What’s the truth about AIDS?


Richard Moore


      A growing group of bio-medical scientists claim the cause of
      AIDS is still unknown. These heretics do not believe in the
      lethal AIDS virus called HIV. They claim that the virus is
      indeed harmless.  Most of them think AIDS is also not sexually
      transmitted; it probably has toxic  causes. People die because
      they are poisoned to death by toxic antiviral drugs.  Part of
      the AIDS dissidents even question the existence of a virus
      entity. These  HIV skeptics say that the AIDS virus has never
      really been isolated, and the AIDS  tests are worthless...
    This website tells you their story. 
overview presentation, very good:

summary statements by doctors:

selected article:


P.H. Duesberg 

Dept. of Molecular and Cell Biology; 
University of California, 
Berkeley, CA 94720 (USA) 

The first 5 AIDS cases, described in 1981, were all male
homosexual drug users with pneumocystis pneumonia and acute
cytomegalovirus infections (Gottlieb et al., 1981). Since
then, over 100,000 cases of about 25 conventional diseases
including predominantly pneumonia, Kaposi's sarcoma, lymphoma,
dementia, tuberculosis, candidiasis and diarrhoea have been
recorded as AIDS diseases in the US (CDC, 1990). Over 90 %
occurred in two major risk groups (CDC, 1990), namely in 20-
to 40-year old intravenous drug users and male homosexuals who
also consume drugs (Gottlieb et al., 1981; Lauritsen and
Wilson, 1986; CDC, 1 987; Darrow et al., 1987; Haverkos and
Dougherty, 1988; Rappoport, 1988; Adams, 1989; Chaisson et
al., 1989; Weiss, S., 1989; Friedman-Kien et a/., 1990).
Because acquired immune deficiency is thought to be the common
cause of these vastly disparate diseases, they were grouped
together as the AIDS syndrome.

There are two competing hypotheses as to what causes AIDS, the
virus-AIDS and the risk-AIDS hypothesis.

The virus-AIDS hypothesis, currently held by most medical
scientists, in particular virologists, proposes that the
retrovirus HIV (human immunodeficiency virus) causes AIDS by
killing billions of T cells but only on average 8 to 10 years
after infection (Institute of Medicine, Natl. Acad. Sci.,
1986, 1988; Coffin et al., 1986; Gallo and Montagnier, 1988;
Blattner et al., 1988; Duesberg, 1989a). HIV was originally
discovered by Montagnier and co-workers in 1983 as a latent
retrovirus in AIDS patients (Barre-Sinoussi et. al., 1983).
Tracking latent viruses, like HIV, depends largely on
technology that was only developed in the 70's and 80's. Prior
to that time, a latent virus such as HIV was practically
undetectable. It is for this reason that the virus is
perceived as "new" (Gallo and Montagnier, 1988; Blattner et
al., 1988). On the basis of the virus-AIDS hypothesis, about
25 conventional diseases are now defined as AIDS if they occur
in the presence of antibody to HIV (Institute of Medicine,
Natl. Acad. Sci., 1986, 1988; CDC, 1987, 1990; Duesberg,
1989a). However, except for antibody to HIV or rare elements
of the latent virus, there is no known distinction between
conventional Kaposi's sarcoma (Friedman-Kien et al., 1990),
Iymphoma, dementia, tuberculosis, candidiasis, diarrhoea, etc.
and their AIDS counterparts.

The fact that antibody to HIV is found in the US predominantly
in AIDS risk groups, and that about 1.5 % of the 1 to 1.5
million antibody-positive Americans develop AIDS diseases
annually (Duesberg, 1989a), are cited as the primary arguments
for the virus-AIDS hypothesis (Coffin et al., 1986; Institute
of Medicine, Natl. Acad. Sci., 1986, 1988; Gallo and
Montagnier, 1988; Blattner et al., 1988). Yet a correlation,
in particular one with antibody to a virus, is not an
unambiguous argument for viral causation of a disease
(Duesberg, 1989a). Moreover, the relevance of this correlation
to the aetiology of AIDS is questionable because it is 100 %
by definition (Institute of Medicine, Natl. Acad. Sci., 1986,
1988; Duesberg, 1989a) rather than by natural coincidence
between the diseases and HIV.

