AIDS-Stretching the Germ Theory Beyond Its Limits
By Peter H. Duesberg
is the first of two in "Controversy: HIV and AIDS," sponsored
by Georg Wick, editor-in-chief of International Archives of Allergy
Archives of Allergy and Immunology, 103: 118-126, 1994
Latent viruses not pathogenic; Infectious diseases equal between
sexes; HIV fails Koch's postulates; AIDS only after HIV neutralization;
HIV-free AIDS; Non-contagious AIDS; Clinical definition of AIDS;
Non-immunodeficiency AIDS diseases; Drug-AIDS hypothesis; Drug use
that human immunodeficiency virus (HIV) causes AIDS was advanced
in 1984, based only on circumstantial evidence. To this date, the
primary evidence are correlations between the presence of antibody
against HIV and AIDS. But these correlations are biased by proponents
of the HIV hypothesis in favour of HIV. They ignore HIV-free AIDS
and they base correlations on selected studies because there are
no national HIV-AIDS statistics. The HIV-AIDS hypothesis has made
the following predictions: (1) AIDS would 'explode' from the original
risk groups into the general population via sexual transmission
of HIV. (2) Health care workers would contract AIDS from their patients,
scientists from propagating HIV, and prostitutes from their clients.
(3) The 150 chimpanzees that have been experimentally inoculated
with HIV, and the 15,000 American hemophiliacs who have been iatrogenically
inoculated before 1984, would develop AIDS. (4) immunity and vaccines
would protect against AIDS. (5) HIV would cause AIDS by killing
T-cells. (6) AIDS would occur only in people infected by HIV. But
none of these predictions proved to be correct. Recent studies show
that HIV is a passenger virus instead of the cause of AIDS: (1)
AIDS occurs at unpredictable intervals after infection; (2) HIV
may be active, passive, or totally absent from otherwise identical
AIDS cases. Indeed, AIDS does not meet one of the classical criteria
of infectious disease: (1) Equal distribution between the sexes;
(2) disease following infection within days or weeks, the time microbes
take to become either immunogenic or pathogenic or both; (3) the
presence of a common active microbe. Therefore it is proposed that
American and European AIDS is caused by the long-term consumption
of recreational drugs and the anti-HIV drug AZT. This hypothesis
is testable and provides a rational basis for AIDS control.
In April 1984,
the retrovirologist Robert Gallo from the National Institutes of
Health in Bethesda and the American Secretary of Health and Human
Services announced, at an international press conference in Washington,
that the acquired immunodeficiency syndrome (AIDS) was caused by
a retrovirus, now termed human immunodeficiency virus (HIV) .
The announcement was made before even one American study on HIV
had appeared in the scientific literature. Gallo and his collaborators
cited antibodies against the virus in "about 85% of patients
with AIDS" as the only evidence for their hypothesis . Although
AIDS occurred despite antiviral antibodies, the researchers expressed
"hope that a vaccine would be ... ready in about two years"
. In the scientific papers that followed the next month, HIV
was said to cause AIDS by depleting T-cells [2, 3]. The hypothesis
proposed that HIV would cause all of the 30 heterogenous AIDS diseases
, including those that are not consequences of immunodeficiency,
such as cancer, weight loss and dementia (Table 1) .
AIDS: From Hypothesis to Dogma
In 1986, the
American Academy of Sciences and the Institute of Medicine assembled
a blue ribbon committee of medical scientists to confront the growing
AIDS epidemic. The committee, chaired by David Baltimore, concluded
that the isolation of HIV by Montagnier et al.  and Gallo et
al.  "led to its definitive identification as the cause
of AIDS" . Without mention of dissent [8, 9], a derivative
committee declared in 1988: "The committee believes that the
evidence that HIV causes AIDS is scientifically conclusive"
[boldface in original] and proposed to rename AIDS "HIV disease"
. The committees had sealed the hypothesis into national dogma.
However, the committee's conclusion was based only on circumstantial
evidence including five questionable assumptions:
(1) The primary
assumption was that, " ... close to 100 percent of the affected
individuals can be found to harbor the virus" and "The
probability that this distribution might have occurred by chance
is less than one in a million" .
no national HIV-AIDS statistics exist , the committee had to
rely on selected individual studies and unpublished observations.
