
Defic. Syndr. 6: 820-822.
1994. Critic still lays blame for AIDS on lifestyle, not HIV. Nature
(London) 369: 434.
1995. Der Tod aus dem Regenwald. Die Woche, 19 May, p26-27.
M., C. Bueso-Ramos, F. Donahoe, J. J. Madden, A. Falek, J. K. A.
Nicholson and P. Bokos, 1987. Mechanistic implications of the findings
that opiates and other drugs of abuse moderate T-cell surface receptors
and antigenic markers. Ann. N.Y. Acad. Sci. 496: 711-721.
P. and H. Haverkos, 1992. What Causes Kaposi's Sarcoma? Inquiring
Epidemiologists Want to Know. Epidemiology 3: 191-193.
1995. Keeping Score-What We Are Getting for Our Federal Drug
Control Dollars. Washington,
P., 1993a. Aetiology of AIDS. Lancet 341: 1544.
P., 1993b. HIV and AIDS. Science 260: 1705.
P., 1993c. HIV and the aetiology of AIDS. Lancet 341: 957-958.
P., 1995. Foreign-protein-mediated immunodeficiency in hemophiliacs
with and without HIV. Genetica 95: 51-70.
P., 1995a. "The Duesberg-Phenomenon": Duesberg and Other
Voices (letter). Science 267: 313.
P., 1995b. Foreign-protein-mediated immunodeficiency in hemophiliacs
with and without HIV. Genetica 95: 51-70.
P. and H. Bialy, 1995. Responding to "Duesberg and the new
view of HIV." In: AIDS: Virus- or Drug-Induced?, (eds.)
Kluwer, Dordrecht, The Netherlands, in press.
P. H., 1987. Retroviruses as carcinogens and pathogens: expectations
and reality. Cancer Res. 47: 1199-1220.
P. H., 1989. Human immunodeficiency virus and acquired immunodeficiency
syndrome: Correlation but not causation. Proc. Natl. Acad. Sci.
USA 86: 755-764.
P. H., 1991. AIDS epidemiology: inconsistencies with human immunodeficiency
virus and with infectious disease. Proc. Natl. Acad. Sci. USA
P. H., 1992. AIDS acquired by drug consumption and other noncontagious
risk factors. Pharmacology & Therapeutics 55: 201-277.
P. H., 1993d. Can epidemiology determine whether drugs or HIV cause
AIDS? AIDS-Forschung 12: 627-635.
P. H., 1993e. HIV and AIDS. Science 260: 1705.
P. H., 1993f. The HIV gap in national AIDS statistics. Biotechnology
P. H., 1994a. Infectious AIDS-stretching the germ theory beyond
its limits. Int. Arch. Allergy Immunol. 103: 131-142.
P. H., 1994b. Results fall short for HIV theory. Insight, February
P. H. and J. R. Schwartz, 1992. Latent viruses and mutated oncogenes:
no evidence for pathogenicity. Prog. Nucleic Acid Res. Mol. Biol.
J. and J. J. Weyer, 1991. Linkage and independence of AIDS Kaposi
disease: The interaction of human immunodeficiency virus and some
coagents. Infection 19: 115-122.
J., A. B. Downey and P. H. Duesberg, 1995. HIV as a surrogate marker
for drug-use: a re-analysis of the San Francisco Men's Health Study.
Genetica 95: 165-171.
P., I. Bouchard, C. Buffet, V. Thiers, J. Pillot and J. P. Etienne,
1987. High prevalence of infection by hepatitis B virus and HIV
in incarcerated French drug addicts. Gastroenterologie Clinique
et Biologique 11: 288-292.
Study, 1991. Children born to women with HIV-1 infection: natural
history and risk of transmission. Lancet 337: 253-260.
S., 1989. Does HIV cause AIDS? An historical perspective. J.
Acquir. Immune Defic. Syndr. 2: 107-113.
L., R. B. Ramsey, D. N. Lawrence, L. D. Zyla and J. W. Curran, 1984.
The acquired immunodeficiency syndrome in patients with hemophilia.
Ann. Intern. Med. 100: 499-505.
1995a. AIDS-Words from the Front. SPIN Magazine, April, 189-193,
1995b. AIDS-Words from the Front. SPIN Magazine, July, 69.
B. R. McAuslan, C. A. Mims, J. Sambrook and D. O. White, 1974. The
Biology of Animal Viruses. Academic Press, Inc., New York.