In addition, a viral aetiology of AIDS is claimed based on
anecdotal cases of transmission (Institute of Medicine, Natl.
Acad. Sci., 1986, 1988; Gallo and Montagnier, 1988; Blattner
et al., 1988). It is claimed that because of infection with
HIV, antibody-positive haemophiliacs or other
antibody-positive recipients of transfusions have developed
diseases otherwise typical of their various conditions,
although these diseases appear on average only 8 to 10 years
after antiviral immunity and only in 1-3 % of them per year
(Duesberg, 1989a). Likewise it is claimed that HIV
transmission from mother to child is the reason some
antibody-positive babies have developed typical pediatric
diseases on the average 2 years after perinatal infection
(Duesberg, 1989a) (but not the diseases typical of the major
AIDS risk groups such as Kaposi's sarcoma) (Duesberg, 1988;
Beral et al., 1990; CDC, 1990). Yet there is not a single
controlled epidemiological study to confirm the postulated
viral aetiologv of AIDS transmission, comparing for example
the incidence of AlDS-like diseases in two groups of matched
haemophiliacs that differ only in antibody to HIV (Duesberg,

Moreover, the virus-AIDS hypothesis is not compatible with
orthodox viral pathology. It is paradoxical that:

a) Unlike all other pathogenic viruses, HIV hardly infects any
cells when it is claimed to be pathogenic (Duesberg, 1987,
1988, i989a). During AIDS, < 1 in 500 lymphocytes contain a
latent HIV provirus and only 1 in 10,000 to 100,000 contain an
active provirus-just as in millions of asymptomatic carriers
(Duesberg, 1987, 1989a, 1989b; Schnittman et al., 1989).
Therefore, it is difficult to explain the loss of billions of
T cells said to be the hallmark of AIDS (Institute of
Medicine, Natl. Acad. Sci., 1986, 1988; CDC, 1987). Like the
rest of us, even viruses need to do something to get something

b) In view of the claims that in vivo HIV kills T cells
directly (Baltimore and Feinberg, 1989; Ho et al., 1989) over
99 % of the few T cells that ever become infected survive
infection to become "reservoirs" of latent HIV (Schnittman et
al., 1989).

c) In view of recent claims that viraemia is necessary for
AIDS (Baltimore and Feinberg, 1989; Coombs et al., 1989; Ho et
al., 1989), the number of infected cells remains low in all
AIDS cases (Duesberg, 1990).

d) AIDS diseases-by definition (Institute of Medicine, Natl.
Acad. Sci., 1986; Coffin et al., 1986)-only occur after the
onset of antiviral immunity, a "positive" AIDS test (Duesberg,
1987, 1988, 1989a). All other viruses cause diseases primarily
before antiviral immunity when they are biochemically most
active (Evans, 1989).

e) AIDS diseases only occur after long, unpredictable latent
periods, averaging 8 to 10 years with a minimum of 2 years in
adults (Duesberg, 1989a), while all other viruses including
pathogenic retroviruses cause primary disease within weeks
after infection. Such long latent periods are particularly
paradoxical if one argues that antiviral immunity is essential
for pathogenicity (Duesberg, 1989a).

f) The same virus would take an average of 2 years to cause
diseases in children and an average of 8 to 10 years in adults
(Institute of Medicine, Natl. Acad. Sci., 1988; Duesberg,

g) The same virus is proposed to cause neoplastic diseases
such as Kaposi's sarcomas and AIDS lymphomas as well as
necrogenic diseases such as T-cell death or AIDS dementia
(Duesberg, 1989a). This, in particular, is implausible, since
neither Kaposi's cells nor neurons are even infected by HIV
(Duesberg, 1989a). Indeed, neurons cannot be infected by HIV
because retroviruses depend on mitosis to initiate infection
(Rubin and Temin, 1958), and neurons don't divide.

h) Immune deficiency should cause neoplasms such as Kaposi's
sarcoma and lymphoma (Duesberg, 1989a). T-cell-deficient
humans or animals such as nude mice have no more tumours than
immune competent counterparts (Kinlen, 1982; Sharkey and Fogh,

i) The most common AIDS disease in the US is pneumocystis
pneumonia while the most common AIDS diseases in Africa are
slim disease, diarrhoea and fever, although Pneumocystis
carinii is ubiquitous in all humans, including Africans
(Duesberg, 1989a).

j) AIDS diseases would occur in the US to over 90 % in males,
but would be equally distributed between the sexes in Africa
if they were caused by a sexually transmitted virus introduced
into each country about 10-20 years ago (Duesberg, 1989a).

k) Among all risk groups in the US, HIV would cause Kaposi's
sarcoma almost exclusively in homosexuals (Duesberg, 1988,
1989a; Beral et al., 1990). It is also incompatible with viral
aetiology that Kaposi's sarcomas in American homosexuals with
HIV are indistinguishable from those without (Friedman-Kien et
al., 1990).

