VIRUSMYTH HOMEPAGE
Pharmac. & Ther. Vol. 55: 201-277, 1992
AIDS ACQUIRED BY DRUG CONSUMPTION AND OTHER NONCONTAGIOUS
RISK FACTORS
PETER
H. DUESBERG
Department of Molecular and Cell Biology, 229 Stanley Hall, University
of California at Berkeley, Berkeley, CA 94720, U.S.A.
3. Discrepancies Between AIDS and Infectious Disease
3.1.Criteria of Infectious and Noninfectious Disease
The correct hypothesis explaining the cause of AIDS must
predict the fundamental differences between the two main AIDS epidemics
and the bewildering heterogeneity of the 25 AIDS diseases. In addition,
the cause of American/European AIDS should make clear why-in an era of
ever-improving health parameters, population growth and decreasing mortality
(The Software Toolworks World Atlas™, 1992; Anderson and May, 1992)-suddenly
a subgroup of mostly 20- to 45-year-old males would die from diverse microbial
and nonmicrobial diseases. The mortality from all infectious diseases combined
has been reduced to less than 1% in the Western World (Cairns, 1978) through
advanced sanitation and nutrition (Section 6) (McKeown, 1979; Moberg and
Cohn, 1991; Oppenheimer, 1992). Further, 20- to 45-year-olds are the least
likely to die from any disease (Mims and White, 1984). Their relative immunity
to all diseases is why they are recruited as soldiers. The correct AIDS
hypothesis would also have to explain why only a small group of about 20,000
Africans have developed AIDS diseases annually since 1985 (Table 1), during
a time in which Central Africa enjoyed the fastest population growth in
the world, i.e. 3% (The Software Toolworks World Atlas™, 1992).
The sudden appearance of AIDS could signal a new microbe, i.e. infectious
AIDS. Yet the suddenness of AIDS could just as well signal one or several
new toxins, such as the many new psychoactive drugs that have become popular
in America and Europe since the Vietnam War (Section 4).
Based on common characteristics of all orthodox infectious
diseases, infectious AIDS would be predicted to:
(1) Spread randomly between the sexes. This is just as
true for venereal as for other infectious diseases (Judson et al.,
1980; Haverkos, 1990).
(2) Cause primary disease within weeks or months after
infection, because infectious agents multiply exponentially in susceptible
hosts until stopped by immunity. They are self-replicating, and thus fast
acting toxins. (Although "slow" viruses are thought to be pathogenic
long after neutralization by antiviral immunity (Evans, 1989c), slow pathogenicity
by a neutralized virus has never been experimentally proven (Section 6.1).)
(3) Coincide with a common, active and abundant microbe
in all cases of the same disease. (Inactive microbes or microbes at low
concentrations are harmless passengers, e.g. lysogenic bacteriophages,
endogenous and latent retroviruses (Weiss et al., 1985), latent
herpes virus or latent ubiquitous Pneumocystis and Candida
infections (Freeman, 1979; Pifer, 1984; Williford Pifer et al.,
1988). Hibernation is a proven microbial strategy of survival, which allows
indefinite coexistence with the host without pathogenicity.)
(4) Coincides with a microbe that lyses or renders nonfunctional
more cells than the host can spare or regenerate.
(5) Generate a predictable pattern of symptoms.
By contrast non-infectious AIDS, caused by toxins, would
be predicted to:
(1) Spread nonrandomly, according to exposure to toxins.
For example, lung cancer and emphysema were observed much more frequently
in men than in women 20 years ago, because men consumed much more tobacco
than women 30-40 years ago (Cairns, 1978).
(2) Follow intoxication after variable intervals as determined
by lifetime dosage and personal thresholds for disease. These intervals
would be considerably longer than those between microbes and disease, because
microbes are self-replicating toxins. For example, lung cancer and emphysema
are "acquired" only after 10-20 years of smoking, and liver cirrhosis
is "acquired" only after 10-20 years of alcoholism.
(3) Manifest toxin-specific and intoxication site-specific
diseases, e.g. cigarettes causing lung cancer and alcohol causing liver
cirrhosis.
3.2. AIDS Not Compatible with Infectious Disease
All direct parameters of AIDS are incompatible with classical
criteria of infectious disease:
(1) Unlike conventional infectious diseases, including
venereal diseases (Judson et al., 1980), American/European AIDS
is nonrandomly (90%) restricted to males, although no AIDS disease is male-specific
(Table 1).
(2) The long and unpredictable intervals between infection
and "acquiring" primary AIDS symptoms-averaging two years in
infants and 10 years in adults, and termed "latent periods of HIV"-stand
in sharp contrast to the short intervals of days or weeks between infection
and primary disease observed with all classical viruses, including retroviruses
(Duesberg, 1987; Duesberg and Schwartz, 1992). These short intervals reflect
the time periods, that all exponentially growing microbes with generation
times of half-hours, and viruses including HIV (Clark et al., 1991;
Daar et al., 1991) with generation times of 8-48 hr need to reach
immunogenic and thus potentially pathogenic concentrations (Fenner et
al., 1974; Freeman, 1979; Mims and White, 1984). Once stopped by immunity,
conventional viruses and microbes are no longer pathogenic. Thus long latent
periods between immunity against a microbe and a given disease are incompatible
with conventional microbial causes, including HIV (Section 3.5.14). The
discrepancy of eight years between the hypothetical "latent periods
of HIV" in infants and adults presents a secondary paradox.
Nevertheless, HIV could possibly play a role in AIDS if
it were consistently reactivated by an "acquired immunodeficiency"-10
years after it was neutralized by antibodies (Section 3.4.2)-just as Candida,
Pneumocystis and cytomegalovirus play roles in AIDS if they are
activated by "acquired immunodeficiency." However, HIV is nearly
always inactive even during acquired immunodeficiency (Sections 3.3.1 and
3.5.6). In the absence of HIV reactivation during AIDS, long hypothetical
latent periods are simply statistical artifacts. They are conceived to
link HIV with AIDS and to buy time for the real causes of AIDS to generate
AIDS-defining diseases.
(3) There is no active microbe common to all AIDS patients,
and no common group of target cells are lysed or rendered nonfunctional
(Sections 3.3 and 3.5.10).
(4) There is no common, predictable pattern of AIDS symptoms
in patients of different risk groups. Instead, different risk groups have
characteristic AIDS diseases (Sections 2.1.3, 3.4.4 and 3.4.5).
Thus AIDS does not meet even one of the classical criteria
of infectious disease. In a recent response to these arguments, Goudsmit,
a proponent of the HIV-AIDS hypothesis, confirmed that "AIDS does
not have the characteristics of an ordinary infectious disease. This view
is incontrovertible" (Goudsmit, 1992). Likewise, the epidemiologists
Eggers and Weyer conclude 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) and hence have "simulated a cofactor
[that] cannot be identified with any known infectious agent" (Weyer
and Eggers, 1990). Anderson and May (1992) had to invent "assortative
scenarios" for different AIDS risk groups to reconcile AIDS with infectious
disease. Indeed, AIDS would never have been accepted as infectious without
the numerous unique assumptions that have been made to accommodate HIV
as its cause (Sections 3.5 and 6.1).
3.3.No Proof for the Virus-AIDS Hypothesis
Despite research efforts that exceed those on all other
viruses combined and have generated over 60,000 papers on HIV (Christensen,
1991), it has not been possible to prove that HIV causes AIDS. These staggering
statistics illustrate that the virus-AIDS hypothesis is either not provable
or is very difficult to prove.
Proof for pathogenicity of a virus depends either on (1)
meeting Koch's classical postulates, (2) preventing pathogenicity through
vaccination, (3) curing disease with antiviral drugs or (4) preventing
disease by preventing infection. However, the HIV-hypothesis fails all
of these criteria.
3.3.1. Virus Hypothesis Fails to
Meet Koch's Postulates
Koch's postulates may be summarized as follows: (i) the
agent occurs in each case of a disease and in amounts sufficient to cause
pathological effects; (ii) the agent is not found in other diseases; and
(iii) after isolation and propagation in culture, the agent can induce
the disease anew (Merriam-Webster, 1965; Weiss and Jaffe, 1990).
But:
(i) HIV is certainly not present in all AIDS patients,
and even antibody against HIV is not found in all patients who have AIDS-defining
diseases. HIV is not even present in all persons who die from multiple
indicator-diseases plus general immune system failure-the paradigm AIDS
cases (Sections 3.4 and 4.5). In addition, HIV is never present "in
amounts sufficient to cause pathological effects" based on the following
evidence:
(1) On average only 1 in 500 to 3000 T-cells, or 1 in
1500 to 8000 leukocytes of AIDS patients are infected by HIV (Schnittman
et al., 1989; Simmonds et al., 1990). (About 35% of leukocytes
are T-cells (Walton et al., 1986).) A recent study, relying on in
situ amplification of a proviral HIV DNA fragment with the polymerase chain
reaction, detects HIV DNA in 1 of 10 to 1 of 1000 leukocytes of AIDS patients.
However, the authors acknowledge that the in situ method cannot
distinguish between intact and defective proviruses and may include false-positives,
because it does not characterize the amplified DNA products (Bagasra et
al., 1992). Indeed the presence of 1 provirus per 10 or even 100 cells
is exceptional in AIDS patients. This is why direct hybridization with
viral DNA, a technique that is capable of seeing 1 provirus per 10 to 100
cells, typically fails to detect HIV DNA in AIDS patients (Duesberg, 1989c).
According to one study, "The most striking feature ... is the extremely
low level of HIV provirus present in circulating PBMCs (peripheral blood
mononuclear cells) in most cases" (Simmonds et al., 1990).
Since on average only 0.1% (1 out of 500 to 3000) of T-cells
are ever infected by HIV in AIDS patients, but at least 3% of all T-cells
are regenerated (Sprent, 1977; Guyton, 1987) during the two days it takes
a retrovirus to infect a cell (Duesberg, 1989c), HIV could never kill enough
T-cells to cause immunodeficiency. Thus even if HIV killed every infected
T-cell (Section 3.5.10), it could deplete T-cells only at 1/30 of their
normal rate of regeneration, let alone activated regeneration. The odds
of HIV causing T-cell deficiency would be the same as those of a bicycle
rider trying to catch up with a jet airplane.
(2) It is also inconsistent with a common pathogenic mechanism
that the fraction of HIV-infected leukocytes in patients with the same
AIDS diseases varies 30- to 100-fold. One study reports that the fraction
of infected cells ranges from 1 in 900 to 1 in 30,000 (Simmonds et al.,
1990), and another reports that it ranges from 1 in 10 to 1 in 1000 (Bagasra
et al., 1992). In all conventional viral diseases the degree of
pathogenicity is directly proportional to the number of infected cells.
(3) It is entirely inconsistent with HIV-mediated pathogenicity
that there are over 40-times more HIV-infected leukocytes in many healthy
HIV carriers than in AIDS patients with fatal AIDS (Simmonds et al.,
1990; Bagasra et al., 1992). Simmonds et al. report that
there are from 1 in 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 1000 infected
leukocytes in healthy carriers and from 1 in 10 to 1 in 1000 in patients
with fatal AIDS. Thus there are healthy persons with 43 times (30,000:700)
and 33 times (1000:30) more HIV-infected cells than in AIDS patients.
(4) In terms of HIV's biological function, it is even
more important that the levels of HIV RNA synthesis in AIDS are either
extremely low or even nonexistent. Only 1 in 10,000 to 100,000 leukocytes
express viral RNA in 50% of AIDS patients. In the remaining 50% no HIV
expression is detectable (Duesberg, 1989c; Simmonds et al., 1990).
The very fact that amplification by the polymerase chain reaction must
be used to detect HIV DNA or RNA (Semple et al., 1991) in AIDS patients
indicates that not enough viral RNA can be made or is made in AIDS patients
to explain any, much less fatal, pathogenicity based on conventional precedents
(Duesberg and Schwartz, 1992). The amplification method is designed to
detect a needle in a haystack, but a needle in a haystack is not sufficient
to cause a fatal disease, even if it consists of plutonium or cyanide.
(5) In several AIDS diseases, that are not caused by immunodeficiency
(Section 3.5.8), HIV is not even present in the diseased tissues, e.g.
there is no trace of HIV in any Kaposi's sarcomas (Salahuddin et al.,
1988) and there is no HIV in neurons of patients with dementia, because
of the generic inability of retroviruses to infect nondividing cells like
neurons (Sections 3.5.8 and 3.5.10) (Duesberg, 1989c).
As a result, there is typically no free HIV in AIDS patients
(Section 3.5.6). Indeed, the scarcity of infectious HIV in typical AIDS
patients is the reason that neutralizing antibodies, rather than virus,
have become the diagnostic basis of AIDS. It is also the reason that on
average 5 million leukocytes of HIV-positives must be cultured to activate
("isolate") HIV from AIDS patients. Even under these conditions
it may take up to 15 different isolation efforts (!) to get just one infectious
virus out of an HIV carrier (Weiss et al., 1988). The scarcity of
HIV and HIV-infected cells in AIDS patients is also the very reason for
the notorious difficulties experienced by leading American (Hamilton, 1991;
Palca, 1991a; Crewdson, 1992) and British (Connor, 1991, 1992; Weiss, 1991)
AIDS researchers in isolating, and in attributing credit for isolating
HIV from AIDS patients.
(ii) HIV does not meet Koch's second postulate, because
it is found not just in one, but in 25 distinct diseases, many as unrelated
to each other as dementia and diarrhea, or Kaposi's sarcoma and pneumonia
(Table 1, Section 2.1.2).
(iii) HIV also fails Koch's third postulate, because it
fails to cause AIDS when experimentally inoculated into chimpanzees which
make antibodies against HIV just like their human cousins (Blattner et
al., 1988; Institute of Medicine, 1988; Evans, 1989b; Weiss and Jaffe,
1990). Up to 150 chimpanzees have been inoculated since 1983 and all are
still healthy (Duesberg, 1989c) (Jorg Eichberg, personal communication,
see Section 1). HIV also fails to cause AIDS when accidentally introduced
into humans (Duesberg, 1989c, 1991a).
There is, however, a legitimate limitation of Koch's postulates,
namely that most microbial pathogens are only conditionally pathogenic
(Stewart, 1968; McKeown, 1979; Moberg and Cohn, 1991). They are pathogenic
only if the immune system is low, allowing infection or intoxication of
the large numbers of cells that must be killed or altered for pathogenicity.
This is true for tuberculosis bacillus, cholera, influenza virus, polio
virus and many others (Freeman, 1979; Mims and White, 1984; Evans, 1989c).