N., 1994. AIDS: time to turn to basic science. Nature (London)
A., 1979. Burrows Textbook of Microbiology. W. B. Saunders
P., K. E. Helfert, M. R. Hamrell and D. S. Stein, 1993. Hepatomegaly
with severe steatosis in HIV-seropositive patients. AIDS 7:
A. E., B. R. Saltzman, Y. Cao, M. S. Nestor, M. Mirabile, J. J.
Li and T. A. Peterman, 1990. Kaposi's sarcoma in HIV-negative homosexual
men. Lancet 335: 168-169.
H., M. von Sydow, P. O. Pehrson and P. Lundbegh, 1988. Clinical
picture of primary HIV infection presenting as a glandular-fever-like
illness. Br. Med. J. 297: 1363-1368.
C., 1991. Virus Hunting-AIDS, Cancer, & the Human Retrovirus:
A Story of Scientific Discovery. Basic Books, New York.
M., M. Belenko, E. Fazzini and R. Schinella, 1987. Pulmonary manifestations
of Kaposi's sarcoma. Chest 91: 39-43.
W., D. P. Drotman and H. W. Jaffe, 1994. What Causes AIDS? The debate
continues. Reason, December, p35.
1995. Love has Helped Keep me Alive. Parade Magazine, April
1994. Heroin Returning to Center Stage. High Times, December,
Gill, P. S.,
B. Akli, P. Coletti, M. Rarick, C. Louriero, M. Bernstein-Singer,
M. Krailo and L. A. M., 1989. Pulmonary Kaposi's sarcoma: clinical
findings and results of therapy. Am. J. Med. 87: 57-61.
Gill, P. S.,
M. Rarick, R. K. Byrnes, D. Causey, C. Loureiro and A. M. Levine,
1987. Azidothymidine associated with bone marrow failure in the
acquired immunodeficiency syndrome (AIDS). Ann. Intern. Med.
J., A. R. Cohen, C. M. Kessler, S. Eichinger, S. V. Seremetis, C.
S. Rabkin, F. J. Yellin, P. S. Rosenberg and L. M. Aledort, 1994.
Risks of immunodeficiency, AIDS, and death related to purity of
factor VIII concentrate. Lancet 344: 791-792.
J., C. Y. Neuland, W. C. Wallen, M. H. Greene, D. L. Mann, C. Murray,
D. M. Strong, J. F. Fraumeni, Jr. and W. A. Blattner, 1982. Amyl
nitrite may alter T lymphocytes in homosexual men. Lancet
1994. Peter Duesberg: Visionary or Public Menace. High Times,
December, p58-61, 66.
J., 1992. Alternative view on AIDS. Lancet 339: 1289-1290.
D. S., 1986. What ever happened to the war on cancer? Discover,
G., 1995. Letter to Dr. Fauci. March 24.
H. W., 1990. Nitrite inhalant abuse and AIDS-related Kaposi's sarcoma.
J. Acquir. Immune Defic. Syndr. 3: Supplement 1, S47-S50.
H. W. and J. A. Dougherty (eds), 1988. Health Hazards of Nitrite
Inhalants. NIDA Research Monograph 83, US. Dept. Health &
Human Services, Washington, DC.
H. W. and D. P. Drotman, 1995. NIDA Technical Review: Nitrite
Inhalants. NIDA, Washington, D.C & CDC, Atlanta, GA, unpublished,
H. W., D. P. Drotman and D. Hanson, 1994. Surveillance for AIDS-related
Kaposi's sarcoma (KS): update. NIDA/CDC, Rockville, MD/Atlanta,
H. W., P. F. Pinsky, D. P. Drotman and D. J. Bregman, 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.
and S. Hulley, 1988. Preventing the heterosexual spread of AIDS:
Are we giving our patients the best advice? J. Am. Med. Assoc.
1995. Gutknecht stands by letter questioning link between HIV, AIDS.
Star Tribune, May, 12, p 5A.
Ho, D. D.,
1995. Time to Hit HIV, Early and Hard. N. Engl J. Med 333:
N., 1994. New Evidence links gay sex drug to AIDS. The London
Sunday Times, April, 10, p 1-2.
P., J. Chua and M. Noel, 1964. Nucleosides.V. The monomesylates
of 1-(2'-deoxy-beta-D-lyxofuranosyl) thymidine. J. Org. Chem.
D., D. S. Stein, H. M. Gundacker, F. T. Valentine, J. P. Phair and
P. A. Volberding, 1994. Within-Subject Variation in CD4 Lymphocyte
Count in Asymptomatic Human Immunodeficiency Virus Infection: Implications
for Patient Monitoring. J. Infectious Diseases 169: 28-36.
of Medicine, 1988. Confronting AIDS-Update 1988. National
Academy Press, Washington, DC.