The virus-AIDS hypothesis is unproven, because (1) HIV as the
hypothetical cause of AIDS fails to meet many classical
criteria of viral pathology, (2) HIV has not been shown to
have any unconventional properties to resolve the above
paradoxa (Duesberg, 1989a), and (3) there are no controlled
epidemiological studies showing a role for HIV in AIDS. The
view that HIV is not sufficient or even not proven to be
necessary for AIDS (Duesberg, 1987, 1988, 1989a) have been
voiced by a number of scientists including: Bialy (1988);
Eigen (1989); Evans (1989; Duesberg, 1989c); Gilbert (Hall,
1988; Liversidge, 1989); Griffin (1989); Haas (1989); Holub
(1988); Root-Bernstein (1990); Rubin (1988a,b); Schwartz
(1989); Sonnabend (1989); Stewart (1989); Weiss, R. (1989) and
at least one non-scientist, Fauci's sister Denise (Fauci,
1989; Duesberg, 1989d). Moreover, Friedman-Kien et al. (1990)
and Beral et al. (1990) have now called HIV into question as a
cause of Kaposi's sarcoma, which used to be the hallmark of
AIDS in the early 80's (Beral et al., 1990) for the same
reasons I have cited above and previously (Duesberg, 1989a).

The risk-AIDS hypothesis suggests that AIDS is caused
primarily by non-infectious agents. These include psychoactive
drugs, overmedication with antibiotics (Rappoport, 1988;
Rubin, 1988a; Adams, 1989; Sonnabend, 1989) and above all AZT,
a chain terminator of DNA synthesis administered to treat HIV
infection since 1987 (Duesberg, 1989a; Farber, 1989;
Lauritsen, 1989). Consumption of psychoactive drugs is often
associated with traditional causes for immune deficiency such
as protein malnutrition and parasitic infections (Seligman et
al., 1984) and AZT is directly immunosuppressive because it is
designed to kill lymphocytes (Duesberg, 1989a; Farber, 1989;
Lauritsen, 1989). This hypothesis is compatible with views
stated by RootBernstein (1990; Rubin (1988a,b); Sonnabend
(1989); and Stewart (1989). The risk hypothesis explains:

a) Why AIDS is limited to risk groups rather than random in
the population, as would be expected from an infectious agent.

b) Why natural vaccination against HIV (a "positive AIDS
test") does not protect against AIDS.

c) The long and unpredictable latent periods between HIV
infection and AIDS, averaging 8 to 10 years in adults, as the
individual reaches a pathogenic threshold of AIDS risks. The
shorter latent periods in children averaging about 2 years
would reflect prenatal and postnatal risk factors, as 90 % of
babies with AIDS are either, born to mothers who are drug
addicts or prostitutes or both, or- are haemophiliacs
(Duesberg, 1988; CDC, l99O).

d) The enormous diversity and risk-group-specificity of AIDS
diseases in terms of the diversity of risk factors. For
example, the incidence of Kaposi's sarcoma exclusively- in
homosexuals correlates and declines directly with their
group-specific use of nitrite inhalants (Lauritsen and Wilson,
1986; Haverkos and Dougherty, 1988; Rappoport, 1988; Duesberg,
1989a; Beral et al., 1990) regardless of the presence of HIV
(Friedman-Kien et al., 1990). The nearly complete difference
between the major AIDS diseases in the US and Africa could be
explained as a consequence of drug consumption in the US and
of malnutrition and conventional parasitic infections in

e) The paradox as to why HIV, unless an innocent bystander,
can afford to infect actively 1 in 10,000 and latently < 1 in
500 susceptible lymphocytes even in those dying from AIDS
(Duesberg, 1989a; Coombs et al., 1989; Ho et al., 1989;
Schnittman el a/., 1989).

f) The recent emergence of AIDS diseases in the US as a
function of the enormous increase during the last 10 to 20
years in the consumption of psychoactive drugs (NNICC Reports,
1978-1988; Rappoport, 1988; Adams, 1989). For instance,
cocaine consumption alone has increased 5-fold during the last
10 years in the US (NNICC Reports, 1978-1988). Indeed, about a
third of the American AIDS patients are confirmed intravenous
drug users (CDC, 1990). In addition many, perhaps most, of the
male homosexuals with AIDS appear to have used various
psychoactive drugs (Gottlieb et al., 1981; Lauritsen and
Wilson, 1986; Darrow et al., 1987; Haverkos and Dougherty,
1988; Rappoport, 1988; CDC, 1990; Adams, 1989; Friedman-Kien
et al., 1990). Together, these two risk groups represent 90 %
of the US AIDS cases (CDC, 1990). Moreover, since 1987, 20,000
antibody-positive symptomatic and asymptomatic persons in the
US (Marx, 1989) and 50,000 worldwide (Deer, 1989) have been
treated with the DNA chain terminator AZT, which is directly
immunosuppressive (Duesberg, 1989a). Thus, the use of drugs
appears to be a common denominator of most AIDS cases in the

g) The preferential occurrence in the US of HIV in AIDS risk
groups can also be reconciled with the risk hypothesis. Since
HIV is not widespread in the US and also very hard to transmit
due to its chronic latency (Duesberg, 1989a), only those who
have intimate contacts with many others are likely to be
infected, as for example promiscuous homosexuals, drug addicts
sharing needles or practicing prostitution, and haemophiliacs.
Thus HIV would serve as an outstanding, but not an absolute
(Friedman-Kien et al., 1990) surrogate marker for AIDS risks
(Darrow et al., 1987; Duesberg, 1989a; Weiss, S., 1989).