However, even with such limitations HIV fails the third
postulate. The scientific literature has yet to prove that even one health
care worker has contracted AIDS from the over 206,000 American AIDS patients
during the last 10 years, and that even one of thousands of scientists
has developed AIDS from HIV, which they propagate in their laboratories
and companies (Section 3.5.16) (Duesberg, 1989c, 1991a). AIDS is likewise
not contagious to family members living with AIDS patients for at least
100 days in the same household (Friedland et al., 1986; Sande, 1986;
Hearst and Hulley, 1988; Peterman et al., 1988). However the CDC
has recently claimed that seven health care workers have developed AIDS
from occupational infection (Centers for Disease Control, 1992c). But the
CDC has failed to provide any evidence against nonoccupational causation,
such as drug addiction (see Section 4). Indeed thousands of health care
workers, e.g. 2586 by 1988 (Centers for Disease Control, 1988), have developed
AIDS from nonprofessional causes. In addition the CDC has failed to report
the AIDS diseases of the seven patients and those of their putative donors,
has failed to report their sex (see next paragraph) and whether these patients
developed AIDS only after AZT treatment (see Section 4) (Centers for Disease
Control, 1992c). The failure of HIV to meet the third postulate is all
the more definitive since there is no antiviral drug or vaccine. Imagine
what would happen if there were 206,000 polio or viral hepatitis patients
in our hospitals and no health care workers were vaccinated!
Contrary to expectations that health care workers would
be the first to be affected by infectious AIDS, the AIDS risk of those
health care workers that have treated the 206,000 American AIDS patients
is in fact lower than that of the general population, based on the following
data. The CDC reports that about 75% of the American health care workers
are females, but that 92% of the AIDS patients among health care workers
are males (Centers for Disease Control, 1988). Thus the AIDS risk of male
health care workers is 35 times higher than that of females, indicating
nonprofessional AIDS causes.
Moreover, the CDC reports that the incidence of AIDS among
health care workers is percentagewise the same as that in the general population,
i.e. by 1988, 2586 out of 5 million health care workers, or 1/2000 had
developed AIDS (Centers for Disease Control, 1988), by the same time 110,000
out of the 250 million Americans, or 1/2250, had developed AIDS (Centers
for Disease Control, 1992b). Since health care workers are nearly all over
20 years old and since there is virtually no AIDS in those under 20 (Table
1), but those under 20 make up about 1/3 of the general population, it
can be estimated that the AIDS risk of health care workers is actually
1/3 lower (1/3 times 1/2000) than that of the general population-hardly
an argument for infectious AIDS.
In view of this, leading AIDS researchers have acknowledged
that HIV fails Koch's postulates as the cause of AIDS (Blattner et al.,
1988; Evans, 1989a,b; Weiss and Jaffe, 1990; Gallo, 1991). Nevertheless,
they have argued that the failure of HIV to meet Koch's postulates invalidates
these postulates rather than HIV as the cause of AIDS (Section 6.1) (Evans,
1989b, 1992; Weiss and Jaffe, 1990; Gallo, 1991). But the failure of a
suspected pathogen to meet Koch's postulates neither invalidates the timeless
logic of Koch's postulates nor any claim that a suspect causes a disease
(Duesberg, 1989b). It only means that the suspected pathogen cannot be
proven responsible for a disease by Koch's postulates-but perhaps by new
laws of causation (Section 6).
3.3.2. Anti-HIV Immunity Does Not Protect Against
AIDS
Natural antiviral antibodies, or vaccination, against
HIV-which completely neutralize HIV to virtually undetectable levels-are
consistently diagnosed in AIDS patients with the "AIDS test."
Yet these antibodies consistently fail to protect against AIDS diseases
(Section 3.5.11) (Duesberg, 1989b,c, 1991a; Evans, 1989a,b). According
to Evans, "The dilemma in HIV is that antibody is not protective"
(Evans, 1989a).
By contrast, all other viral diseases are prevented or
cured by antiviral immunity. Indeed, since Jennerian vaccination in the
late 18th century, antiviral immunity has been the only protection against
viral disease. In view of this HIV researchers have argued that antibodies
do not neutralize this virus (Section 3.5.11) instead of considering that
HIV may not be the cause of AIDS.
3.3.3. Antiviral Drugs Do Not Protect Against
AIDS
All anti-HIV drugs fail to prevent or cure AIDS diseases
(Section 4).
3.3.4. All AIDS-defining Diseases Occur in the
Absence of HIV
The absence of HIV does not prevent AIDS-defining diseases
from occurring in all AIDS risk groups, it only prevents their diagnosis
as AIDS (Sections 3.4.4, 4.5 and 4.7).
Thus, there is no proof for the virus-AIDS hypothesis-not even that
AIDS is contagious. Instead, the virus-AIDS hypothesis is based only on
circumstantial evidence, including epidemiological correlations and anecdotal
cases (Sections 3.4 and 3.5)
3.4. Noncorrelations Between HIV and AIDS
Leading AIDS researchers acknowledge that correlations
are the only support for the virus-AIDS hypothesis. For example, Blattner
et al. state, "... overwhelming seroepidemiologic evidence
(is) pointing toward HIV as the cause of AIDS ... Better methods ... show
that HIV infection is present in essentially all AIDS patients" (Blattner
et al., 1988). According to an editorial in Science, Baltimore
deduces from studies reporting an 88% correlation between antibodies to
HIV and AIDS: "This was the kind of evidence we are looking for. It
distinguishes between a virus that was a passenger and one that was the
cause" (Booth, 1988). The studies Baltimore relied on are those published
by Gallo et al. in Science in 1984 that are the basis for
the virus-AIDS hypothesis (Gallo et al., 1984; Sarngadharan et
al., 1984), but their authenticity has since been questioned on several
counts (Beardsley, 1986; Schupach, 1986; Connor, 1987; Crewdson, 1989;
Hamilton, 1991; Palca, 1991a; Crewdson, 1992). Weiss and Jaffe concur that
"the evidence that HIV causes AIDS is epidemiological ..." (Weiss
and Jaffe, 1990), although Gallo concedes that epidemiology is just "one
hell of a good beginning" (Gallo, 1991). In view of correlations it
is argued that "persons infected with HIV will develop AIDS and those
not so infected will not" (Evans, 1989a), or that "HIV ... is
the sine qua non for the epidemic" (Gallo, 1991).
But correlations are only circumstantial evidence for
a hypothesis. According to Sherlock Holmes, "Circumstantial evidence
is a very tricky thing. It may seem to point very straight to one thing,
but if you shift your point of view a little, you may find it pointing
in an equally uncompromising manner to something entirely different"
(Doyle, 1928). The risk in epidemiological studies is that the cause may
be difficult to distinguish from noncausal associations. For example, yellow
fingers are noncausally and smoking is causally associated with lung cancer.
"In epidemiological parlance, the issue at stake is that of confounding"
(Smith and Phillips, 1992). This is true for the "overwhelming seroepidemiologic
evidence" claimed to support the virus-AIDS hypothesis on the following
grounds.
3.4.1. Only about Half of American
AIDS is Confirmed HIV-antibody-positive
In the U.S. antibodies against HIV are only confirmed
in about 50% of all AIDS diagnoses; the remainder are presumptively diagnosed
(Institute of Medicine, 1988; Selik et al., 1990). Several studies
indicate that the natural coincidence between antibodies against HIV and
AIDS diseases is not perfect, because all AIDS defining diseases occur
in all AIDS risk groups in the absence of HIV (Section 4). Ironically,
the CDC never records the incidence of HIV in its HIV/AIDS Surveillance
Reports (Centers for Disease Control, 1992b).
It follows that the reportedly perfect correlation between
HIV and AIDS is in reality an artifact of the definition of AIDS and of
allowances for presumptive diagnoses (Centers for Disease Control, 1987;
Institute of Medicine, 1988). Since AIDS has been defined exclusively as
diseases occurring in the presence of antibody to HIV (Section 2.2), the
diagnosis of AIDS is biased by its definition toward a 100% correlation
with HIV. That is why "persons infected by HIV will develop AIDS and
... those not so infected will not" (Evans, 1989a), and why HIV is
the "sine qua non" of AIDS (Gallo, 1991).
3.4.2. Antibody-positive, but Virus-negative
AIDS
The correlations between AIDS and HIV are in fact not
correlations with HIV, but with antibodies against HIV (Sarngadharan et
al., 1984; Blattner et al., 1988; Duesberg, 1989c). But antibodies
signal immunity against viruses, signal neutralization of viruses, and
thus protection against viral disease-not a prognosis for a future disease
as is claimed for antibodies against HIV. For example, antibody-positive
against polio virus and measles virus means virus-negative, and thus protection
against the corresponding viral diseases. The same is true for antibodies
against HIV: antibody-positive means very much virus-negative. Residual
virus or viral molecules are almost undetectable in most antibody-positive
persons (Sections 3.3 and 3.5.6). Thus antibodies against HIV are not evidence
for a future or current HIV disease unless additional assumptions are made
(Section 3.5.11).
3.4.3. HIV: Just One of Many Harmless Microbial
Markers of Behavioral and Clinical AIDS Risks
In addition to antibodies against HIV, there are antibodies
against many other passenger viruses and microbes in AIDS risk groups and
AIDS patients (Sections 2.3 and 4.3.2). These include cytomegalovirus,
hepatitis virus, Epstein-Barr virus, Human T-cell Leukemia Virus-I (HTLV-I),
herpes virus, gonorrhea, syphilis, mycoplasma, amoebae, tuberculosis, toxoplasma
and many others (Gallo et al., 1983; Sonnabend et al., 1983;
Blattner et al., 1985; Mathur-Wagh et al., 1985; Darrow et
al., 1987; Quinn et al., 1987; Messiah et al., 1988;
Stewart, 1989; Goldsmith, 1990; Mills and Masur, 1990; Root-Bernstein,
1990a,c; Duesberg, 1991a; Buimovici-Klein et al., 1988). In addition,
there are between 100 and 150 chronically latent retroviruses in the human
germ line (Martin et al., 1981; Nakamura et al., 1991). These
human retroviruses are in every cell, not just in a few like HIV, and have
the same genetic structure and complexity as HIV and all other retroviruses
(Duesberg, 1989c). According to Quinn et al., "Common to African
patients with AIDS and outpatient controls and American patients with AIDS
and homosexual men was the finding of extremely high prevalence rates of
antibody to CMV (range, 92-100%), HSV (range, 90-100%), hepatitis B virus
(range, 78-82%), hepatitis A virus (range, 82-95%), EBV capsid antigen
(100%), syphilis (11-23%), and T. gondii (51-74%). In contrast,
the prevalence of antibody to each of these infectious agents was significantly
lower among the 100 American heterosexual men ..." (Quinn et al.,
1987). Thus, the incidence of many human parasites, both rare and common,
is high in typical AIDS patients and in typical AIDS risk groups (Sections
2.3 and 5). However, none of these microbes are fatal and nearly all are
harmless to a normal immune system (Section 2.3).
Most of these parasites, including HIV, have been accumulated
by AIDS risk behavior and by clinical AIDS risks (Blattner et al.,
1985; Institute of Medicine, 1988; Stewart, 1989). Such behavior includes
the long-term injection of unsterile, recreational "street" drugs
and large numbers of sexual contacts promoted by oral and injected aphrodisiac
drugs (Section 4) (Dismukes et al., 1968; Darrow et al.,
1987; Des Jarlais et al., 1987; Espinoza et al., 1987; Moss,
1987; Moss et al., 1987; van Griensven et al., 1987; Des
Jarlais et al., 1988; Messiah et al., 1988; Chaisson et
al., 1989; Weiss, S.H., 1989; Deininger et al., 1990; McKegney
et al., 1990; Stark et al., 1990; Luca-Moretti, 1992; Seage
et al., 1992). Clinical risk groups, such as hemophiliacs, accumulate
such viruses and microbes from occasionally contaminated transfusions (Section
3.4.4).
It follows that a high correlation between AIDS and antibodies
against one particular virus, such as HIV, does not "distinguish between
a virus that was a passenger and one that was a cause" (Baltimore,
see above) (Booth, 1988). It is an expected consequence or marker of behavioral
and clinical AIDS risks, particularly in countries where the percentage
of HIV carriers is low (Duesberg, 1991a). In addition to HIV, many other
microbes and viruses which are rare and inactive, or just inactive, in
the general population, such as hepatitis virus, are "specific"
for AIDS patients, and thus markers for AIDS risks (Sections 2.2, 2.3 and
4.3.2). For example, 100% of AIDS patients within certain cohorts, not
just 50% as with HIV (Section 2.2), were shown to have antibodies against,
or acute infections of, cytomegalovirus (Gottlieb et al., 1981;
Francis, 1983; van Griensven et al., 1987; Buimovici-Klein et
al., 1988). A comparison of 481 HIV-positive with 1499 HIV-negative
homosexual men in Berlin found that the HIV-positives were "significantly
more often carriers of antibodies against hepatitis A virus, hepatitis
B virus, cytomegalovirus, Epstein-Barr virus and syphilis" (Deininger
et al., 1990). And the frequent occurrence of antibodies against
hepatitis B virus in cohorts of homosexual AIDS patients, termed "hepatitis
cohorts," was a precedent, that helped to convince the CDC to drop
the "lifestyle" hypothesis of AIDS in favor of the "hepatitis
analogy" (Francis et al., 1983; Centers for Disease Control,
1986; Oppenheimer, 1992) (Section 2.2).
The higher the consumption of unsterile, injected drugs,
the more sexual contacts mediated by aphrodisiac drugs and the more transfusions
received, the more accidentally contaminating microbes will be accumulated
(Sections 3.4.4.5, 4.3.2 and 4.5). In Africa antibodies against HIV and
hepatitis virus are poor markers for AIDS risks, because millions carry
antibodies against these viruses (Table 1) (Quinn et al., 1987;
Evans, 1989c; Blattner, 1991). Thus it is arbitrary to consider HIV the
AIDS "driver" rather than just one of the many innocent microbial
passengers of AIDS patients (Francis, 1983), because it is neither distinguished
by its unique presence nor by its unique biochemical activity.
3.4.4. Annual AIDS Risks of Different HIV-infected
Risk Groups, Including Babies, Homosexuals, Drug Addicts, Hemophiliacs
and Africans, Differ over 100-fold
If HIV were the cause of AIDS the annual AIDS risks of
all infected persons should be similar, particularly if they are from the
same country. Failure of HIV to meet this prediction would indicate that
HIV is not a sufficient cause of AIDS. The occurrence of the same AIDS-defining
diseases in HIV-free controls would indicate that HIV is not even necessary
for AIDS.