H. and L. D. Kaplan, 1993. Pulmonary manifestations of acquired
immunodeficiency syndrome-associated malignancies. Seminars in
Respiratory Infections 8: 139-148.
A., J. S. Koopman, C. P. Simon and I. M. Longini Jr., 1994. Role
of the primary infection in epidemics of HIV infection in gay chorts.
J. Acquired Immune Deficiency Syndromes 7: 1169-1184.
W., K. Choi, P. A. Thomas, H. W. Haverkos, D. M. Auerbach, M. E.
Guinan, M. F. Rogers, T. J. Spira, W. W. Darrow, M. A. Kramer, S.
M. Friedman, J. M. Monroe, A. E. Friedman-Kien, L. J. Laubenstein,
M. Marmor, B. Safai, S. K. Dritz, S. J. Crispi, S. L. Fannin, J.
P. Orkwis, A. Kelter, W. R. Rushing, S. B. Thacker and J. W. Curran,
1983. National case-control study of Kaposi's sarcoma and Pneumocystis
carinii pneumonia in homosexual men: Part 1, Epidemiologic results.
Ann. Intern. Med. 99: 145-151.
1994. Why Do Doctors Hate This Man? Genre, June, p39-43,
1994. On-line journal to track new diseases. Science 266:
M., B. Tindall, P. Williamson, J. Elford and D. A. Cooper, 1993.
Factors Associated with Kaposi's Sarcoma in a Cohort of Homosexual
and Bisexual Men. J. of Acquired Immune Deficiency Syndromes
1872. Idiopathisches multiples Pigmentsarkom der Haut. Archiv
für Dermatologie und Syphilis 2: 265-273.
M. Lowdell, S. K. Jacobson and F. Hill, 1992. Inhibition of human
immunodeficiency virus and growth of infected T cells by the immunosuppressive
drugs cyclosporin A and FK 506. Proc. Natl. Acad. Sci. USA 89:
A., W. C. Blackwelder, D. G. Ostrow, D. Yerg, J. Palenicek, A. H.
Coulson and R. O. Valdiserri, 1989. No evidence for a role of alcohol
or other psychoactive drugs in accelerating immunodeficiency in
HIV-1-positive individuals. J. Am. Med. Assoc. 261: 3424-3429.
A., J. P. Phair, H. B. Freidman, R. E. Lyter, R. E. Solomon, J.
Dudley, F. Polk and W. Blackwelder, 1987. Infection with the Human
Immunodeficiency Virus: clinical manifestations and their relationship
to immunodeficiency. Ann. Intern. Med. 107: 474-480.
A., B. Blaauw, J. Spear, D. A. Paul, L. A. Falk and A. Landay, 1987.
Diagnosis of human immunodeficiency virus infection in seronegative
homosexuals presenting with an acute viral syndrome. J. Am. Med.
Assoc. 258: 1196-1199.
1987. Imminent marketing of AZT raises problems; Marrow suppression
hampers AZT use in AIDS victims. Science 235: 1462-1463.
M., P. F. Hughes and A. Khurranna, 1994. Zidovudine Use in Pregnancy:
A Report on 104 Cases and the Occurence of Birth Defects. J.
of Acquired Immune Deficiency Syndromes 7: 1034-1039.
1994. HIV and Aids: Questions of Scientific and Journalistic Responsibility.
Yale Scientific, Fall, p8-23.
R. E. Anderson, H. Perkins, R. M. Grant, D. Lyman, W. Winkelstein,
R. Royce and J. A. Levy, 1987. Clinical, Immunologic, and Serologic
Findings in Men at Risk for Acquired Immunodeficiency Syndrome.
J. Am. Med. Assoc. 257: 326-330.
H. Perkins, R. E. Anderson, R. Royce, N. Jewell and W. Winkelstein,
Jr., 1989. Patterns of T lymphocyte changes with human immunodeficiency
virus infection: from seroconversion to the development of AIDS.
J. Acquir. Immune Defic. Syndr. 2: 63-69.
E. and S. Zierler, 1993. Entangled epidemics: cocaine use and HIV
disease. J. Psychoactive drugs 25: 207-221.
J., 1990. Poison by Prescription-The AZT Story. Asklepios
Press, New York.
J., 1992. FDA documents show fraud in AZT trials. New York Native,
March 30, p 20-23.
J., 1994. NIH reconsiders nitrites' link to AIDS. Biotechnology
J. and H. Wilson, 1986. Death Rush, Poppers and AIDS. Pagan
Press, New York.