For example, the committee selected a Science News &
Comment article entitled "A rebel without a cause of AIDS"
, an unpublished speech of the epidemiologist Winkelstein and
the papers of Montagnier and Gallo as the source for the "close
to 100%" correlation . But the original paper by Montagnier
et al.  only reported a single isolation of HIV from the lymph
node of a person who did not have AIDS, and Gallo's isolate proved
to be Montagnier's virus . And the authenticity of the HIV-AIDS
correlations from Gallo's group has since been questioned on several
(2) The committee
also believed that "The virus is not found in persons who are
not at risk for infection"-assuming that infection was restricted
to AIDS risk groups, e.g. male homosexuals, intravenous drug users
and recipients of transfusions . However, HIV has since been
found in 1 million healthy Americans, 0.5 million healthy Europeans,
1.5 million healthy South Americans, 1.5 million healthy Asians
and 8 million healthy Africans .
(3) The committee
further believed that " ... AIDS is unknown in populations
that are free of HIV antibodies," i.e. that there is no HIV-free
AIDS . However, many HIV-free AIDS cases had already been reported
by 1986 and 1988, when the committees confronted AIDS .
(4) The committee
accepted without questioning the unique practice of the HIV researchers
to present antibodies against HIV as pathogenic powers of HIV. Proponents
of the HIV-AIDS hypothesis interpret these antibodies as indicators
of current and future HIV disease. However, antibodies against all
other microbes are signs of rejection of the microbe and protection
against future disease.
(5) The committee
accepted uncontrolled statistics as evidence for AIDS from transfusion
of HIV . For example, AIDS researchers blame HIV for pneumonia
and other opportunistic infections that occur in about 2% of HIV-positive
hemophiliacs per year [5, 10]. However, controlled studies have
since shown that the incidence of immunodeficiency in matched groups
of HIV-positive and negative hemophiliacs is the same .
Thus the committee
had adopted the virus-AIDS hypothesis on the basis of questionable
assumptions, primarily the assumption that all AIDS correlates with
is the Correlation between HIV and AIDS?
coincidence between HIV and AIDS can only be determined by first
diagnosing AIDS clinically and then testing for HIV. However, since
the HIV-AIDS hypothesis has been accepted in 1986, the definition
of AIDS by clinical criteria alone has been abandoned in America
and Europe in favor of an HIV-based definition . Moreover all
HIV-AIDS correlations are based on selected individual studies,
because to date no national and international AIDS statistics reporting
HIV tests exist . As a result, proponents of the HIV-AIDS hypothesis
bias HIV-AIDS correlations in several ways:
(1) They cite
HIV-AIDS correlations from selected, individual studies which are
frequently based on non-standardized and unconfirmed HIV antibody
tests [11, 14].
(2) They present
antibodies against HIV, instead of activities and titers of HIV,
as a rational cause of AIDS.
(3) They exclude
clinically diagnosed, HIV-free AIDS defining diseases from their
statistics, e.g., the 4,621 cases cited below , because the
HIV-AIDS hypothesis postulates that HIV causes AIDS. Therefore HIV-free
AIDS cases are either diagnosed by their old names, e.g. Kaposi
sarcoma, pneumonia, etc., or renamed "idiopathic CD4 lymphocytopenia,"
or ICL .
But the effort
to set apart HIV-positive from HIV-negative AIDS cases is not based
on any clinical or convincing epidemiological criteria [11, 16].
According to an editorial by Fauci: "Given the heterogeneity
of the [ICL] syndrome, it is highly likely that there is no common
cause" . Yet at the same time the proponents of the HIV
hypothesis, including Fauci, insist that HIV must be the common
cause of the 30 heterogenous AIDS diseases.
also argues that the HIV-free AIDS or ICL cases are unlike the HIV-positive
cases because "Approximately one third of the patients are
women, as compared with 11% among those with HIV ..." (in America).
But proponents of the HIV-AIDS hypothesis, including Fauci, insist
that HIV also causes African AIDS, despite about 50% of the African
patients being women .
retroviruses have been proposed as causes of HIV-free AIDS, particularly
at the VIII International AIDS Conference in 1992 in Amsterdam [17,
18], because these cases were clinically indistinguishable from
HIV-positive AIDS. Following the HIV precedent, these retroviruses
were considered "new" AIDS causes simply because of their
presence in these cases.
that the primary argument for the HIV-AIDS hypothesis, the HIV-AIDS
correlation, is a circular argument. It is in reality an artefact
of the HIV-based AIDS definition, which is a restatement of the
To date the
virus-AIDS hypothesis has been a complete failure in terms of public
health benefits: no vaccine has been developed, AIDS continues to
spread despite efforts to stop the spread of HIV, and nobody has
ever been cured from AIDS. However the acid test of a hypothesis
is not to produce useful results, but to make accurate predictions.
of the HIV-AIDS Hypothesis
hypothesis makes the following testable predictions, none of which
proved to be correct [5, 19]:
to make valid predictions is the hallmark of a flawed hypothesis.