3.4.4.1. Critically ill recipients of transfusions.
The annual AIDS risk of HIV-infected American recipients of transfusions
(other than hemophiliacs) is about 50%, as half of all recipients die within
one year after receiving a transfusion (Table 2) (Ward et al., 1989).
Table 2. Annual AIDS Risks of HIV-infected Groups*
HIV-infected group Annual AIDS in % Group-specific
American recipients 50 pneumonia, opportunistic
of transfusions infections
American babies 25 dementia, bacterial
Male homosexuals 4-6 Kaposi's sarcoma
using sexual stimulants
Intravenous drug users 4-6 tuberculosis, wasting
American hemophiliacs 2 pneumonia, opportunistic
infections
German hemophiliacs 1 pneumonia, opportunistic
infections
American teenagers 0.16-1.7 hemophilia-related
American general population 0.1-1 opportunistic infections
Africans 0.3 fever, diarrhea,
tuberculosis
Thais 0.05 tuberculosis
* Based on controlled studies, it is proposed that the
health risks of all HIV-infected AIDS risk groups are the same as those
of matched HIV-free controls (Sections 3.4.4, 4 and 5). The virus hypothesis
simply claims the specific morbidity of each of these groups for HIV.
Since the AIDS risk of transfusion recipients is much higher
than the national 3-4% average, nonviral factors must play a role (Table
1). Indeed, about 50% of American recipients of transfusions without HIV
also die within 1 year after receiving a transfusion (Hardy et al.,
1985; Ward et al., 1989), and over 60% within 3 years (Bove et
al., 1987). Moreover, the AIDS risk of transfusion recipients increases
3-6 times faster with the volume of blood received than their risk of infection
by HIV (Hardy et al., 1985; Ward et al., 1989). This indicates
that the illnesses that necessitated the transfusions are responsible for
the mortality of the transfusion recipients. Yet the virus hypothesis claims
the relatively high mortality of American transfusion patients for HIV
without considering HIV-free controls. The hypothesis also fails to consider
that the effects of HIV on transfusion mortality should be practically
undetectable in the face of the high mortality of transfusion recipients
and its postulate that HIV causes AIDS on average only 10 years after infection.
3.4.4.2. HIV-infected babies. The second highest
annual AIDS risk is reported for perinatally infected American babies,
whose health has been compromised by maternal drug addiction or by congenital
diseases like hemophilia (Section 2.1.3). They develop AIDS diseases on
average two years after birth (Anderson and May, 1988; Blattner et al.,
1988; Institute of Medicine, 1988; Blattner, 1991). This corresponds to
an annual AIDS risk of 25% (Table 2).
Since the AIDS risk of babies is much higher than the
national average of 3-4% (Table 1), nonviral factors must play a role in
pediatric AIDS. Based on correlations and controlled studies documenting
AIDS-defining diseases in HIV-free babies, it is proposed below that maternal
drug consumption (Section 4) and congenital diseases, like hemophilia (Section
3.4.4.5), are the causes of pediatric AIDS. Indeed, before AIDS surfaced,
many studies had shown that maternal drug addiction was sufficient to cause
AIDS-defining diseases in newborns (Section 4.6.1). In accord with this
proposal it is shown that HIV is naturally a perinatally transmitted retrovirus-and
thus harmless (Section 3.5.2).
3.4.4.3. HIV-positive homosexuals. The annual AIDS
risk of HIV-infected male homosexuals with hundreds of sex partners, who
frequently use aphrodisiac drugs (Section 4), was originally estimated
at about 6% (Mathur-Wagh et al., 1985; Anderson and May, 1988; Institute
of Medicine, 1988; Lui et al., 1988; Moss et al., 1988; Turner
et al., 1989; Lemp et al., 1990; van Griensven et al.,
1990; Blattner, 1991). As more HIV-positives became identified, lower estimates
of about 4% were reported (Table 2) (Rezza et al., 1990; Biggar
and the International Registry of Seroconverters, 1990; Munoz et al.,
1992).
Since the annual AIDS risk of such homosexual men is higher
than the national average, group-specific factors must be necessary for
their specific AIDS diseases. Based on correlations with drug consumption
and studies of HIV-free homosexuals, it is proposed here that the cumulative
consumption of sexual stimulants and psychoactive drugs determines the
annual AIDS risk of homosexuals (Sections 4.4 and 4.5). Indeed, all AIDS-defining
diseases were observed in male homosexuals from behavioral risk groups
before HIV was discovered and have since been observed in HIV-free homosexuals
from AIDS risk groups (Sections 4.5 and 4.7).
In the spirit of the virus-AIDS hypothesis, many of these
HIV-free homosexual AIDS cases have been blamed on various retrovirus-like
particles, papilloma viruses, other viruses and microbes by researchers
who have not investigated drug use, particularly not oral drug use. These
cases include 153 immunodeficient HIV-free homosexuals with T4/T8-cell
ratios below 1 (Drew et al., 1985; Weber et al., 1986; Novick
et al., 1986; Collier et al., 1987; Bartholomew et al.,
1987; Buimovici-Klein et al., 1988) and 23 HIV-free Kaposi's sarcomas
(Afrasiabi et al., 1986; Ho et al., 1989b; Bowden et al.,
1991; Safai et al., 1991; Castro et al., 1992; Huang et
al., 1992) (see also Note added in proof).
3.4.4.4. HIV-positive intravenous drug users. Application
of the annual AIDS risk of male homosexual risk groups led to valid predictions
for the annual AIDS risk of intravenous drug users (Lemp et al.,
1990). Therefore the annual AIDS risk of HIV-infected intravenous drug
users was originally estimated to be 6% (Table 2) (Lemp et al.,
1990; Blattner, 1991; Goudsmit, 1992). More recent studies have concluded
that the annual AIDS risk of intravenous drug users is about 4% (Table
2) (Rezza et al., 1990; Munoz et al., 1992).
These findings argue against a sexually transmitted cause,
because sexual transmission predicts a much higher AIDS risk for homosexuals
with hundreds of sexual partners than for intravenous drug users (Section
4) (Weyer and Eggers, 1990; Eggers and Weyer, 1991). Indeed, numerous controlled
studies have indicated that the morbidity and mortality of intravenous
drug users is independent of HIV (Sections 4.4, 4.5 and 4.7). On the basis
of such studies it is proposed that the lifetime dose of drug consumption
determines the annual AIDS risk of intravenous drug users (Section 4).
3.4.4.5. HIV-positive hemophiliacs. The hemophiliacs provide
the most accessible group to test the virus hypothesis, because the time
of infection can be estimated and because the role of other health risks
can be controlled by studying HIV-free hemophiliacs.
About 15,000, or 75% of the 20,000 American hemophiliacs
have HIV from transfusions received before the "AIDS test" was
developed in 1984 (Tsoukas et al., 1984; Hardy et al., 1985;
Institute of Medicine, 1986, 1988; Stehr-Green et al., 1988; Goedert
et al., 1989; Koerper, 1989). Based on limited data and antibodies
against selected viral antigens, it is generally estimated that most of
these infections occurred between 1978 and 1984 (Evatt et al., 1985;
Johnson et al., 1985; McGrady et al., 1987; Goedert et
al., 1989). This high rate of infection reflects the practice, developed
in the 1960s and 1970s, of preparing factor VIII from blood pools collected
from large numbers of donors (Johnson et al., 1985; Aronson, 1988;
Koerper, 1989). Since only about 300 of the 15,000 HIV-infected American
hemophiliacs have developed AIDS annually over the last 5 years (Morgan
et al., 1990; Centers for Disease Control, 1992a,b), the annual
AIDS risk of HIV-infected American hemophiliacs is about 2% (Table 2).
Data from Germany extend these results: about 50% of the 6000 German hemophiliacs
are HIV-positive (Koerper, 1989), and only 37 (1%) of these developed AIDS-defining
diseases during 1991 and 303 (1% annually) from 1982 until 1991 (Bundesgesundheitsamt
(Germany), 1991; Leonhard, 1992). An international study estimated the
annual AIDS risk of adult hemophiliacs at 3% and that of children at 1%
over a 5-year period of HIV-infection (Biggar and the International Registry
of Seroconverters, 1990).
According to the virus-AIDS hypothesis, one would have
expected that by now (about one 10-year-HIV-latent-period after infection)
at least 50% of the 15,000 HIV-positive American hemophiliacs would have
developed AIDS or died from AIDS. But the 2% annual AIDS risk indicates
that the average HIV-positive hemophiliac would have to wait for 25 years
to develop AIDS diseases from HIV, which is the same as their current median
age. The median age of American hemophiliacs has increased from 11 years
in 1972, to 20 years in 1982 and to over 25 years in 1986, despite the
infiltration of HIV in 75% (Johnson et al., 1985; Institute of Medicine,
1986; Koerper, 1989). Thus, one could make a logical argument that HIV,
instead of decreasing the lifespan of hemophiliacs, has in fact increased
it.
Considering the compromised health of many hemophiliacs
compared to the general population, it is also surprising, that the 1-2%
annual AIDS risk of HIV-infected hemophiliacs is lower than the 3-4% risk
of the average HIV-infected, nonhemophilic European or American (Table
1). There is even a bigger discrepancy between the annual AIDS risks of
hemophiliacs and those of intravenous drug users and male homosexuals,
which are both about 4-6% (Table 2). In an effort to reconcile the relatively
low annual AIDS risks of hemophiliacs with that of homosexuals, the hematologists
Sullivan et al. (1986) noted "The reasons for this difference
remain unclear." And Biggar and colleagues (1990) noted that "AIDS
incubation ... was significantly faster" for drug users and homosexuals
than for hemophiliacs.
In view of the many claims that HIV causes AIDS in hemophiliacs,
it is even more surprising that there is not even one controlled study
from any country showing that the morbidity or mortality of HIV-positive
hemophiliacs is higher than that of HIV-negative controls.
Instead, controlled studies show that immunodeficiency
in hemophiliacs is independent of HIV, and that the lifetime dosage of
transfusions is the cause of AIDS-defining diseases of hemophiliacs. Studies
describing immunodeficiency in HIV-free hemophiliacs are summarized in
Table 3 (Tsoukas et al., 1984; AIDS Hemophilia French Study Group,
1985; Ludlam et al., 1985; Gill et al., 1986; Kreiss et
al., 1986; Madhok et al., 1986; Sullivan et al., 1986;
Sharp et al., 1987; Matheson et al., 1987; Antonaci et
al., 1988; Mahir et al., 1988; Aledort, 1988; Jin et al.,
1989; Jason et al., 1990; Lang, et al., 1989; Becherer et
al., 1990). One of these studies even documents an AIDS-defining disease
in an HIV-free hemophiliac (Kreiss et al., 1986). Immunodeficiency
in these studies is typically defined by a T4 to T8-cell ratio of about
1 or less than 1, compared to a normal ratio of 2.
Most of the studies listed in Table 3 and additional ones
conducted before HIV had been discovered have concluded or noted that immunodeficiency
is directly proportional to the number of transfusions received over a
lifetime (Menitove et al., 1983; Kreiss et al., 1984; Johnson
et al., 1985; Hardy et al., 1985; Pollack et al.,
1985; Prince, 1992; Ludlum et al., 1985; Gill et al., 1986).
According to the hematologists Pollack et al. (1985) "derangement
of immune function in hemophiliacs results from transfusion of foreign
proteins or a ubiquitous virus rather than contracting AIDS infectious
agent." The "ubiquitous virus" was a reference to the virus-AIDS
hypothesis but a rejection of HIV, because in 1985 HIV was extremely rare
in blood concentrates outside the U.S., but immunodeficiency was observed
in Israeli, Scottish and American hemophiliacs (Pollack et al.,
1985). Madhok et al. also arrived at the conclusion that "clotting
factor concentrate impairs the cell mediated immune response to a new antigen
in the absence of infection with HIV" (Madhok et al., 1986).
Aledort observed that "chronic recipients ... of factor VIII, factor
IX and pooled products ... demonstrated significant T-cell abnormalities
regardless of the presence of HIV antibody" (Aledort, 1988). Even
those who claim that clotting factor does not cause immunodeficiency show
that immunodeficiency in hemophiliacs increases with both the age and the
cumulative dose of clotting factor received during a lifetime (Becherer
et al., 1990).
One controlled study showed directly that protein impurities
of commercial factor VIII, rather than factor VIII or HIV, were immunosuppressive
among factor VIII-treated, HIV-positive hemophiliacs. Over a period of
two years the T-cells of HIV-positive hemophiliacs treated with commercial
factor VIII declined two-fold, while those of matched HIV-positive controls
treated with purified factor VIII remained unchanged (Table 3) (de Biasi
et al., 1991).
Before AIDS, a multicenter study investigating the immune
systems of 1551 hemophiliacs treated with factor VIII from 1975 to 1979
documented lymphocytopenia in 9.3% and thrombocytopenia in 5% (Eyster et
al., 1985). Accordingly, AIDS-defining opportunistic infections, including
60% pneumonias and 20% tuberculosis, have been recorded in hemophiliacs
between 1968 and 1979 (Johnson et al., 1985). These transfusion-acquired
immunodeficiencies could more than account for the 2% annual incidence
of AIDS-defining diseases in HIV-positive hemophiliacs recorded now (Centers
for Disease Control, 1992b). An American hematologist who recorded opportunistic
infections in hemophiliacs occurring between 1968 and 1979, including 2
candidiasis and 66 pneumonia deaths, commented in 1983 "... it seems
possible that many of the unspecified pneumonias in hemophiliacs in the
past would be classified today as AIDS" (Aronson, 1983).
It follows that long-term transfusion of foreign proteins
causes immunodeficiency in hemophiliacs with or without HIV. The virus
hypothesis has simply claimed normal morbidity and mortality of hemophiliacs
for HIV, by ignoring HIV-free controls.
Nevertheless several investigators comparing HIV-negative
to HIV-positive hemophiliacs have noted that immunodeficiency is more often
associated with HIV-positives (Table 3), and have observed that HIV correlates
with the number of transfusions received (Tsoukas et al., 1984;
Kreiss et al., 1986; Sullivan et al., 1986; Koerper, 1989;
Becherer et al., 1990). According to Kreiss et al. "seropositive
hemophiliac subjects, on average, had been exposed to twice as much concentrate
... as seronegative[s]" (Kreiss et al., 1986). And according
to Goedert et al. "the prevalence of HIV-1 antibodies was directly
associated with the degree of severity (of hemophilia)" (Goedert et
al., 1989). Thus HIV appears just to be a marker of the multiplicity
of transfusions, rather than a cause of immunodeficiency.