D. N., J. M. Jason, R. C. Holman and J. J. Murphy, 1990. HIV transmission
from hemophilic men to their heterosexual partners. In: Heterosexual
Transmission of AIDS, pp. 35-53, Alexander, N. J., Gabelnick,
H. L. and Spieler, J. M. (eds.) Wiley-Liss, New York.
A. Idris, M. Warzynski, R. Sherer, D. Brauner, O. Patch, D. McCulley
and P. Orris, 1984. Altered T-lymphocyte subsets in hospitalized
intravenous drug abusers. Arch. Intern. Med. 144: 1376-1380.
J., B. Tindall, L. Evans, A. Cunningham, P. Cunningham, J. Wells,
R. Penny, J. Kaldor and D. A. Cooper, 1992. Long-term symptomless
HIV-1 infection in recipients of blood products from a single donor.
Lancet 340: 863-867.
M., D. Guetard, Y. Henin, L. Montagnier and A. Zerial, 1990. Protective
activity of tetracycline analogs against the cytopathic effect of
the human immunodeficiency viruses in CEM cells. Res. Virol.
W. R., R. D. Gelber, D. J. Cotton, B. F. Cole, A. Goldhirsch, P.
A. Volberding and M. A. Testa, 1994. Evaluation of the quality of
life associated with Zidovudine treatment in asymptomatic Human
Immunodeficiency Virus infection. N. Engl. J. Med. 330: 738-743.
D., 1989. Cocaine abuse and acquired immunodeficiency syndrome:
tale of two epidemics. Am. J. Med. 87: 661-663.
1994. Down the tabloid slope. New York Times, July, 4, Monday,
J. S., 1989. Food additives handbook. Van Nostrand Reinhold,
New York, NY 19793.
R., 1994. Facing AIDS. Essence (New York), December, p63,
64, 124, 126, 130.
R., W. W. Darrow, N. A. Hessol, P. M. O'Malley, J. L. Barnhart,
H. W. Jaffe and G. W. Rutherford, 1990. Kaposi's sarcoma in a cohort
of homosexual and bisexual men: epidemiology and analysis for cofactors.
Am. J. Epidemiol. 131: 221-231.
U., F. Wischhusen, K. Pueschel and et al., 1995. Vergleich der HIV-1-Praevalenz
bei Drogentodesfaellen in Deutschland sowie in verschiedenen europaeischen
Grosstaedten (Stand: 31. 12. 1993). AIDS Forschung 10: 253-256.
A., 1992. AIDS: the alternative view (letter). Lancet 339:
1991. AIDS research turned upside down. Nature (London) 353:
1993a. Has Duesberg a right of reply? Nature (London) 363:
1993b. New-style abuse of press freedom. Nature (London)
1995. Duesberg and the new view of HIV. Nature (London) 373:
S. and G. Owen (1993) The Use of Ecstasy and Other Recreational
Drugs in Patients Attending an HIV Clinic in London and its Association
with Sexual Behaviour. IX International Conference on AIDS, Berlin.
and the CDC Cooperative Needlestick Surveillance Group, 1988. Surveillance
of health care workers exposed to blood from patients infected with
the human immunodeficiency virus. N. Engl. J. Med. 319: 118-1123.
A., M. T. Schechter, M. S. Weaver, W. A. McLeod, W. J. Boyko, B.
Willoughby, B. Douglas, K. J. P. Craib and M. O'Shaughnessy, 1989.
Evidence that prior immune dysfunction predisposes to human immunodeficiency
virus infection in homosexual men. J. Acquir. Immune Defic. Syndr.
A. E. Friedman-Kien, L. Laubenstein, R. D. Byrum, D. C. William,
S. D'Onofrio and N. Dubin, 1982. Risk factors for Kaposi's sarcoma
in homosexual men. Lancet i: 1083-1087.
J., J. G. M. Sim, G. J. Sole, L. Rymer, S. Shalekoff, A. B. N. van
Niekerk, P. Becker, C. N. Weilbach, J. Iwanik, K. Keddy, G. B. Miller,
B. Ozbay, A. Ryan, T. Viscovic and M. Woolf, 1995. CD4+ Lymphocyte
Count in African Patients Co-Infected with HIV and Tuberculosis.
Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology
U., R. W. Enlow, I. Spigland, R. J. Winchester, H. S. Sacks, E.
Rorat, S. R. Yancovitz, M. J. Klein, D. C. William and D. Mildwan,
1984. Longitudinal study of persistent generalized lymphadenopathy
in homosexual men: Relation to acquired immunodeficiency syndrome.