It raises two fundamental questions: (1) Is HIV a passenger virus
rather than the cause of AIDS? (2) Is AIDS infectious?
a Passenger Virus Rather than the Cause of AIDS?
argument assumes that the presence of a virus in a disease is sufficient
proof of causation. But the presence of a virus in a disease is
by no means proof of causation. Particularly since HIV does not
cause AIDS if inoculated into chimpanzees or if iatrogenically introduced
into hemophiliacs, it could be just a harmless passenger virus.
Passenger viruses are "widely distributed ... in mammals, causing
no obvious disease" . In the absence of functional proof,
the distinction between a causative and a passenger virus can be
made by the temporal relations between infection and disease, by
the consistency of its presence, and by the biochemical activity
of the virus during the course of the disease as follows:
all criteria of a harmless passenger virus in AIDS:
(1) HIV infection
precedes AIDS by unpredictable intervals that average about 10 years.
This time is referred to as latent period of HIV by proponents of
the HIV-AIDS hypothesis, although HIV typically remains latent even
when AIDS occurs . Several groups report that HIV may reach high
titers during the primary infection [40-42]. According to Piatak
et al., these titers range from 10 to 104 infectious units per milliliter
. Despite these relatively high HIV titers in some people, and
despite the absence of antiviral immunity in all, there is no AIDS
during the primary infection [40-42]. In addition, the T-cell counts
are normal [42, 43].
When the primary
infection is terminated by antiviral immunity, no infectious HIV
remains, the T-cell are normal and there is also no AIDS . In
the face of antiviral immunity, the virus persists as a latent provirus
in healthy hosts (fig. 2).
(2) HIV also
meets one of the most telling criteria of a passenger virus in relation
to a disease: HIV-free AIDS (see above, fig. 2). At least 4,621
AIDS cases have been documented in the literature since 1984 in
whom there is no HIV . About a third of these, 1,691, were recorded
in the US, 475 in Europe and 2,555 in Africa . Since Africa
uses the clinical, rather than the HIV-based AIDS definition, most
of these cases were observed in Africa. The US and Europe bias AIDS
statistics against HIV-free AIDS, because they use the HIV-based
AIDS definition (see above).
groups have documented that HIV may be either active or passive
once immunodeficiency is acquired and AIDS appears [42, 44, 45]:
Piatak et al. observe either no infectious HIV, e.g. 0 infectious
units per milliliter plasma in 5 out of 27 HIV-antibody-positive
AIDS cases, or fewer than 25 infectious HIVs per milliliter in 6
out of 27 cases, or 102-105 in 16 out of 27 otherwise identical
AIDS cases [42, 43]. Others have reported similar noncorrelations
between virus titers and AIDS [44-46].
there is no correlation between AIDS and the number of HIV-infected
cells. Simmonds et al. report that there are from 1 to 700
to 1 in 83,000 HIV-infected leukocytes in healthy HIV carriers and
from 1 in 900 to 1 in 30,000 in AIDS patients . Bagasra et
al. report that there are from 1 in 30 to 1 in 1,000 infected
leukocytes in healthy carriers and from 1 in 10 to 1 in 1,000 in
patients with fatal AIDS.  Thus there are healthy persons with
43 times (30,000:700) and 33 times (1,000:30) more HIV-infected
cells than in AIDS patients.
that there is neither a correlation between HIV titers, nor between
the number of HIV-infected cells and AIDS-the hallmark of a passenger
(4) Even as
an active passenger, HIV does not aggravate the course of AIDS by
any HIV-specific symptom, as some other passenger viruses or microbes
do. For example, cytomegalovirus, herpes virus, Pneumocystis
carinii and Candida each cause corresponding opportunistic
infections if they are activated by acquired immunodeficiency (table
1). By contrast, the AIDS cases with active or passive HIV appear
to be identical, according to several groups of investigators [42,
44, 45, 48]. Indeed no HIV-specific AIDS symptom has ever been described,
as all AIDS-defining diseases have been known previously [10, 49]
and occur in HIV-free AIDS patients . Thus HIV is not even a
cofactor for AIDS.
that HIV is a harmless passenger virus that does neither cause AIDS
nor even contribute an HIV-specific symptom to AIDS. Since AIDS
is not caused by HIV nor consistently associated with another active
infectious agent , it may not be infectious.