The conclusion that long-term transfusion of foreign proteins
causes immunodeficiency makes three testable predictions:
(1) It predicts that hemophiliacs with "AIDS"
would be older than average hemophiliacs. Indeed, the median age of hemophiliacs
with AIDS in the U.S. (Evatt et al., 1984; Koerper, 1989; Stehr-Green
et al., 1989), England (Darby et al., 1989) and other countries
(Biggar and the International Registry of Seroconverters, 1990; Blattner,
1991) is significantly higher (about 34 years in the U.S.; Johnson et
al., 1985; Koerper, 1989; Becherer et al., 1990) than the average
age of hemophiliacs (20-25 years in the U.S., see above). Goedert et
al. reported that the annual AIDS risk of 1- to 17-year-old hemophiliacs
was 1.5%, that of 18- to 34-year-old hemophiliacs was 3% and that of 64-year-old
hemophiliacs was 5% (Goedert et al., 1989). This confirms that the
cumulative dose of transfusions received is the cause of AIDS-defining
diseases among hemophiliacs. According to the hematologist Koerper, "this
may reflect lifetime exposure to a greater number of units of concentrate,
..." and to Evatt et al., "This age bias may be due to
differences in duration of exposure to blood products ..." (Evatt
et al., 1984; Koerper, 1989).
By contrast, AIDS caused by an autonomous infectious pathogen
would be largely independent of the age of the recipient. Even if HIV were
that pathogen, the hemophiliac population with AIDS should have the same
age distribution as the hemophiliac population over 10 years, because HIV
is thought to take 10 years to cause AIDS and nearly all hemophiliacs were
infected about 10 years ago (Johnson et al., 1985; McGrady et
al., 1987; Koerper, 1989).
(2) Foreign protein-mediated immunodeficiency further
predicts that all AIDS diseases of hemophiliacs are opportunistic infections.
If hemophilia AIDS were due to HIV only 62% of their AIDS diseases would
be opportunistic infections, because 38% of all American AIDS patients
have diseases, that are not dependent on, and not consistently associated
with, immunodeficiency (Table 1, Section 3.5.8). These include wasting
disease (19%), Kaposi's sarcoma (10%), dementia (6%) and lymphoma (3%)
(Table 1).
The AIDS pathology of hemophiliacs confirms the prediction
of the foreign protein-hypothesis exactly. In America 99% of the hemophiliacs
with AIDS have opportunistic infections, of which about 70% are fungal
and viral pneumonias, and less than 1% have Kaposi's sarcoma (Evatt et
al., 1984; Selik et al., 1987; Stehr-Green et al., 1988;
Goedert et al., 1989; Koerper, 1989; Becherer et al., 1990).
The small percentage of Kaposi's sarcoma is due to the nitrite inhalants
used by male homosexual hemophiliacs as sexual stimulants (Section 4).
There are no reports of wasting disease and dementia in hemophiliacs.
(3) If hemophilia AIDS is due to transfusion of foreign
proteins, the wives of hemophiliacs should not contract AIDS from their
mates. But if it were due to a parenterally or sexually transmitted virus,
hemophilia AIDS would be sexually transmissible. Indeed, AIDS researchers
claim that the wives of hemophiliacs develop AIDS from sexual transmission
of HIV (Lawrence et al., 1990; Weiss and Jaffe, 1990; Centers for
Disease Control, 1992b). For example AIDS researcher Fauci asks: "How
about the 60-year-old wife of a hemophiliac who gets infected? Is she cruising,
too?" (Booth, 1988).
However, (a) statistical scrutiny and (b) a controlled
study unconfirm the hypothesis that hemophilia AIDS is sexually transmissible:
(a) The CDC reports that 94 wives of hemophiliacs have been diagnosed with
unnamed AIDS diseases since 1985 (Centers for Disease Control, 1992b).
If one considers that there have been 15,000 HIV-positive hemophiliacs
in the U.S. since 1985 and assumes that a third are married, then there
are 5000 wives of HIV-positive hemophiliacs. About 13 of these women have
developed AIDS annually during the 7 years (94:7) from 1985 to 1991 (Centers
for Disease Control, 1992b). By contrast, at least 80 of these women would
be expected to die per year, considering the human lifespan of about 80
years and that on average at least 1.6% of all those over 20 years of age
die annually. Thus, until controls show that among 5000 HIV-negative wives
of hemophiliacs only 67 (80-13) die annually, the claim that wives of hemophilics
die from sexual transmission of HIV is unfounded speculation.
Moreover, it has been pointed out that all AIDS-defining
diseases of the wives of hemophiliacs are typically age-related opportunistic
infections, including 81% pneumonia (Lawrence et al., 1990). Kaposi's
sarcoma, dementia, lymphoma and wasting syndrome are not observed in wives
of hemophiliacs (Lawrence et al., 1990). Thus the virus-AIDS hypothesis
seems to claim, once more, normal morbidity and mortality of the wives
of hemophiliacs for HIV.
(b) To test the hypothesis that immunodeficiency of hemophiliacs
is sexually transmissible the T4 to T8 cell-ratio of 41 spouses and female
sexual partners of immunodeficient hemophiliacs were analyzed (Kreiss et
al., 1984). Twenty-two of the females had relationships with hemophiliacs
with T-cell ratios below 1 and 19 with hemophiliacs with ratios of 1 and
greater. The mean duration of relationships was 10 years, the mean number
of sexual contacts was 111 during the previous year, and only 12% had used
condoms (Kreiss et al., 1984). Since the T-cell ratios of all spouses
were normal, averaging 1.68-exactly like those of 57 normal controls, the
authors concluded that "there is no evidence to date for heterosexual
or household-contact transmission of T-cell subset abnormalities from hemophiliacs
to their spouses ..." (Kreiss et al., 1984).
It follows that the foreign protein-hypothesis, but not
the HIV-hypothesis, correctly predicts (1) the pathology, (2) the age bias,
(3) the noncontagiousness of hemophilia AIDS and (4) HIV-free immunodeficiency
in hemophiliacs. It also explains the discrepancies between the annual
AIDS risks of hemophiliacs and other risk groups (Table 2).
Since the virus hypothesis has become totally dominant
in 1988, no new studies have described HIV-free immunodeficient hemophiliacs
(Table 3) and the question whether HIV-free immunodeficient hemophiliacs
ever developed AIDS-defining diseases became a taboo. The study by Jason
et al. described data collected in the mid 1980s, the studies by
Jin et al. and Becherer et al. collected data before 1988
and the one by de Biasi et al. compared the effects of purified
to unpurified factor VIII only in HIV-positive hemophiliacs (Table 3).
In response to the argument that hemophiliacs only began
to develop AIDS diseases when HIV appeared (Centers for Disease Control,
1986; Oppenheimer, 1992), it is proposed that "new" AIDS-defining
diseases among hemophiliacs are an indirect consequence of extending their
life with factor VIII treatment. Long-term treatment with factor VIII has
prolonged the median life of hemophiliacs from 11 in 1972 to 25 in 1986.
But contaminating foreign proteins received over periods of 10 years of
treatment have also caused immunodeficiencies, and various viral and microbial
contaminants have caused infections in some, and HIV infection in 75%.
HIV has been a marker for the number of transfusions and factor VIII treatments
received, just like hepatitis virus infection was a marker of the number
of transfusions received until it was eliminated from the blood supplies
(Anonymous, 1984; Koerper, 1989). Prior to factor VIII therapy most hemophiliacs
died as adolescents from internal bleeding (Koerper, 1989).
3.4.4.6. HIV-positive teenagers. The annual AIDS
risk of HIV-infected American teenagers can be calculated as follows: There
are about 30 million American teenagers, of which 0.03% (10,000) (Burke
et al., 1990) to 0.3% (100,000) (St Louis et al., 1991) are
HIV-positive. Since only 160 developed AIDS in 1991 and only 170 in 1990
(Centers for Disease Control, 1992b), their annual AIDS risk is between
0.16% and 1.7% (Table 2).
Thus the AIDS risk of teenagers with HIV is less than
the national average of 3-4%. There are no statistics to indicate that
the annual risk for AIDS-defining diseases of the HIV-infected teenage
population is higher than that of HIV-free controls (Section 3.5.2). Since
most American teenagers with AIDS are either hemophiliacs (38%), intravenous
drug users (25%) or male homosexuals (25%) (Section 2.1.3), it is proposed
that the associated risk factors, rather than HIV, are the cause of teenage
AIDS (Sections 3.4.4.5 and 4).
3.4.4.7. HIV-positive general U.S. population.
The CDC reports that 3% of all American AIDS cases are from the general
population, corresponding to 900-1200 of the 30,000~40,000 annual AIDS
cases (Table 1) (Centers for Disease Control, 1992b). Since at least 0.03%
to 0.3%, or 80,000 to 800,000, of the general American population of 250
million are infected (Section 3.5.2) (U.S. Department of Health and Human
Services, 1990; Burke et al., 1990; Morgan et al., 1990;
St Louis et al., 1991), the annual AIDS risk of the general population
must be between 0.1% and 1% (Table 2). Thus the annual AIDS risk of HIV-infected
Americans of the general population is similar to that of teenagers.
There are no statistics to indicate that the annual AIDS
risk of the general HIV-infected population is higher than the annual risk
for AIDS-defining diseases in HIV-free controls. Because the incidence
of AIDS in the general population is exceedingly low, it is proposed again
that it reflects the normal, low incidence of AIDS-defining diseases, rather
than HIV-mediated diseases.
3.4.4.8. HIV-positive Africans. The annual AIDS
risks of HIV-infected Africans is only 0.3% (Tables 1 and 2), because 6
million HIV carriers generated 129,000 AIDS cases from 1985 to the end
of 1991 (Table 1). There are no controlled studies indicating that the
risk for AIDS-defining diseases of HIV-infected Africans differs from that
of HIV-negative controls.
Since the annual AIDS risk of HIV-infected Africans is
(1) 10-times lower than the average American and European risk, (2) up
to 100-fold less than that of American/European risk groups, (3) the same
for both sexes unlike that in America and Europe and (4) very low considering
that the annual mortality in Africa is around 2% and that AIDS includes
the most common African diseases, it is proposed that African AIDS is just
a new name for indigenous African diseases (Section 2.1.2).
Instead of a new virus, malnutrition, parasitic infections
and poor sanitary conditions have all been proposed as causes of African
AIDS-defining diseases (Editorial, 1987; KonoteyAhulu, 1987, 1989; Rappoport,
1988; Adams, 1989). Further, it has been proposed that the incidence of
tuberculosis, diarrhea, fever and other African AIDS-defining diseases
may be the same in Africans with and without HIV (Editorial, 1987). And
prior to the discovery of HIV, protein malnutrition was identified by the
AIDS researchers Fauci et al. as the world's leading cause of immunodeficiency,
particularly in underdeveloped countries (Seligmann et al., 1984).
Indeed, recent studies document that only 2168 out of
4383 (49.5%) African AIDS patients with slim disease, tuberculosis and
other Africa-specific diseases, who all met the WHO definition of AIDS,
were infected by HIV. These patients were from Abidjan, Ivory Coast (De
Cock et al., 1991; Taelman et al., 1991), Lusaka, Zambia
and Kinshasa, Zaire (Taelman et al., 1991). Another study reports
135 (59%) HIV-free AIDS patients from Ghana out of 227 diagnosed by clinical
criteria of the WHO. These patients suffered from weight loss, diarrhea,
chronic fever, tuberculosis and neurological diseases (Hishida et al.,
1992). An earlier study documents 116 HIV-negatives among 424 African patients
that meet the WHO definition of AIDS (Widy-Wirski et al., 1988).
According to an African AIDS doctor, "Today, because of AIDS, it seems
that Africans are not allowed to die from these conditions any longer"
(Konotey-Ahulu, 1987). Another asks "What use is a clinical case definition
for AIDS in Africa?" (Gilks, 1991).
The 10-fold difference between the average annual AIDS
risks of Africans and Americans/ Europeans (Table 1) can thus be resolved
as follows: (1) The high AIDS risk of HIV-positive Americans and Europeans
is the product of the low absolute numbers of HIV carriers in the U.S.
and Europe compared to Africa (Table 1) and of the concentration of HIV
in AIDS risks groups, e.g. consumers of recreational drugs and the antiviral
drug AZT (Section 4) and recipients of transfusions (Section 3.4.3). (2)
The low AIDS risk of Africans is a product of large absolute numbers of
HIV carriers and their relatively low, spontaneous and malnutrition-mediated
AIDS risks.
3.4.4.9. HIV-positive Thais. Given that there have
been only 123 Thai AIDS cases in the last 1-2 years and an estimated 300,000
HIV carriers in Thailand (Weniger et al., 1991), the annual AIDS
risk of HIV-infected Thais can be calculated to be less than 0.05% (Table
2). Since most of these 123 were either intravenous drug users or "sex
workers" (Section 2.1.3), it is proposed that these specific health
risks are their cause of AIDS (Section 4), rather than the HIV that they
share, unspecifically, with 300,000 healthy Thais.
The over 100-fold range in the annual AIDS risks of different
AIDS risks groups, summarized in Table 2, clearly indicates that HIV is
not sufficient to cause AIDS. It confirms and extends an earlier CDC conclusion:
"The magnitude of some of the differences in rates is so great that
even gross errors in denominator estimates can be overcome" (Hardy
et al., 1985). Moreover, analysis of the specific health risks of
each risk group has identified nonviral health risks that are necessary
and sufficient causes of AIDS (Table 3 and Section 4.5).
3.4.5. Specific AIDS Diseases Predetermined
by Prior Health Risks
If HIV were the cause of AIDS, every AIDS case should
have the same risk of having one or more of the 25 AIDS diseases. However,
the data listed above (Section 2.1) and in Table 2 indicate that per AIDS
case different risk groups have very specific AIDS diseases:
(1) Male homosexuals have 20 times more Kaposi's sarcoma
than all other American and European AIDS risk groups.
(2) Hemophiliacs and other recipients of transfusions
have fungal and viral pneumonia and other opportunistic infections, and
practically no Kaposi's sarcoma or dementia.
(3) The AIDS diseases of the "general population"
are either spontaneous, hemophilia- or age-related opportunistic infections.
Typical examples are cited below (Section 3.5.16).
(4) Babies exclusively have bacterial infections (18%)
and a high rate of dementia (14%), compared to adults (6%) (Table l).
(5) Africans develop Africa-specific AIDS diseases 10
times more and Kaposi's sarcoma 10 times less often than Americans or Europeans.