Lancet i: 1033-1038.
X. and S. M. Hammer, 1992. Zidovudine: Five Years Later. Ann.
Intern. Med. 117: 487-501.
V., 1994. Heroin use said to near crisis level. USA Today, May
25, p 1, 3A.
U., D. E. Stover, M. Lee, P. L. Myskowski, J. F. Caravelli and M.
B. Zama, 1986. Pulmonary Kaposi's sarcoma in the acquired immune
deficiency syndrome: clinical, radiographic, and pathologic manifestations.
Am. J. Med. 81: 11-18.
Laboratories, 1992. The Merck Manual of Diagnosis and Therapy.
Merck & Co., Inc., Rahway, NJ.
H., 1993. Slowing the spread of HIV: Agenda for the 1990's. Science
1994. Woman wins $390,000 from HRS for AIDS misdiagnosis. Miami
Herald, September 23, 1994, p Obituary page.
G. H. C., E. J. C. van Ameijden, H. M. Weigel, J. A. R. van den
Hoek and R. A. Countinho, 1993. Clinical symptoms associated with
seroconversion for HIV-1 among misusers of intravenous drugs: comparison
with homosexual seroconverters and infected and non-infected intravenous
drug misusers. Br. Med. J. 306: 371-373.
Mims, C. and
D. O. White, 1984. Viral Pathogenesis and Immunology. Blackwell
Scientific Publications, Oxford.
Mir, N. and
C. Costello, 1988. Zidovudine and bone marrow. Lancet ii:
1995. Everything you always wanted to know about poppers; the "gay
drug" is still here despite a ban, and so is the controversy.
San Francisco Frontiers Newsmagazine, July 20, p16-19.
S., J. Williamson, D. Babcook and C. Sheng-Chong, 1993. Mutagenicity
of iso-butyl nitrite vapor in the Ames test and some relevant chemical
properties, including the reaction of iso-butyl nitrite with phosphate.
Environ. Mol. Mutagen. 21: 247-252.
Mok, J. Q.,
A. De Rossi, A. E. Ades, C. Giaquinto, I. Grosch-Woerner and C.
S. Peckham, 1987. Infants born to mothers seropositive for human
immunodeficiency virus. Lancet i: 1164-1168.
S. and Y. Chang, 1995. Detection of Herpesvirus-like DNA Sequences
in Kaposi's Sarcoma in Patients With and Those Without HIV Infection.
N. Engl J. Med 332: 1181-1185.
Moss, A. R.,
1987. AIDS and intravenous drug use: the real heterosexual epidemic.
Br. Med. J. 294: 389-390.
Moss, A. R.,
D. Osmond and P. Bacchetti, 1988. The cause of AIDS. Science
B., 1995. A hypothetical disease of the immune system that may bear
some relation to the Acquired Immune Deficiency Syndrome. Genetica
1995. Disease progression 15 percent of HIV-infected men will be
long-term survivors. AIDS Weekly, (News Report) May, 15 &
29: 5-6 & 3-4.
W., D. A. Scavuzzo, C. D. Kelly, B. Y. Rubin and R. B. Roberts,
1988. T4+ cell production of interferon gamma and the clinical spectrum
of patients at risk for and with acquired immunodeficiency syndrome.
Arch. Intern. Med. 148: 1613-1616.
on AIDS, 1991. The Twin Epidemics of Substance Use and HIV. National
Commission on AIDS, Washington, D.C., July.
of Allergy and Infectious Diseases, 1994. NIAID Backgrounder:
How HIV Causes AIDS. NIH, Washington D.C., April.
Council, 1982. Diet, nutrition, and cancer. National Acad.
Press, Washington, D.C.,
R., P. W. A. Mansell, M. R. Spitz, J. M. Reuben and E. M. Hersh,
1985a. Volatile nitrites: Use and adverse effects related to the
current epidemic of the acquired immune deficiency syndrome. Am.
J. Med. 78: 811-816.
R., P. W. A. Mansell, M. B. Wilson, H. K. Lynch, M. R. Spitz and
E. M. Hersh, 1985b. Risk factor analysis among men referred for
possible acquired immune deficiency syndrome. Preventive Med.
A., M. Musico, A. Saracco, S. Molinari, N. Ziliani and A. Lazzarin,
1990. Incidence and risk factors of HIV infection: A prospective
study of seronegative drug users from Milan and Northern Italy,
1987-1989. Epidemiology 1: 453-459.
B., J. Fleming, R. J. Coker, J. R. Harris and D. M. Mitchell, 1993.