It is concluded that in the US and probably in Europe, AIDS is
a collection of non-infectious deficiencies of which about 90
% are acquired by drug consumption associated with
malnutrition and parasitic infections and other specific
risks, such as chronic transfusions for treatment of
haemophilia. The 10 % of AIDS cases occurring outside the risk
groups in the US. (CDC, 1990) are consequences of the clinical
definition of AIDS, namely conventional diseases occurring in
persons accidentally infected by HIV. The African AIDS
epidemic would also appear to be the product of the
all-embracing AIDS definition, namely a widespread
heterosexual distribution of the newly detectable, dormant HIV
together with old African diseases like slim disease, fever
and diarrhoea. For example, about 10-20 % of the 30 million
Zairens carry latent HIV in Africa, but only 335 developed
AIDS in the period from 1985 to 1988 (Duesberg, 1989a). Like
nearly all retroviruses in wild animals endemic human
retroviruses are probably transmitted perinatally (Duesberg,
1989a). This would more convincingly explain the heterosexual
distribution in Africa of HIV, and hence diseases now termed
AIDS because of HIV, than theories about peculiar sexual
practices (G. Klein, 1988; Institute of Medicine, Natl. Acad.
Sci., 1988).


I thank Harry Rubin and Bryan Ellison for cutical comments.

I am supported by Outstanding Investigator Grant
#5-R35-CA39915 04 from the National Cancer Institute


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Note added in proof:

The following new information in support of the risk-AIDS
hypothesis is added:

1) Recent surveys have indicated that the incidence of
AlDS-like diseases in matched risk groups is independent of
HIV up to one year after receiving HIV in general patients
(Ward et al., 1989) and probably for over 4 years in
haemophiliacs (din et al., 1989).

2) Further, it was shown that among HIV-positive mothers, drug
addiction was the only consistent risk factor for deficiencies
among newborns (Blanche et al., 1989).

3) The CDC has now retroactively revised downward the
estimates of HlV-infected persons in the US from 1-2 million
in the period of 1985-89 to 0.75 million in 1986 and about I
million in 1990 (CDC, 1990a). During the same interval, the
"latent" period from HIV to AIDS was increased from initially
three years to currently over ten years (Duesberg, 1989a).
These apparently are attempts to close the gaps that I have
pointed out between the number of AIDS cases predicted by the
virus-AIDS hypothesis and those actually recorded (Duesberg,
1989a). Moreover, the prediction of the virus-AIDS hypothesis
that, due to sexually-transmitted virus, AIDS would spread
into the heterosexual population (Institute of Medicine,
1988), has not materialized.

4) Finally, several defences of the virus-AIDS hypothesis have
failed to refute or prove erroneous the central arguments I
have raised against it. These include defences by Blattner,
Gallo and Temin (1988) / Duesberg (1988), Eigen (1989) /
Duesberg (199Oa), Evans (1989) / Duesberg (1989c), Klein
(1988)-,-Kurth (1989) / Duesberg (1989e), Velimirovic (1989) /
Duesberg (1989f), Fauci (1989) / Duesberg (1989d), Linz (1989)
/ Duesberg (1989g), and Baltimore and Feinberg (1989) /
Duesberg (1990).

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KURTH, R. (1989), Is HIV the cause of AIDS? An up-to-date
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LINZ, U. (1989), HIV und AIDS. Nachr. Chem. Tech. Lab., 37
(9), 930.

VELIMIROVIC, B. (1989), What actually are the postulates of
causation? Some remarks on Duesberg's article "HIV and AIDS:
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WARD, J.W., BUSH, T.J., PERKINS, H.A. et. al. (1989), The
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JIN, Z., CLEVELAND, R.P. & KAUFMAN, D.B. (1989),
Immunodefciency in patients with hemophilia: an underlying
deficiency and lack of correlation with factor replacement
therapy or exposure to human immunodeficiency virus. J.
Allergy. Clin. Immunol., 83, 165.

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Richard Moore (rkm)
Wexford, Ireland

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