The epidemiological data summarized in Section 3.4 indicate
that HIV is sufficient to determine neither the annual AIDS risk, nor the
type of AIDS disease an infected person may develop. Instead, prior health
risks including drug consumption, malnutrition and congenital diseases
like hemophilia and their treatments and even the country of residence,
predetermine AIDS diseases. The correlations between HIV and AIDS that
are claimed to support the virus-AIDS hypothesis are not direct, not complete,
not distinctive and, above all, not controlled. Controlled studies indicate
that the incidence of AIDS-defining diseases in intravenous drug users,
male homosexuals practicing risk behavior and hemophiliacs is independent
of HIV.
Therefore, it is proposed that various group-specific
health risk factors, including recreational and antiviral drugs (Section
4) and malnutrition, are necessary and sufficient causes of AIDS. The existence
of risk group-specific AIDS-defining diseases in the absence of HIV confirms
this conclusion (Sections 3.4.4 and 4.5).
3.5 Assumptions and Anecdotal Cases that Appear
to Support the Virus-AIDS Hypothesis
The following assumptions and anecdotal cases are frequently
claimed to prove the virus-AIDS hypothesis. Despite the popularity 0f these
claims they are either uncontrolled for alternative explanations or they
are natural coincidences between HIV infection and naturally-occurring
diseases.
3.5.1. HIV is Presumed New Because AIDS is New
HIV is presumed new in all countries with AIDS, because
AIDS is new (Blattner et al., 1988; Gallo and Montagnier, 1988;
Weiss and Jaffe, 1990). The presumed newness of HIV is used as a primary
argument for the virus-AIDS hypothesis: ... the time of occurrence of AIDS
in each country is correlated with the time of introduction of HIV into
that country; first HIV is introduced, then AIDS appears" (Blattner
et al., 1988) or: "In every country and city where AIDS has
appeared, HIV infection preceded it just by a few years" (Weiss and
Jaffe, 1990).
However, according to Farr's law, the age of a microbe
in a population is determined by changes in its incidence over time (Bregman
and Langmuir, 1990). If a microbe is spreading from a low to a high incidence
it is new; however, if its incidence in a population is constant, it is
old (Fig. 1) (Freeman, 1979; Duesberg, 1991a). Figure 1 shows the incidences
of long established microbes in the U.S. population, i.e. Candida
and Pneumocystis each at about 100% (Freeman, 1979; Pifer, 1984;
Williford Pifer et al., 1988), and cytomegalovirus and herpes virus
at about 50% and 40%, respectively (Evans, 1989c). In addition, it shows
the typical exponential rise and subsequent fall of a hypothetical epidemic
by a new influenza virus strain (Freeman, 1979).
Ever since antibodies against HIV were first detected
by the "AIDS test" in 1985, the number of antibody-positive Americans
has been fixed at a constant population of 1 million, or 0.4% (Section
2.2. and Table 1). The U.S. Army also reports that from 1985 to 1990 an
unchanging 0.03% of male and female applicants have been HIV-positive (Burke
et al., 1990). This is the predicted distribution of a long established
virus (Fig. 1 ). Since there are over 250 million uninfected Americans,
and since there is no antiviral vaccine or drug to stop the spread of HIV,
the non-spread of HIV in the U.S. in the last 7 years is an infallible
indication that the American "HIV epidemic" is old. The Central
African HIV epidemic has also remained fixed at about 10% of the population
since 1985 (Section 2.2). Likewise, HIV has remained fixed at 500,000 Europeans
since 1988 (World Health Organization, 1992a). The non-spread of HIV confirms
exactly the conclusion reached below that HIV behaves in a population as
a quasi-genetic marker (Section 3.5.2). Hence, the assumption that HIV
is new in the U.S. or in Africa is erroneous.
Indeed HIV existed in the U.S. long before its fictitious
origin in Africa (Gallo, 1987; Gallo and Montagnier, 1988; Anderson and
May, 1992) and its fictitious entry into this country in the 1970s (Shilts,
1987). For example, in the U.S. in 1968 an HIV-positive, male homosexual
prostitute died from Kaposi's sarcoma and immunodeficiency (Garry et
al., 1988), and 45 out of 1129 American intravenous drug users were
found to be HIV-positive in 1971 and 1972 (Moore et al., 1986).
The putative novelty of HIV is an anthropocentric interpretation
of new technology that made it possible to discover HIV and many other
latent retroviruses like HTLV-I (Duesberg and Schwartz, 1992). Indeed,
the technology to detect a latent virus like HIV only became available
around the time AIDS appeared. Given a new virus-scope, the assertion that
HIV is new is just like claiming the appearance of "new" stars
with a new telescope. Thus the claims that "... first HIV is introduced,
then AIDS appears" (Blattner et al., 1988) and that "HIV
... preceded it (AIDS)" (Weiss and Jaffe, 1990) are ironically more
true than the proponents of the virus hypothesis had anticipated. HIV preceded
AIDS by many, perhaps millions, of years.
3.5.2. HIV-Assumed to be Sexually Transmitted-Depends
on Perinatal Transmission for Survival
AIDS is said to be a sexually transmitted disease, because
HIV is thought to be a sexually transmitted virus (Section 2.2). However,
HIV is not by nature a sexually transmitted virus. Sexual transmission
of HIV is extremely inefficient. Based on studies measuring heterosexual
and homosexual transmission, it depends on an average of 1000 heterosexual
contacts and 100-500 homosexual contacts with antibody-positive people
(Rosenberg and Weiner, 1988; Lawrence et al., 1990; Blattner, 1991;
Hearst and Hulley, 1988; Peterman et al., 1988). 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" (Rosenberg and Weiner, 1988). Moreover, unwanted pregnancies
and venereal diseases, but not HIV infections, have increased significantly
in the U.S. since HIV has been known (Institute of Medicine, 1988; Aral
and Holmes, 1991). This argues directly against sexual transmission of
HIV.
Sexual transmission is so inefficient because there is
no free, non-neutralized HIV anywhere in antibody-positive persons, particularly
not in semen (Section 3.3). In a group of 25 antibody-positive men, only
one single provirus of HIV could be found in over 1 million cells of semen
in one of the men and no HIV at all was found in the semen of the other
24 (Van Voorhis et al., 1991). Likewise, HIV could only be isolated
or reactivated from ejaculates of 9 out of 95 antibody-positive men by
cocultivation with 2 million phytohemagglutinin-activated leukocytes (Anderson
et al., 1992). No virus or microbe could survive if it depended
on a transmission strategy that is as inefficient as 1 in 1000 contacts.
Indeed, HIV depends on perinatal, instead of sexual, transmission
for survival-just like other animal and human retroviruses. Therefore,
the efficiency of perinatal transmission must be high. This appears to
be the case. Based on HIV-tracking via the "AIDS test," perinatal
transmission from the mother is estimated to be 13-50% efficient (Blattner
et al., 1988; Blattner, 1991; Duesberg, 1991a; Institute of Medicine,
1988; European Collaborative Study, 1991). This number does not include
paternal HIV transmission to the baby via semen, for which there are currently
no data. The real efficiency of perinatal transmission must be higher than
the antibody-tests suggest, because in a fraction of recipients HIV only
becomes immunogenic when its hosts are of an advanced age (Quinn et
al., 1986; St Louis et al., 1991). During the antibody-negative
phase, latent HIV can be detected by the polymerase chain reaction (Rogers
et al., 1989, European Collaborative Study, 1991). This is also
true for other perinatally transmitted human (Blattner, 1990; Duesberg,
1991a) and animal retroviruses (Rowe, 1973; Duesberg, 1987).
HIV survival via perinatal transmission leads to two predictions: (1)
HIV cannot be inherently pathogenic-just like all other perinatally transmitted
viruses and microbes (Freeman, 1979; Mims and White, 1984). No microbe-host
system could survive if the microbe were perinatally transmitted and at
once fatal. (2) HIV must function as a quasi-genetic marker, because it
is quasi-nontransmissible by sex, or other natural horizontal modes of
transmission, just like known murine retrovirus prototypes (Rowe, 1973;
Duesberg, 1987). Both predictions are confirmed:
(1) Overwhelming statistical evidence from the U.S. and
Africa documents that the risk for AIDS-defining diseases for HIV-positive
babies, in the absence of other risk factors (Sections 3.4.4 and 4), is
the same as that of HIV-free controls:
(a) "AIDS tests" from applicants to the U.S.
Army and the U.S. Job Corps indicate that between 0.03% (Burke et al.,
1990) and 0.3% (St Louis et al., 1991) of the 17- to 19-year-old
applicants are HIV-infected but healthy. Since there are about 90 million
Americans under the age of 20, there must be between 27,000 and 270,000
(0.03%-0.3% of 90 million) HIV carriers. In Central Africa there are even
more, since 1-2% of healthy children are HIV-positive (Quinn et al.,
1986).
Most, if not all, of these adolescents must have acquired
HIV from perinatal infection for the following reasons: sexual transmission
of HIV depends on an average of 1000 sexual contacts, and only 1 in 250
Americans carries HIV (Table 1). Thus, all positive teenagers would have
had to achieve an absurd 1000 contacts with a positive partner, or an even
more absurd 250,000 sexual contacts with random Americans to acquire HIV
by sexual transmission. It follows that probably all of the healthy adolescent
HIV carriers were perinatally infected, as for example the 22-year-old
Kimberly Bergalis (Section 3.5.16).
The AIDS risk of perinatally infected babies of the general
population can be estimated as follows. Between 27,000 and 270,000 Americans
under the age of 20 carry HIV. But only about 4260 AIDS cases have been
recorded in this age group in the last 10 years (Centers for Disease Control,
1992b). Therefore, between 85% and 98% of HIV-infected youths do not develop
AIDS up to 20 years after perinatal infection (Section 2.1). Since the
above number includes the AIDS babies from drug-addicted mothers (Sections
3.4.2 and 4), the AIDS risk of HIV-infected babies from mothers that don't
use drugs probably reflects normal infant mortality.
(b) A controlled study from Africa compared 218 newborns
from HIV-positive mothers to 218 from HIV-negative mothers, and the "rates
of prematurity, low birth weight, congenital malformations and neonatal
mortality were comparable in the two groups" (Lepage et al.,
1991). The mothers were matched for age and parity and the "frequency
of signs and symptoms was not statistically different in the two groups."
(2) The incidence of HIV in American teenagers of different
ethnic backgrounds is predictable on genetic grounds. It is about 10-fold
higher in blacks than in whites, i.e. 0.3% compared to 0.03% (U.S. Department
of Health and Human Services, 1990; Burke et al., 1990; Blattner,
1991; Palca, 1991b; St Louis et al., 1991; Vermund, 1991). HIV was
even 50-fold more common in black mothers in inner-city hospitals in New
York (36%) than in whites (0.7%) (Landesmann et al., 1987). This
reflects the 25- to 50-fold higher incidence of HIV in the blacks' African
ancestors (10%) compared to the whites' European ancestors (0.2 to 0.4%)
(Section 2.2, Table 1). Likewise, the different ethnic groups of the Caribbean
reflect the distinct HTLV-I incidences of their ancestors in Africa, Europe
and Japan, despite generations of coexistence on the Caribbean islands
(Blattner, 1990). The unchanging incidence of HIV in the American population
(Fig. 1) also confirms the view that HIV is a quasi-genetic marker. Since
there is virtually no horizontal transmission of retroviruses, murine retroviruses
have functioned as classical genetic markers of mice that could only be
distinguished from cellular genes by fastidious genetic crosses (Rowe,
1973).
Thus the assumption that AIDS is sexually transmitted
by HIV is not consistent with the natural perinatal mode of HIV transmission.
If natural transmission of HIV caused a disease, AIDS would be a pediatric
disease. Instead, HIV is merely a marker of either an average of 1000 sexual
contacts and thus of many other possible AIDS risks associated with very
high sexual activity or of long-term intravenous drug use (Sections 3.4.3
and 5).
3.5.3. AIDS Assumed to be Proportional to HIV
Infection
The incidence of AIDS is assumed to be proportional to
the incidence of HIV via a constant factor. For example, a 10-fold higher
incidence of AIDS in American and European males compared to females is
assumed to reflect a 10-fold higher incidence of HIV in men (Blattner et
al., 1988; Blattner, 1991; Goudsmit, 1992).
However, there is no evidence that the incidence of HIV
is 10 times higher in males than in females of the general American and
European population, although this is the case for AIDS (Table l). Indeed,
the most recent claim for a 90% bias of HIV for males of the general population
(Blattner, 1991) is only supported by a reference to an editorial (Palca,
1991b), which itself provides nothing more than an unreferenced cartoon
showing global patterns of HIV infection. According to a CDC epidemiologist,
estimates of how HIV is distributed between the sexes of the general population
are "approximations" based on the distribution of AIDS (Tim Dondero,
CDC, personal communication; see also Anderson and May, 1992)-a tautology.
Proportionality between HIV and AIDS via a constant is
also incompatible with the following statistics. The U.S. Army (Burke et
al., 1990) and the U.S. Job Corps (St Louis et al., 1991) report,
based on millions of tests, that HIV has been equally distributed between
the sexes among 17- to 21-year-olds of the general population over the
last five years for which data were available (Sections 3.5.1 and 3.5.2).
Since testing 17- to 19-year-olds annually for 5 years is equivalent to
testing 17- to 24-year-olds, the U.S. Army data predict that among 17-
to 24-year-olds, AIDS risks should be distributed equally between the sexes.
However, the CDC documents that 85% of the AIDS cases among 17- to 24-year-olds
were males (Centers for Disease Control, 1992b).
In response to this, some proponents of the virus-AIDS
hypothesis have speculated that teenage homosexuals exclude themselves
from the Army. However, Randy Shilts, a homosexual writer, reports that
just the opposite is true (Shilts, 1991). Moreover, most teenagers are
not as yet aware of a definite homosexual persuasion and are not likely
to understand the implications nor to fear the consequences of a positive
"AIDS test."
The over 100-fold discrepancies between the AIDS risks
of different HIV-infected risk groups also disprove the claim that the
incidence of AIDS is proportional via a constant to the incidence of HIV
(Table 2). The proportionality between HIV and AIDS only holds if the analysis
is restricted to groups with the same AIDS risks. In groups with the same
percentage of HIV but with different AIDS risks, AIDS segregates specifically
with nonviral AIDS risks, e.g. illicit recreational drugs, the antiviral
drug AZT (Section 4) and frequent transfusions (Section 3.4.4).