The effect of cigarette smoking on the development of AIDS in HIV-1-seropositive
individuals. AIDS 7: 705-710.
Niu, M. T.,
D. S. Stein and S. M. Schnittmann, 1993. Primary human immunodeficiency
virus type 1 infection: review of pathogenesis and early treatment
intervention in humans and animal retrovirus infections. J. Infect.
Dis. 168: 1490-1501.
B., 1990. Good Intentions: How Big Business, Politics, and Medicine
are Corrupting the Fight Against AIDS. Atlantic Monthly Press,
E. Z., P. Cowper, J. D. Hamilton, D. B. Matchar, P. Hartigan, G.
Samsa, M. Simberkoff and J. R. Feussner, 1993. Cost effectiveness
analysis of early zidovudine treatment of HIV infected patients.
Br. Med. J. 307: 1322-1325.
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, pp. 49-83, Fee, E. and Fox, D. M. (eds.)
University of California Press, Berkeley.
G., 1994. Substance abuse and HIV infection. Psychiatric Manifestations
of HIV Disease 17: 69-89.
G., M. J. Van Raden, R. Fox, L. A. Kingsley, J. Dudley, R. A. Kaslow
and the Multicenter AIDS Cohort Study (MACS), 1990. Recreational
drug use and sexual behavior change in a cohort of homosexual men.
AIDS 4: 759-765.
E., V. F. Turner and J. M. Papadimitriou, 1993. Is a positive Western
blot proof of HIV infection? Biotechnology 11: 696-707.
1993. Key factor. The Sunday Times, Dec. 19, p letter.
B. and Y. C. Cheng, 1994. Mitochondrial Toxicity of Antiviral Nucleoside
Analogs. The Journal of NIH Research 6: 57-61.
C., E. Dickmeiss, J. Gaub, L. P. Ryder, P. Platz, B. O. Lindhardt
and J. D. Lundgren, 1990. T-cell subset alterations and lymphocyte
responsiveness to mitogens and antigen during severe primary infection
with HIV: a case series of seven consecutive HIV seroconverters.
AIDS 4: 523-526.
T. A., R. L. Stoneburner, J. R. Allen, H. W. Jaffe and J. W. Curran,
1988. Risk of human immunodeficiency virus transmission from heterosexual
adults with transfusion-associated infections. J. Am. Med. Assoc.
L. Jacobson, R. Detels, C. Rinaldo, A. Saah, L. Schrager and A.
Munoz, 1992. Acquired immune deficiency syndrome occuring within
5 years of infection with human immunodeficiency virus type-1: The
multicenter AIDS cohort study. J. Acquired Immune Deficiency
Syndromes 5: 490-496.
A. N., C. A. Sabin, J. Elford, M. Bofill, G. Janossy and C. A. Lee,
1994. Use of CD4 lymphocyte count to predict long term survival
free of AIDS after HIV infection. Br. Med. J. 309: 309-313.
Desk Reference, 1994. Retrovir. Medical Economics Co., Orandell,
L. C. Saag, S. C. Yang, S. J. Clark, J. C. Kappes, K.-C. Luk, B.
H. Hahn, G. M. Shaw and J. D. Lifson, 1993. High levels of HIV-1
in plasma during all stages of infection determined by competitive
PCR. Science 259: 1749-1754.
B. S. Nair and R. R. Watson, 1991. AIDS, drugs of abuse and the
immune system: a complex immunotoxicological network. Arch. Toxicol.
M., R. Yarchoan, E. S. Jaffe, I. M. Feuerstein, D. Solomon, S. Steinberg,
K. M. Wyvill, A. Raubitschek, D. Katz and S. Broder, 1990. Development
of non-Hodgkin lymphoma in a cohort of patients with severe human
immunodeficiency virus (HIV) infection on long-term antiretroviral
therapy. Ann. Intern. Med. 113: 276-282.
M. C., R. Coker, C. Skinner, A. Hill, S. Bailey, L. Whitaker, A.
Renton and J. Weber, 1995. HIV positive patients first presenting
with an AIDS defining illness: characteristics and survival. Br.
Med. J. 311: 156-158.
1992. Is HIV the cause of AIDS? Project Discussion Paper #5,
San Francisco, May 27, p 1-6.
J., 1988. AIDS INC. Human Energy Press, San Bruno, CA.
1994, 1995. Starke Nachfrage nach synthetischen Drogen. Deutsches
Aerzteblatt 92: C-422.
R. S., 1995a. "The Duesberg Phenomenon": What Does it
Mean? (letter). Science 267: 159.