All Criteria of Infectious Disease
of the HIV-AIDS hypothesis acknowledge that "AIDS does not
have the characteristics of an ordinary infectious disease. This
view is incontrovertible" . More specifically, the epidemiologists
Eggers and Weyer  state that "the spread of AIDS does not
behave like the spread of a disease that is caused by a single sexually
transmitted agent." To reconcile AIDS with infectious disease
they "simulated a cofactor [that] cannot be identified with
any known infectious agent" . The epidemiologists Anderson
and May  had to invent "assortative scenarios" for
different AIDS risk groups to match AIDS with infectious disease.
Indeed, AIDS does not meet even one of the common criteria of all
known infectious diseases:
does not fit even one of the classical criteria of an infectious
of the virus-AIDS hypothesis are all readily resolved by postulating
noninfectious AIDS. In view of this I have proposed that AIDS in
America and Europe is caused by the long-term consumption of recreational
drugs and AZT [5, 59]. African AIDS has been proposed to be an unrelated
epidemic caused by malnutrition, parasitic infections and poor sanitation
AIDS in America and Europe fits all classical criteria of a drug-induced
disease syndrome. AIDS correlates epidemiologically and chronologically
with the drug epidemics that started in America and Europe after
the Vietnam war:
30% of all American and European AIDS patients are intravenous drug
users [4, 5]. This group includes nearly all heterosexuals with
AIDS [4, 5]. It also includes 80% of all American and European babies
with AIDS who were intrauterine drug users, because their mothers
injected drugs during pregnancy .
It is known
since 1982 that virtually 100% of homosexual males with AIDS or
at risk for AIDS have been longterm users of oral, aphrodisiac drugs,
particularly nitrite inhalants, that confer euphoria and facilitate
anal intercourse [60-69]. Epidemiological studies from San Francisco
and Vancouver have just confirmed, in 1993, that 100% of several
hundred male homosexuals with AIDS had used multiple recreational
drugs [70, 71, 81]. In addition some had also used the cytotoxic
DNA chain terminator AZT as antiviral drug [72-75, 81]. The immunotoxicity
of these recreational drugs has been documented in the literature
since 1909 [5, 76].
HIV-positive healthy people and AIDS patients are currently treated
four times daily with AZT and other DNA chain terminators as anti-HIV
drugs. These drugs kill all growing cells, particularly those of
the highly proliferative immune system . Thus AZT is AIDS by
(2) In the
US recreational drug use increased over the last years at about
the same rate as AIDS . For example, 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 . During the same time
cocaine-related hospital emergencies increased 24-fold from 3,296
cases in 1981 to 80,355 cases in 1990  (fig. 1b). Note the parallelisms
between the spreads of AIDS (fig. 1a) and the spreads of cocaine
and cocaine-related hospital emergencies since 1981, and the contrast
with the non-spread of HIV since 1984 (fig. la).
(3) 90% of
the American AIDS patients are male, because according to the US
Bureau of Justice Statistics males consume about 75% of all illicit
injected drugs, and because homosexual males are virtually the only
consistent users of aphrodisiac drugs like alkyl nitrites [5, 59].
(4) AIDS occurs
on average 10 years after initiation of risk behavior, because it
takes years of recreational drug consumption to cause disease [5,
63, 77], e.g., 20 years of smoking to get lung cancer  or emphysema,
or years of alcoholism to develop liver cirrhosis. The great variations
in "latent periods" from HIV to AIDS that currently average
10 years  are euphemisms for the time required by individuals
to accumulate sufficient drug toxicity to generate AIDS diseases
risk groups have risk-group-specific AIDS diseases, e.g., Kaposi
sarcoma is observed almost exclusively in homosexuals , because
homosexuals are the almost-exclusive users of aphrodisiac nitrite
inhalants [5, 65]; tuberculosis and weight loss is observed in intravenous
drug users, because intravenous drugs cause those symptoms ;
anemia and lymphocytopenia is observed in recipients of AZT which
kills proliferating bone marrow cells [5, 80]; and hemophiliacs
get pneumonias and candidiases almost exclusively, because long-term
transfusion of foreign proteins is immunosuppressive .
hypothesis is experimentally and epidemiologically testable and
provides a rational basis for AIDS prevention and control.
I thank Jody
Schwartz for a critical review and Bryan Ellison for discussions.
Supported in part by the Council for Tobacco Research, USA, and
private donations from Glenn Braswell (Los Angeles, Calif., USA),
Dr. Richard Fischer (Annandale, Va., USA), Dr. Fabio Franchi (Trieste,
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