3.5.4. AIDS Assumed to be Homosexually Transmitted
in the U.S. and Europe
In view of a sexually transmitted AIDS virus, it is paradoxical
that AIDS is 90% male in America and 86% male in Europe (Sections 3.1 and
3.2). Therefore it is assumed that "the virus first got its footing
in the U.S." in male homosexuals (Booth, 1988) and has remained with
homosexuals because it is transmitted preferentially by anal intercourse
and because homosexuals have no sex with heterosexuals (Centers for Disease
Control, 1986; Shilts, 1987; Blatter et al., 1988; Institute of
Medicine, 1988; Blattner, 1991; Bardach, 1992; Project Inform, 1992).
However, this assumption is inconsistent with the fact
that about 10% of all males and females prefer anal intercourse (Bolling
and Voeller, 1987; Turner et al., 1989) and that American and European
heterosexuals have sufficient access to HIV. The females would be infected
by HIV-positive, heterosexual intravenous drug users, hemophiliacs, and
bisexual males. Thus, if HIV were transmitted by anal intercourse, about
the same percentage of women as men should develop AIDS, particularly since
the efficiencies of transmission of anal and vaginal intercourse are approximately
the same, e.g. between 1 to 100 and 1 to 500 for anal and 1 to 1000 for
vaginal intercourse (Blattner, 1991) (see also Section 3.5.2). Yet, despite
widespread alarm, this has not occurred in the last 10 years in the U.S.
(Table 1), although the first women with AIDS had been diagnosed as early
as in 1981 (Centers for Disease Control, 1986; Guinan and Hardy, 1987).
The risk of women for both HIV infection and AIDS is the same for those
who practice anal intercourse as for those who practice other types of
intercourse (Guinan and Hardy, 1987).
The preferred anal-transmission hypothesis is also incompatible
with the sexually equal distribution of HIV and AIDS in Africa. Since it
is postulated that HIV appeared in America and Africa at about the same
time 10-20 years ago (Institute of Medicine, 1986; Blattner et al.,
1988; Gallo and Montagnier, 1988), HIV should have reached the same equilibria
between the sexes in all countries.
Instead it is shown below that the male bias for AIDS
in America and Europe reflects male-specific behavior, including the facts
that over 75% of all intravenous drug users are males and that long-term
consumption of sexual stimulants, like amylnitrite and ethylchloride inhalants,
is almost entirely restricted to male homosexuals (Section 4). HIV is just
a marker of the many sexual stimulants used to achieve 500-1000 sexual
contacts (Section 4). The difference between the AIDS risks of men in America
and Europe, namely drugs, and those of Africans, namely country-specific,
but not sex-specific, risk factors (Section 3.4.4.8) resolves the paradox
between the different sexual distributions of AIDS in these countries.
3.5.5. AIDS Assumed to be Heterosexually Transmitted
by African "Life-style"
AIDS in Africa is assumed to affect both genders equally,
because HIV is distributed equally between the sexes by "prostitution"
(Institute of Medicine, 1988), lack of "circumcision" (Klein,
1988; Marx, 1989; Blattner, 1991), African "lifestyle" (Quinn
et al., 1987; Blattner et al., 1988; Goodgame, 1990) and
"voodoo rituals" (Gallo, 1991). These assumptions are compatible
with the sexually equal distributions of HIV and AIDS in Africa.
However, AIDS in Africa is hard to reconcile with the
known efficiency of sexual transmission of HIV. Since it takes 1000 HIV-positive
sexual contacts to transmit HIV and about 10% of all Central Africans,
or 6 million, are HIV-positive (Section 2.2), 6 million Africans would
have had to achieve on average at least 10,000 sexual contacts with random
Africans to pick up HIV. Since this is highly improbable, it is also highly
improbable that sexual transmission of HIV is the cause of AIDS in Africa.
The true reason for the sexually equal distribution of HIV in Africa is
perinatal transmission of HIV (Section 3.5.2). Nonsexual, country-specific
risk factors are the reason for the "sexually" equal distribution
of AIDS in Africa (Section 3.4.4.8).
3.5.6. HIV Claimed to be Abundant in AIDS Cases
HIV is said to be abundant or viremic in AIDS patients
(Baltimore and Feinberg, 1989; Coombs et al., 1989; Ho et al.,
1989a; Semple et al., 1991) and thus compatible with orthodox viruses
which cause disease only at high titers (Duesberg and Schwartz, 1992).
In other words HIV is assumed to meet Koch's first postulate (Section 3.3).
The assumption is based on two papers which reported HIV titers of 102
to 103 infectious units per mL of blood in 75% of AIDS patients and in
25-50% of asymptomatic HIV carriers (Coombs et al., 1989; Ho et
al., 1989a). The authors and an accompanying editorial, HIV Revealed,
Toward a Natural History of the Infection (Baltimore and Feinberg,
1989), concluded that these findings established HIV viremia as an orthodox
criterion of viral pathogenicity. Viremia of similar titers was recently
also implied in some AIDS patients and asymptomatic carriers based on an
indirect assay that amplifies HIV RNA in vitro (Semple et al.,
1991).
However, several arguments cast doubt on the claim that
HIV viremia is relevant for AIDS:
(1) Since viremia was observed in 25-50% of asymptomatic
HIV carriers (Coombs et al., 1989; Ho et al., 1989a; Semple
et al., 1991), it cannot be sufficient for AIDS.
(2) Since no viremia was observed in 25% of the AIDS cases
studied by two groups (Coombs et al., 1989; Ho et al., 1989a),
it is not necessary for AIDS.
(3) Viremia initiated from a previously suppressed virus
and observed years after infection is a classical consequence, rather than
the cause of immunodeficiency. Indeed, many normally latent parasites become
activated and may cause chronic "opportunistic infections" in
immunodeficient persons, as for example Candida, Pneumocystis,
herpes virus, cytomegalovirus, hepatitis virus, tuberculosis bacillus,
toxoplasma (Sections 2.3 and 3.4.3)-and sometimes even HIV. It is consistent
with this view that HIV viremia is observed more often in AIDS patients
than in asymptomatic carriers (Duesberg, 1990c).
(4) The HIVs that make up the "viremias" are
apparently not infectious in vivo, because only a negligible fraction
of leukocytes, on average only 1 in 1500 to 8000, of AIDS patients are
infected (Section 3.3). The probable reason is that the "viremias"
consist of viruses that are neutralized by the antiviral antibodies of
"seropositive" AIDS patients (Duesberg, 1992d). Since viruses,
as obligatory cellular parasites, can only be pathogenic by infecting cells,
these noninfectious viremias cannot be relevant to the cause of AIDS. If
assayed in vitro, in the absence of free antiviral antibodies, antibodies
may dissociate from neutralized viruses and thus render the virus infectious
for cells in culture. This explains the discrepancy between the noninfectious
"viremias" in vivo and the relatively high infectivity
recorded in vitro (Coombs et al., 1989; Ho et al.,
1989a).
Thus HIV viremia is a rare, predictable consequence of
immunodeficiency rather than its cause.
3.5.7. HIV to Depend on Cofactors for AIDS
Conceding that HIV is not sufficient to cause AIDS, it
is assumed to depend on cofactors. Montagnier (Goldsmith, 1990; Lemaitre
et al., 1990; Balter, 1991) and Lo (Lo et al., 1991) have
proposed mycoplasmas that were discovered in their laboratories; Gallo
has proposed two viruses, herpes virus-6 and HTLV-I, which were both discovered
in his laboratory (Cotton, 1990; Gallo, 1990, 1991; Lusso et al.,
1991). Others have proposed cytomegalovirus, Epstein-Barr virus (Quinn
et al., 1987; Evans, 1989a; Root-Bernstein, 1990c), "age"
(Evans, 1989a; Goedert et al., 1989; Weiss and Jaffe, 1990; Biggar
and the International Registry of Seroconverters, 1990), unidentified "coagents"
(Weyer and Eggers, 1990; Eggers and Weyer, 1991), "clinical illness
promotion factors" (Evans, 1989b, 1992) and even "pre-existing
immune abnormalities" (Ludlam et al., 1985; Marion et al.,
1989; Ludlam, 1992) as cofactors of HIV.
However, cofactor hypotheses only replace HIV-specific
AIDS problems with the following HIV-plus-cofactor-specific AIDS problems:
(1) Since HIV is extremely rare and dormant in most antibody-positive
AIDS patients (Sections 2.2 and 3.3), it is hard to imagine how its various
AIDS-allies could benefit from their dormant "cofactor" HIV.
(2) Since HTLV-I is just as dormant and unable to kill
cells as HIV (Duesberg, 1987; Blattner, 1990; Duesberg and Schwartz, 1992),
it is even harder to imagine how one dormant virus could help another dormant
virus to generate the biochemical activity that would be necessary to cause
a fatal disease.
(3) Since mycoplasma (Freeman, 1979; Cotton, 1990; Goldsmith,
1990; Balter, 1991), herpes virus-6 (Cotton, 1990; Lusso et al.,
1991), cytomegalovirus and Epstein-Barr virus (Mims and White, 1984; Evans,
1989c) are each very common, if not ubiquitous, parasites (Freeman, 1979;
Froesner, 1991), AIDS should develop in most people as soon as they are
infected by HIV. Likewise, "aged" people should develop AIDS
as soon as they are infected by HIV. Yet not more than 3-4% of HIV-antibody-positive
Americans or Europeans and 0.3% of antibody-positive Africans develop AIDS
per year (Tables 1 and 2).
Moreover, if infectious cofactors helped HIV to cause
AIDS, the AIDS risk of Africans would be expected to be higher than that
of Americans. This is because the incidence of hypothetical, microbial
cofactors in Africans without AIDS was found to be the same as in those
with AIDS, while the incidence of microbial cofactors in Americans without
AIDS risks was significantly lower than in those with AIDS (Section 3.4.3)
(Quinn et al., 1987). Even the cofactor HIV was present in 6% of
African AIDS-free controls (Quinn et al., 1987). Yet the annual
AIDS risk of HIV-infected Africans is 10-times lower than that of Americans
(Table 1).
(4) Contrary to the claims that "age" is an
AIDS cofactor of HIV, the virus-AIDS hypothesis postulates that the latent
period for HIV is longer in adults (10 years) than in children (2 years)
(Section 2.2). However, the proposal that "age" is a cofactor
for HIV becomes more compelling the more the hypothetical "latent
period" of HIV grows. Clearly, if a 70-year-old will be infected by
a virus with a "latent period" of 10 years, "age" will
be a predictable cofactor (see, for example, hemophiliacs, Section 3.4.4.5
and Paul Gann, Section 3.5.16).
(5) The claims that HIV depends on "clinical illness
promotion factors" (Evans, 1992) or on a "pre-existing immune
abnormality" (Marion et al., 1989; Ludlam, 1992) for AIDS are
euphemisms for saying that HIV cannot cause AIDS until something else does
(Duesberg, 1989b). The additional hypothesis that a "pre-existing
immune abnormality" (Ludlam, 1992) or a "prior immune dysfunction"
(Marion et al., 1989) makes a subject more susceptible to HIV is
erroneous, because a pre-existing immune deficiency only affects the progression
of an infection, but not the risk of infection.
In view of this, I share Gallo's concerns about cofactors
of HIV, which he expresses with a quotation from Lewis Thomas: "Multifactorial
is multi-ignorance. Most factors go away when we learn the real cause of
a disease" (Gallo, 1991). The "cofactor" HIV may be no exception.
Until any one of these hypothetical cofactors is actually shown to depend
on HIV to cause AIDS, HIV must be considered just one of many innocent
bystanders found in AIDS patients (Section 3.4.3).
3.5.8. All AIDS Diseases to Result from Immunodeficiency
All AIDS diseases are said to reflect a primary immunodeficiency
(Coffin et al., 1986; Institute of Medicine, 1986; Blattner et
al., 1988).
However, immunodeficiency is not a common denominator
of all AIDS diseases. About 38% of all AIDS diseases, i.e. dementia, wasting
disease, Kaposi's sarcoma and lymphoma (Table 1), are neither caused by,
nor necessarily associated with, immunodeficiency. Cancer is not a consequence
of immunodeficiency (Stutman, 1975; Duesberg, 1989c). Indeed, Kaposi's
sarcoma frequently has been diagnosed in male homosexuals in the absence
of immunodeficiency. For example, the immune systems of 20 out of 37 HIV-positive
homosexuals with Kaposi's sarcoma were normal when their disease was first
diagnosed (Spornraft et al., 1988). Another study also describes
19 male homosexual Kaposi's sarcoma patients with normal immune systems
(Murray et al., 1988). Likewise, Kaposi's sarcomas have been diagnosed
in HIV-free male homosexuals with normal immune systems (Afrasiabi et
al., 1986; Archer et al., 1989; Friedman-Kien et al.,
1990; Marquart et al., 1991).
Dementia and wasting disease also are not consequences
of immunodeficiency (Duesberg, 1989c, 1991a). Thus, the assumption that
all AIDS diseases are caused by immunodeficiency is erroneous.
3.5.9. HIV to Induce AIDS via Autoimmunity and
Apoptosis
In view of the extremely low number of HIV-infected cells
in AIDS patients (Section 3.3), HIV has recently been proposed to cause
AIDS by inducing autoimmunity (Hoffmann, 1990; Maddox, 1991a; Mathé,
1992) or apoptosis (Laurent-Crawford et al., 1991; Goudsmit, 1992).
According to these new ideas HIV is assumed either to confuse the immune
system into attacking itself or to persuade the immune cells to commit
suicide, termed apoptosis. The autoimmune hypothesis postulates homology
between HIV and human cells, and currently relies only on mouse and monkey
models (Hoffmann, 1990; Maddox, 1991a), and on precedents for autoimmunity
induced in humans as a consequence of graft rejection and blood transfusions
(Root-Bernstein, 1990a,b; Mathe, 1992). One autoimmunologist claims that
"each of Duesberg's paradoxes might be understood in the context of
the model without sacrificing the idea that HIV is usually involved in
pathogenesis" (Hoffmann, 1990). This strategy of crediting me rather
than the virus-AIDS hypothesis for its paradoxes shifts the discussion
from a problem with science to a problem with a scientist (Booth, 1988;
Weiss and Jaffe, 1990).
However, both the autoimmune and the apoptosis hypotheses
are incompatible with human AIDS on several grounds:
(1) Autoimmunity or apoptosis cannot account for all those
AIDS diseases that are not caused by immunodeficiency, e.g. Kaposi's sarcoma,
dementia, wasting disease and lymphoma (Section 3.5.8).
(2) Autoimmunity or apoptosis fail to explain risk group-specific
AIDS diseases (Section 2.1.3, Tables 1 and 2).