R. S., 1995b. Five myths about AIDS that have misdirected research
and treatment. Genetica 95: 111-132.
M. J. and J. M. Weiner, 1988. Prostitutes and AIDS: A health department
priority? Am. J. Public Health 78: 418-423.
E., 1990. II: The untold story of HUT78. Science 248: 1499-1507.
Saah, A. J.,
D. R. Hoover, Y. Peng, J. P. Phair, B. Visscher, L. A. Kingsley,
L. K. Schrager and for the Multicenter AIDS Cohort Study, 1995.
Predictors for failure of Pneumocystis carinii pneumonia prophylaxis.
J. Am. Med. Assoc. 273: 1197-1202.
D., 1994. Kneeling at the Crystal Cathedral. Genre, December/January
1994, p40-45, 86-90.
Project Inform, 1992. HIV=AIDS? Part One: Is HIV the Cause of
AIDS? Part Two: How Does HIV Cause AIDS? San Francisco Project
Inform, June 25, 1992.
M. A. Nardi, E. T. Lenette and S. Karpatkin, 1985. Thrombocytopenic
purpura in narcotics addicts. Ann. Intern. Med. 102: 737-741.
M. T., K. J. P. Craib, K. A. Gelmon, J. S. G. Montaner, T. N. Le
and M. V. O'Shaughnessy, 1993a. HIV-1 and the aetiology of AIDS.
Lancet 341: 658-659.
M. T., K. J. P. Craib, K. A. Gelmon, J. S. G. Montaner, T. N. Le
and M. V. O'Shaughnessy, 1993b. HIV-1 and the aetiology of AIDS.
Lancet 341: 658-659.
M. T., K. J. P. Craib, J. S. G. Montaner, T. N. Le, M. V. O'Shaughnessy
and K. A. Gelmon, 1993c. Aetiology of AIDS. Lancet 341: 1222-1223.
1992a. Covering AIDS and Living it: A Reporter's Testimony. New
York Times, December 20, p Sec 4.
1992b. Holidays and the bad tidings of H.I.V. (personal story of
Jeannie Pejko, who has AIDS). New York Times, 31 December,
p A20 (L).
1994. A conversation with Kary Mullis. California Monthly 105:
C. R., 1984. Foreword. In: Cocaine: Pharmacology, Effects and
Treatment of Abuse, NIDA Research Monograph 50, pp. VII-VIII,
Grabowski, J. (eds.) National Institute on Drug Abuse, Washington,
R. Durham and G. Pieczenik, 1991. Potential molecular competitor
for HIV. Lancet 337: 731-732.
N. and R. O. Rieder, 1994. A Review of Sexual Behaviour in the United
States. The American Journal of Psychiatry 151: 330-341.
M., L. Chess, J. L. Fahey, A. S. Fauci, P. J. Lachmann, J. L'Age-Stehr,
J. Ngu, A. J. Pinching, F. S. Rosen, T. J. Spira and J. Wybran,
1984. AIDS-an immunologic reevaluation. N. Engl. J. Med.
M., D. A. Warrell, J.-P. Aboulker, C. Carbon, J. H. Darbyshire,
J. Dormont, E. Eschwege, D. J. Girling, D. R. James, J.-P. Levy,
P. T. A. Peto, D. Schwarz, A. B. Stone, I. V. D. Weller, R. Withnall,
K. Gelmon, E. Lafon, A. M. Swart, V. R. Aber, A. G. Babiker, S.
Lhoro, A. J. Nunn and M. Vray, 1994. Concorde: MRC/ANRS randomised
double-blind controlled trial of immediate and deferred zidovudine
in symptom-free HIV infection. Lancet 343: 871-881.
S. V., L. M. Aledort, G. E. Bergman, R. Bona, G. Bray, D. Brettler,
M. E. Eyster, C. Kessler, T.-S. Lau, J. Lusher and F. Rickles, 1993.
Three-year randomised study of high-purity or intermediate-purity
factor VIII concentrates in symptom-free HIV-seropositive haemophiliacs:
effects on immune status. Lancet 342: 700-703.
1987. And the Band Played On. St. Martin's Press, New York.
P., P. Balfe, J. F. Peutherer, C. A. Ludlam, J. O. Bishop and A.
J. Leigh-Brown, 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.
P. N. Kumar and P. F. Pierce, 1993. Chemotherapy for patients with
pulmonary Kaposi's sarcoma: benefit of filgrastim (G-CSF) in supporting
dose administration. Southern Medical Journal 86: 1219-1224.
D. and A. N. Phillips, 1992. Confounding in epidemiological studies:
why "independent" effects may not be all they seem. Br.
Med. J. 305: 757-759.
P., M. Froschl, J. Ring, M. Meurer, F. D. Goebel, H. W. Ziegler-Heitbrock,
G. Riethmüller and O. Braun-Falco, 1988. T4/T8 ratio and absolute
T4 cell numbers in different clinical stages of Kaposi's sarcoma
in AIDS. Br. J. Dermatol. 119: 1-9.
J. K., J. M. Jason, B. L. Evatt and the Hemophilia-Associated AIDS
Study Group, 1989. Geographic variability of hemophilia-associated
AIDS in the United States: effect of population characteristics.
Am. J. Hematol. 32: 178-183.
and J. Cohen, 1995. Congressman Uncovers the HIV Conspiracy. Science
R. L., D. C. Des Jarlais, D. Benezra, L. Gorelkin, J. L. Sotheran,
S. R. Friedman, S. Schultz, M. Marmor, D. Mildvan and R. Maslansky,
1988. A larger spectrum of severe HIV-I-related disease in intravenous
drug users in New York City. Science 242: 916-919.
D., 1994. AIDS chief promises a shift towards basic research. Nature
(London) 370: 494.
Collaborative Study, 1994. Natural History of Vertically Acquired
Human Immunodeficiency Virus-1 Infection. Pediatrics 94:
1994. Zidovudine for mother, fetus, and child: hope or poison? Lancet
1995. Risky Business: taking stock of AZT's future. Men's Style,
May/June, p54-56, 102-106.
C. A., K. B. Mullis and P. E. Johnson, 1994. What causes AIDS ?
Reason, June, p18-23.
Till, M. and
K. B. MacDonnell, 1990. Myopathy with human immunodeficiency virus
type 1 (HIV-1) infection: HIV-1 or zidovudine? Ann. Intern. Med.
D. A. Cooper, B. Donovan and R. Penny, 1988. Primary human immunodeficiency
virus infection. Clinical and serologic aspects. Infectious Disease
Clinics of North America 2: 329-341.
I., R. Marcus, D. H. Culver, C. A. Schable, P. S. McKibben, C. I.
Bandea and D. M. Bell, 1993. Surveillance of HIV Infection and Zidovudine
Use among Health Care Workers after Occupational Exposure to HIV-infected
Blood. Ann. Intern. Med. 118: 913-919.
P. A., S. W. Lagakos, J. M. Grimes, D.S. Stein, J. Rooney, T.-C.
Meng, M.A. Fischl, A.C. Collier, J.P. Phair, M.S. Hirsch, W.D. Hardy,
H.H. Balfour, R.C. Reichman for the AIDS Clinical Trials Group,
1995. A comparison of immediate with deferred Zidovudine therapy
for asymptomatic HIV-infected adults with CD4 cell counts of 500
or more per cubic millimeter. N. Engl. J. Med. 333:
A., 1994. Drogen: Poppers, Speed und XTC: "Am Wochenende bin
ich nicht auf dieser Welt." Magnus (Germany), Februar,
1995. Contrarians at the gate. The New York Times, Jan. 8,
S., 1995. Virological mayhem. Nature (London) 373: 102.
W. Ledergerber, M. Opravil, W. Siegenthaler and R. Lüthy, 1990.
Progression of HIV infection in misusers of injected drugs who stop
injecting or follow a programme of maintenance treatment with methadone.
Br. Med. J. 301: 1362-1365.
Weil, A. and
W. Rosen, 1983. Chocolate and morphine. Houghton Mifflin
and H. Jaffe, 1990. Duesberg, HIV and AIDS. Nature (London)
N. Teich, H. Varmus and J. Coffin, 1985. Molecular Biology of
RNA Tumor Viruses. Cold Spring Harbor Press, Cold Spring Harbor,
H., C. Weston Klein, R. K. Mayur, J. Besra and T. N. Denny, 1992.
Idiopathic CD4+ T-lymphocytopenia. Lancet 340: 608-609.
1993. We have to question the so-called "facts." Capital
Gay, August 20th, p 14-15.
1989. A consumer's dictionary of food additives. Crown Publishers,
Inc., New York, NY 10022.
Organization, 1995. The Current Global Situation of the HIV/AIDS
Pandemic. Geneva, Jan.
A., 1994. Rushing to Judgement. Barron's, August, 15, p23-27.
1994. Verdict in case of false HIV diagnosis yields more clients.
The Daily Business Review, Nov. 18, p A14.