(3) Autoimmunity and apoptosis fail to explain the long
average intervals, "latent periods," from conventional immunity
against HIV, detected by the "AIDS test," to hypothetical autoimmunity
10 years later (Section 3.2).
(4) Autoimmunity and apoptosis fail to explain the over
100-fold discrepancies between the annual AIDS risks of different HIV-infected
groups (Table 2).
(5) HIV-induced autoimmunity or apoptosis fail to explain the consistent
90% bias of American/European AIDS for males (2.1, Table 1).
(6) In view of the autoimmunity or apoptosis hypothesis,
it is paradoxical that 80% of antibody-positive Americans (1 million minus
the 206,000 who have developed AIDS) and 98% of antibody-positive Africans
(6 million minus the 129,000 who have developed AIDS) have not developed
AIDS since 1984 (Table 1). Obviously, these figures are not even corrected
for the normal and drug-induced incidence of AIDS-defining diseases in
those groups (Section 3.4.4, Table 2).
(7) There is no sequence homology between HIV and human
DNA detectable by hybridization to predict autoimmunity (Shaw et al.,
1984). Therefore, autoimmunologists argue that antibodies against those
antibodies, which are directed at the viral proteins that bind to cellular
receptors, would also react with cellular receptors and thus cause AIDS
(Hoffmann, 1990). However, if this were true, all viruses should cause
AIDS.
Thus the HIV-autoimmunity and apoptosis hypotheses of
AIDS are (a) not compatible with essential parameters of human AIDS and
(b) arbitrary, because they are not based on an autoimmunogenic or apoptogenic
property of HIV that is distinct from all other viruses.
3.5.10. HIV Assumed to Kill T-cells
Based on an early observation by Gallo et al. HIV
is assumed to cause immunodeficiency by specifically killing T-cells (Gallo
et al., 1984; Weiss and Jaffe, 1990). Gallo's observation was restricted
to primary T-cells (Gallo et al., 1984) but not to established T-cell
lines (Rubinstein, 1990). However, according to Montagnier, the discoverer
of HIV, "In a search for a direct cytopathic effect of the virus on
(primary) T-lymphocytes, no gross changes could be seen in virus-producing
cultures, with regard to cell lysis or impairment of cell growth"
(Montagnier et al., 1984). Others have confirmed that HIV does not
kill infected, primary T-cells in vitro (Hoxie et al., 1985;
Anand et al., 1987; Langhoff et al., 1989; Duesberg, 1989c).
Moreover HIV-infected primary T-cells are considered the natural "reservoir"
of HIV in vivo (Schnittman et al., 1989).
Thus Gallo's controversial observation probably reflects
the notorious difficulties experienced by his laboratory in maintaining
primary blood cells alive in culture instead of a genuine cytocidal function
of HIV (Crewdson, 1989; Culliton, 1990; Rubinstein, 1990; Hamilton, 1991).
Gallo showed in a later study from his laboratory that about 50% of uninfected
T-cells died within 12 days in culture (Gallo, 1990).
Indeed, the assumption that HIV is cytocidal is incompatible
with generic properties of retroviruses and with specific properties of
HIV:
(1) The hallmark of retrovirus replication is to convert
the viral RNA into DNA and to deliberately integrate this DNA as a parasitic
gene into the cellular DNA (Weiss et al., 1985). This process of
integration depends on mitosis to succeed, rather than on cell death (Rubin
and Temin, 1958; Duesberg, 1989c). The resulting genetic parasite can then
be either active or passive, just like other cellular genes (Duesberg,
1987). Transcription of viral RNA from chromosomally integrated proviral
DNA also only works if the cell survives infection, because dying cells
are not transcriptionally active. Thus, this strategy of replication depends
entirely on the survival of the infected cell.
Noncytocidal replication is the reason that retroviruses
were all considered potential carcinogens before AIDS (Weiss et al.,
1985; Duesberg, 1987). For example, Gallo's first candidate for an AIDS
virus is called Human T-cell Leukemia Virus-I (Gallo et al., 1983),
and Gallo's second candidate for an AIDS virus was originally described
at a press conference in April 1984 by Gallo and the Secretary of Health
and Human Services as "a variant of a known human cancer virus called
HTLV III" (Crewdson, 1989; Rubinstein, 1990). It used to be called
Human T-cell Leukemia Virus-III by Gallo (Gallo et al., 1984; Shaw
et al., 1984) before it was renamed HIV in 1986 (Coffin et al.,
1986).
(2) Limited cytotoxicity of HIV has been observed soon
after infection of cells in vitro (Duesberg, 1989c; Bergeron and
Sodroski, 1992). Therefore, it has been proposed that multiple copies of
unintegrated proviral DNA, generated by multiple infections before all
cellular receptors are blocked by newly replicated viruses, could kill
T-cells (Bergeron and Sodroski, 1992). However, cells infected by every
retrovirus, including HIV (Bergeron and Sodroski, 1992), survive multiple
unintegrated proviral DNAs during the early phase of the infection (Weiss
et al., 1985). Rare cell death during this phase of infection is
a consequence of cell fusion, which is mediated by viruses on the surface
of infected cells binding to receptors of uninfected cells. In some conditions
retrovirus-mediated fusion occurs so reliably that it has been used to
quantitate retroviruses in tissue culture. However, virus-mediated fusion
is blocked by antiviral antibodies and thus not relevant to the loss of
T-cells in persons with antibodies against HIV (Duesberg, 1989c).
Alternatively, it has been proposed that HIV proteins
are directly toxic because of structural similarities with scorpion and
snake poisons (Gallo, 1991; Garry et al., 1991; Garry and Koch,
1992). However, no such toxicity is observed in millions of asymptomatic
HIV carriers, and there is no reason that it should occur, if it did, only
after latent periods of 10 years.
(3) The propagation of HIV in indefinitely growing human
T-cells for the "AIDS test" was patented by Gallo et al.
in 1984 (Rubinstein, 1990) and was recently confirmed by Montagnier (Lemaître
et al., 1990). It is totally incompatible with Gallo's claim that
HIV kills T-cells. Such HIV-producing T-cells have been growing in many
laboratories and companies since 1984 producing virus at titers of up to
106 virus particles per mL, which is many orders of magnitude more than
is ever observed in humans with or without AIDS (Duesberg, 1989c, 1991a).
In view of this, Gallo postulates that T-cell lines in
culture have all acquired resistance to HIV killing (Gallo, 1991). However,
there is no precedent for this ad hoc hypothesis, as no other cytocidal
virus has ever been observed that is cytocidal in vivo and in primary
cells in vitro, but is noncytocidal in cell lines in culture. It
is also implausible that a potentially life-saving cellular mutation, such
as resistance to the hypothetical "AIDS virus," would be restricted
just to cells in culture, particularly if these mutations occur so readily
that they are found in all T-cell lines. There is not even one T-cell line
that is consistently killed by HIV.
(4) HIV, like all other retroviruses, does not specifically
infect Tcells. It also infects monocytes, epithelial cells, B-cells,
glial cells and macrophages, etc. and none of these are killed by HIV (Levy,
1988; Duesberg, 1991a). Most other retroviruses also infect T-cells, which
is why so many of them are suspected "T-cell leukemia" viruses
(Weiss et al., 1985; Duesberg, 1987; Blattner, 1990).
Thus, the assumption that HIV causes AIDS by killing T-cells
is not tenable.
3.5.11. Antibodies Assumed not to Neutralize
HIV
Antibodies against HIV, detected by a positive "AIDS
test," are claimed not to protect against AIDS because they do not
neutralize HIV (Institute of Medicine, 1988; Evans, 1989a; Weiss and Jaffe,
1990; Gallo, 1991). "It is a test for anti-HIV antibodies and not,
as Duesberg states, 'neutralizing antibodies'" (Baltimore and Feinberg,
1990).
However, antiviral immunity completely neutralizes HIV
and restricts it to undetectable levels in healthy HIV-carriers as well
as in AIDS patients (Section 3.3.1) (Duesberg, 1989b,c). Indeed, two recent
studies have just confirmed that HIV activity is "rapidly and effectively
limited" by antiviral immunity (Clark et al., 1991; Daar et
al., 1991) to less than 1 in 1000 T-cells (Section 3.3). By contrast,
HIV replicates in the absence of antiviral immunity in human T-cells in
culture to titers of 106 virus particles per mL (Section 3.5.10). Thus,
the assumption that HIV causes AIDS because of inadequate antiviral immunity
is unconfirmed. Baltimore's, Feinberg's and Evans' paradox "that antibody
is not protective" (Evans, 1989a) is their failure to recognize the
non-role of HIV in AIDS (Section 3.3.2).
3.5.12. HIV Claimed to Cause AIDS in 50% Within
10 Years
All HIV-infected persons are said to die from AIDS after
a medium latent period of 10 years (Anderson and May, 1988; Institute of
Medicine, 1988; Moss et al., 1988; Lemp et al., 1990; Blattner,
1991; Duesberg, 1991a).
However, according to statistics from the CDC, only about
30,000-40,000, or 3-4%, of a reservoir of 1 million HIV-infected Americans
develop AIDS annually (Table 1). Likewise, 3% of infected Europeans develop
AIDS per year (Table 1). Accordingly, 50% of HIV-infected Americans and
Europeans would have to wait 12-16 years and 100%, 24-33 years to develop
AIDS. During this time, many would die from other causes. Since only 0.3%
of infected Africans develop AIDS diseases annually (Tables 1 and 2), 50%
of Africans would have to wait about 150 years and 100% would have to wait
300 years to develop AIDS.
Thus, it is presumptuous to claim that HIV causes AIDS
in 50% of infected persons after median latent periods of 10 years, particularly
since the virus has only been known for nine years.
3.5.13. HIV Said to Derive Pathogenicity from
Constant Mutation
During its long latent periods, HIV is claimed to acquire
pathogenicity by mutation, for example by generating variants that escape
immunity (Hahn et al., 1986; Levy, 1988; Eigen, 1989; Gallo, 1990;
Weiss and Jaffe, 1990; Anonymous, 1992; Anderson and May, 1992) or by generating
defective variants (Eigen, 1989; Haas, 1989; Weiss, R.A., 1989).
However, a recent study just demonstrated that the replicative
and functional properties of HIVs from AIDS patients are the same as those
from asymptomatic carriers (Lu and Andrieu, 1992). Indeed, most essential
structural and replicative proteins of a virus cannot be mutated without
eliminating its viability. Functionally relevant mutations of any virus
are also severely restricted by the necessity to remain compatible with
the host (Duesberg, 1990b). Moreover, there is no precedent for an immune
system that has been able to neutralize a virus completely and is then
unable to catch up with an occasional subsequent mutation. If viruses in
general could evade the immune system by mutation, the immune system would
be a useless burden to the host.
Likewise, the proposals that defective HIVs could generate
pathogenicity is untenable. Defective viruses are only viable in the presence
of nondefective helper viruses and thus unlikely to survive in natural
transmission from host to host at low multiplicity of infection, particularly
with helper viruses that never achieve high titers like HIV (Duesberg,
1989a).
There are, however, examples of new antigenic variants
of retroviruses (Beemon et al., 1974) or influenza viruses (Duesberg,
1968), that have arisen upon rare double infection by two antigenically
distinct virus strains via genetic recombination. Yet antigenically new
variants of HIV have never been observed in American and European AIDS
patients, as all HIV strains diagnosed to date crossreact with the very
same standard HIV-1 strain that is patented in America and Europe for the
"AIDS test" (Connor, 1991, 1992; Palca, 1991a; Weiss, 1991).
Moreover, if recombination or spontaneous mutation could
generate pathogenic HIV mutants from nonpathogenic strains, one would expect
all those who are infected by HIV from AIDS patients to develop AIDS within
weeks after infection. Such HIV mutants should be pathogenic just as soon
as conventional, nonpathogenic HIV strains are immunogenic. But this is
not observed.
Thus, the assumption that HIV acquires pathogenicity by
mutation during the course of the infection is not tenable.
3.5.14. HIV Assumed to Cause AIDS with Genes
Unique Among Retroviruses
AIDS researchers assert that HIV causes AIDS with unique
genetic information that all other animal and human retroviruses lack and
that these unique genes would regulate HIV down during the "latent
period" and up during AIDS (Gallo and Montagnier, 1988; Haseltine
and Wong-Staal, 1988; Institute of Medicine, 1988; Eigen, 1989; Temin,
1990; Fauci, 1991; Gallo, 1991). Further, it is claimed that HIV-infected
cells export factors encoded by these genes that promote neoplastic growth
of uninfected cells to cause, for example, Kaposi's sarcoma (Salahuddin
et al., 1988; Ensoli et al., 1990; Gallo, 1990); at the same
time such genes are said to export "scorpion poison"-related
toxins that kill uninfected neurons to cause dementia (Gallo, 1991; Garry
et al., 1991; Garry and Koch, 1992). By contrast, all other known
bacterial, animal and human viruses, including retroviruses, are only able
to kill or alter those cells they infect, because viruses are manufactured
inside cells and would not benefit from proteins released to uninfected
cells.
However, the claims of unique retroviral HIV genes with
unique control functions raises several unresolvable problems:
(1) Despite its presumed unique properties HIV has the
same genetic complexity, i.e. 9000 nucleotides, and the same genetic structure
as all other retroviruses (Beemon et al., 1974; Wang et al.,
1976; Institute of Medicine, 1988). It shares with other retroviruses the
three major genes gag-pol-env, which are linked in this order in
all animal and human retroviruses (Wang et al., 1976). Although
"novel" genes that overlap with the major retroviral genes have
been discovered in HIV by computerized sequence analysis, and by new protein
detection technology (Varmus, 1988), such genes have also been found with
the same technology in other retroviruses that do not cause AIDS, such
as HTLV-I, other human retroviruses, bovine retroviruses, simian retroviruses
and sheep retroviruses (Varmus, 1988; Weiss, 1988; Duesberg, 1989c; Palca,
1990). Thus there is no unique genetic material and no uncommon genetic
structure in HIV RNA that could indicate where this unique AIDS-specific
information of HIV is hiding.
(2) Since all retroviral genes share just one common promoter,
it would be impossible to differentially activate one HIV gene while the
others are latent. Thus the idea that different viral genes would regulate
latency and virulence, as with lambda phage, is not compatible with HIV
(Haseltine and Wong-Staal, 1988; Eigen, 1989; Temin, 1990; Fauci, 1991).
Since all HIV genes share the same promotor, latent HIV can only be activated
by the host-just like all other latent retroviruses. In addition HIV cannot
make specific AIDS factors, while its major genes are dormant. Since viral
RNA synthesis in vivo is only detectable in 1 out of 10,000 to 100,000
leukocytes and then only in half of all AIDS patients (Section 3.3), HIV
cannot make Kaposi's sarcomagenic and neurotoxic factors in amounts sufficient
to cause fatal tumors and dementias. This is why such factors have not
been detectable in vivo (Weiss and Jaffe, 1990; Gallo, 1991).
Thus, based on the structure, information and function
of its RNA, HIV is a profoundly conventional retrovirus. It does not contain
unique genes that distinguish it from other retroviruses, nor can its genes
be differentially regulated at the transcriptional level.
3.5.15. Simian Retroviruses to Prove that HIV
Causes AIDS
Animal retroviruses may cause diseases in experimental
animals that overlap with the wide spectrum of AIDS diseases. Such systems
are now studied for analogies to gain experimental support for the virus-AIDS
hypothesis (Blattner et al., 1988; Weiss and Jaffe, 1990; Goudsmit,
1992). For example, a retrovirus isolated from macaques (Fultz et al.,
1990), termed simian immunodeficiency virus (SIV), that is 40% related
to HIV, is said to cause AIDS-like diseases in rhesus monkeys (Kestler
et al., 1990; Temin, 1990). According to an editorial in Science,
"if SIV infection is all that is needed to cause simian AIDS, that's
one more indication that HIV is all that is needed to cause human AIDS"
(Palca, 1990).
However, the presumed role of SIV in the diseases of infected
monkeys is very different from that of HIV in human AIDS:
(1) According to one study, about half of the infected
monkeys developed diseases within several months to one year after infection
(Kestler et al., 1990). By contrast only 3-4% of HIV-infected Americans
or Europeans and 0.3% of infected Africans develop AIDS annually (Table
1).
(2) In the same study, the absence of antiviral antibodies
predicted the incidence of diseases in monkeys, while the opposite is claimed
for humans infected with HIV. Another study has confirmed that the monkey's
risk of disease is directly proportional to the titer of SIV (Fultz et
al., 1990).
(3) The simian retroviruses barely reduce the T-cell levels
of ill monkeys (Kestler et al., 1991), while HIV is claimed to deplete
T-cells in humans.
(4) The spectrum of diseases observed in the SIV-infected
monkeys is different from AIDS, including bacteremia and lacking, among
others, Kaposi's sarcoma and dementia (Kestler et al., 1990; Fultz
et al., 1990).
(5) In follow-up studies, SIV failed to cause disease
in rhesus and mangabey monkeys despite extensive sequence variation which
is thought to enhance pathogenicity of the virus (Fultz et al.,
1990; Burns and Desrosiers, 1991; Villinger et al., 1991).
(6) Since SIV has never caused any disease in wild monkeys,
although about 50% are naturally infected (Duesberg, 1987, 1989c; Blattner
et al., 1988; Fultz et al., 1990; Burns and Desrosiers, 1991;
Villinger et al., 1991), SIV is not an appropriate model for the
hypothesis that HIV causes AIDS in naturally infected humans.
It would appear that SIV causes disease in monkeys like
all viruses cause disease soon after infection and in the absence of effective
immunity. This is not a model for the hypothesis that HIV causes AIDS 10
years after it is neutralized by antibodies. Indeed, in the vast literature
on retroviruses there is not even one proven example of a latent retrovirus
that, in the presence of antiviral immunity, has ever caused a disease
in any animal, including chickens, mice, cattle, and monkeys (Weiss et
al., 1985; Duesberg, 1987, 1989c).
Moreover, the observation that a retrovirus that is 60%
unrelated to HIV causes disease in monkeys cannot prove that HIV causes
AIDS in humans, even if all parameters of infection were completely analogous.
It can only prove that under analogous conditions other retroviruses may
also cause disease, which has been demonstrated with numerous avian and
murine retroviruses long ago (Weiss et al., 1985).
3.5.16. Anecdotal AIDS Cases from the General
Population
Rare AIDS cases occurring outside the major risk groups
are claimed to prove that HIV alone is sufficient to cause AIDS in persons
with no other AIDS risks (Blattner et al., 1988; Booth, 1988; Baltimore
and Feinberg, 1989; Weiss and Jaffe, 1990). Four examples illustrate this
point:
(1) Ryan White, an 18-year-old hemophiliac, was said to have died from
AIDS in April 1990. However, information from the National Hemophilia Foundation
revealed that White had died from unstoppable internal bleeding and had
also been treated for an extended period with the cytotoxic DNA chain terminator
AZT prior to his death (Duesberg and Ellison, 1990). It appears that hemophilia
and AZT (Section 4) would each be sufficient causes of death, and certainly
a combination of both would be more than adequate to explain the death
of Ryan White. Thus there is no convincing evidence that White died from
HIV.
To prove that HIV played a role in White's death, it would
be necessary to compare mortality of matched hemophiliacs with and without
HIV. To prove that AZT contributed to his death, matched HIV-positive hemophiliacs
with and without AZT must be compared. Without such evidence the HIV-death
of White is just a hypothesis. Yet White was generally described as an
innocent victim of HIV (practicing no risk behavior), which is why the
U.S. Senate approved the Ryan White Comprehensive AIDS Resources Act for
over $550 million in aid to hospitals for AIDS emergencies and treatment
of children (Anonymous, 1990).
(2) In 1989 the California tax-reformer Paul Gann was
reported to have died from AIDS at the age of 77 after receiving HIV from
a blood transfusion. However, a close examination of Gann's case reveals
that he had 5-bypass heart surgery for blocked arteries in 1982, when he
may have received the blood transfusion with HIV. In 1983 he needed further
bypass surgery for blocked intestinal arteries. In 1989, at the age of
77, he was hospitalized again for a broken hip. While recovering from the
hip fracture, Gann was immobilized for weeks and developed a pneumonia
from which he died (Folkart, 1989). This is a rather typical death for
a 77-year-old man in poor health.
To determine whether HIV played any role at all in his
death, a controlled study would be necessary showing that the mortality
of HIV-positive 77-year-old bypass patients with broken hips is higher
than that of HIV-negative counterparts. No such study exists.
(3) Kimberly Bergalis, a 22-year-old woman, developed
candidiasis and a transient pneumonia 17 and 24 months, respectively, after
the extraction of two molars (Centers for Disease Control, 1990). After
her dentist had publicly disclosed that "he had AIDS," she was
tested for HIV, although Bergalis was a virgin and did not belong to an
AIDS risk group (Breo and Bergalis, 1990). Since she was HIV-antibody-positive
the CDC concluded that she had contracted AIDS from her dentist (Centers
for Disease Control, 1990), who was a homosexual with Kaposi's sarcoma
(Ou et al., 1992).
Clearly prior to the virus-AIDS hypothesis, the story
of a doctor transmitting his Kaposi's sarcoma in the form of a yeast infection
to his client via a common infectious cause would have hardly made The
New York Times and certainly not the scientific literature (Lambert,
1991). But since the two entirely unrelated diseases are both labeled AIDS
and because of the tremendous popularity of the virus-AIDS hypothesis,
the paradoxical story became a case célèbre for AIDS in the
general population.
Once diagnosed for AIDS Bergalis was treated with the
cytotoxic DNA chain terminator AZT, which is prescribed to inhibit HIV,
until she died in December 1991 with weight loss (15 kg), hair loss, uncontrollable
candidiasis, anemia and muscle atrophy (requiring a wheelchair) (Breo and
Bergalis, 1990; Anonymous, 1991; Lauritsen, 1991)-the symptoms of chronic
AZT toxicity (Section 4). It is not clear whether her AZT therapy started
before or after her pneumonia, since it was only mentioned in an edited
interview conducted for the American Medical Association (Breo and Bergalis,
1990) and in some newspapers (Anonymous, 1991), but not in a single one
of several scientific reports (Centers for Disease Control, 1990; Witte
and Wilcox, 1991; Ou et al., 1992; Palca, 1992a,b) and not in The
New York Times (Lambert, 1991). Since her fatal condition was attributed
to HIV, she received $1 million in compensation from her dentist's, rather
than from her AZT doctor's (Section 4), malpractice insurance (Palca, 1992a).
In view of the celebrity of the case and the fear it inspired
among patients, 1100 further patients of the dentist came forward to be
tested for HIV (Ou et al., 1992; Palca, 1992a). Seven of these,
including Bergalis, tested positive. Four or 5 of these, including Bergalis
and another woman, did not belong to an AIDS risk group, but 2 or 3 did.
At least three of those who did not belong to a risk group received $1
million settlements from the dentist's malpractice insurance (Palca, 1992b).
However, a plausible mechanism of HIV transmission from the dentist to
his 4-5 positive clients without AIDS risks was never identified, and there
is no consensus as to whether the viruses of the three carriers studied
by the CDC and the insurance companies were sufficiently related to claim
a common source (Palca, 1992a,b).
Statistically, it can be shown that the incidence of HIV-infections
among the dentist's clients reflects, almost to the decimal point, the
national incidence of the virus in the U.S. The national incidence of HIV-positives
among all Americans is 0.4% (1 out of 250) (Table 1), the incidence of
HIV-positives among 1100 patients of the Florida dentist was 0.4% (4 to
5 out of 1100) and the incidence among 15,795 patients from 32 HIV-positive
doctors, determined by the CDC for the Bergalis case, was 0.5% (84 out
of 15,795). Thus the incidence of HIV in patients from HIV-positive doctors
reflects the national incidence of HIV. This suggests noniatrogenic and,
most likely, perinatal infection as the source of HIV in these patients,
particularly in the case of the virgin Bergalis (Section 3.5.2). In addition,
it identifies a rich source of insurance income for 0.4% of American patients
of HIV-positive doctors!
To determine whether HIV had contributed to Bergalis'
death, a controlled study would be necessary comparing the mortality of
women with yeast infections, with and without antibodies against HIV, and
with and without AZT therapy. Since such a study is not available, the
assumption that Bergalis died from HIV is pure speculation.
(4) A doctor, presumably infected with HIV from a needle
stick in 1983 (Aoun, 1992), described himself in a letter to the New
England Journal of Medicine as an AIDS patient (Aoun, 1989). He was
diagnosed HIV-positive in 1986 (Aoun, 1992). His only AIDS symptom at that
time was a weight loss of 4.5 kg (Aoun, 1989). In 1991, then 8 years after
the presumed date of the infection, the doctor described his case again
in a speech "From the eye of the storm ..." published in the
Annals of Internal Medicine (Aoun, 1992). The speech did not describe
any current AIDS symptoms. This case has been cited as an example that
HIV is sufficient to cause AIDS (Baltimore and Feinberg, 1989).
However, the weight loss diagnosed in 1986 could have
been the result of the anxiety that HIV infection causes in believers of
the HIV-AIDS hypothesis, rather than the work of HIV. This interpretation
is consistent with the fact that since 1985 at least 800,000 Americans
(1 million minus the 206,000 AIDS cases recorded by the end of 1991; see
Table 1) have not lost weight or developed other AIDS diseases (Duesberg,
1991a). Likewise, 6 million Central Africans (minus the 129,000 with AIDS)
have been healthy HIV-carriers since at least 1985 (Table 1).
Thus, there are no convincing anecdotal cases to prove
that HIV causes AIDS in persons outside the major risk groups. The use
of the above assumptions and anecdotal cases as proof for the virus-AIDS
hypothesis is misleading, although they may provide valuable clues for
future research.
3.6. Consequences of the Virus-AIDS Hypothesis
Despite the lack of proof and numerous discrepancies with
orthodox criteria of infectious disease, the virus-AIDS hypothesis has
remained since 1984 the only basis for all efforts in predicting, preventing,
investigating and even treating AIDS. AIDS prevention is based entirely
on preventing the spread of HIV. This includes promotion of safe sex (Booth,
1988; Institute of Medicine, 1988; Weiss and Jaffe, 1990; Mann and the
Global AIDS Policy Coalition, 1992; Anderson and May, 1992), clean injection
equipment for intravenous drugs (National Commission on AIDS, 1991) and
the exclusion of HIV antibody-positive blood donations from transfusions
(Vermund, 1991; Duesberg and Schwartz, 1992).
The Food and Drug Administration mandated in 1985 that
the 12 million plus annual blood donations in the U.S. (Williams et
al., 1990) are tested for HIV-1, and as of 1992 also for HIV-2, although
there is as yet only one single American AIDS patient infected by HIV-2
(O'Brien et al., 1992). Since 1985 over 2 million tests have also
been performed annually by the U.S. Army (Burke et al., 1990). By
1986 already over 20 million "AIDS tests" were performed in the
U.S. (Institute of Medicine, 1986), at a minimum cost to the client of
$12 to $70 (Irwin Memorial Blood Bank, San Francisco, personal communication)
or $45 (U.S. Immigration Service). The former U.S.S.R. conducted 20.2 million
"AIDS tests" in 1990 and 29.4 million in 1991 to detect 112 and
66 antibody-positives, respectively (Voevodin, 1992).
The detection of antibodies in healthy persons is interpreted
as a 50% certain prognosis for AIDS within 10 years (Section 3.5.12). Therefore,
a positive "AIDS test" is psychologically toxic (Grimshaw, 1987;
Albonico, 1991b) and often the basis for the physiologically toxic antiviral
therapy with AZT (Section 4) (Duesberg, 1992b,d). A negative test for HIV
is a condition for admission to the U.S. Army (Burke et al., 1990),
for admission to health insurance programs, for residence in many countries
and even for travel into the U.S. and China. Currently, over 50 countries
restrict one or more classes of entrants based on positive antibody-tests
for HIV (Duckett and Orkin, 1989). Antibody-positive Americans who had
sex with antibody-negatives have been convicted of "assault with a
deadly weapon" (Duesberg, 1991c; McKee, 1992). In communist Cuba about
600 antibody-positive persons are quarantined in the name of the virus-AIDS
hypothesis (Scheper-Hughes and Herrick, 1992; Treichler, 1992).
Based on the assumption that HIV had either originated
recently or spread recently from isolation to its current levels, at the
same rates as AIDS had spread in the risk groups in the U.S. and Europe,
and on the assumption that AIDS would follow the presumed spread of HIV
with a hiatus of 10 years, epidemiologists have made apocalyptic predictions
about an AIDS epidemic that has raised fears and funding to unprecedented
levels (Heyward and Curran, 1988; Mann et al., 1988; Mann and the
Global AIDS Policy Coalition, 1992; Anderson and May, 1992).
Above all, over 180,000 antibody-positives, with and without
AIDS, are currently treated indefinitely with the cytotoxic DNA chain terminator
AZT in an effort to inhibit HIV (Section 4.4).
Continue
VIRUSMYTH HOMEPAGE