Inconsistencies with Human Immunodeficiency Virus
and with Infectious Disease
By Peter H. Duesberg
Natl. Acad. Sci. USA, Vol. 88, pp. 1575-1579, February 1991
Contributed by Peter H. Duesberg, October 11, 1990.
defined syndrome AIDS includes 25 unrelated parasitic, neoplastic,
and noninfectious indicator diseases. Based on epidemiological correlations,
the syndrome is thought to be due to a new, sexually or parenterally
transmitted retrovirus termed human immunodeficiency virus (HIV).
The following epidemiological data conflict with this hypothesis.
(i) Noncorrelations exist between HIV and AIDS; for example, the
AIDS risks of infected subjects vary >10-fold with their gender
or country. Abnormal health risks that are never controlled as independent
AIDS causes by AIDS statistics, such as drug addiction and hemophilia,
correlate directly with an abnormal incidence of AIDS diseases.
Above all, the AIDS diseases occur in all risk groups in the absence
of HIV. (ii) American AIDS is incompatible with infectious disease,
because it is almost exclusively restricted to males (91%), because
if it occurs, then only on average 10 years after transfusion of
HIV, because specific AIDS diseases are not transmissible among
different risk groups, and because unlike a new infectious disease,
AIDS has not spread exponentially since the AIDS test was established
and AIDS received its current definition in 1987. (iii) Epidemiological
evidence indicates that HIV is a long-established, perinatally transmitted
retrovirus. HIV acts as a marker for American AIDS risks, because
it is rare and not transmissible by horizontal contacts other than
frequent transfusions, intravenous drugs, and repeated or promiscuous
sex. It is concluded that American AIDS is not infectious, and suggested
that unidentified, mostly noninfectious pathogens cause AIDS.
is like a bikini: what is revealed is interesting; what is concealed
AIDS is a
newly defined syndrome of 25 old parasitic, neoplastic, and noninfectious
diseases, including in the United States 53% pneumonia, 19% wasting
disease, candidiasis, 11% Kaposi sarcoma, 6% dementia, 3% lymphoma,
and 2% tuberculosis (1). These unrelated diseases are grouped together
because they are all thought to be indicators of an acquired immunodeficiency
(2). In America AIDS is almost completely restricted (91%) to males
(1). About 90% of all AIDS patients are 20- to 40-year-olds, 30%
are intravenous drug users and their children, 60% are male homosexuals
and some heterosexuals who frequently use oral psychoactive drugs
(3-7), and 7% are hemophiliacs and other recipients of transfusions
As of 1982,
the Centers for Disease Control (CDC) considered AIDS infectious
because it appeared to be transmitted among intravenous drug users
and homosexuals by sexual contact or by contaminated blood (8).
Among infectious agents, cytomegalovirus and various bacteria were
proposed as causes of AIDS (6, 8, 10). In 1983 Montagnier and coworkers
(11) suggested lymphadenopathy-associated virus [now termed human
immunodeficiency virus (HIV)] and Gallo et al. (12) human T-cell
leukemia virus (HTLV) as causes of AIDS. However, psychoactive drugs,
like aphrodisiac nitrite inhalants ("poppers"), were also
proposed as causes for Kaposi sarcoma and pneumonia in homosexuals
In April 1984
the Secretary of Health and Human Services announced that HIV was
the cause of AIDS, and an antibody test for HIV, termed the AIDS
test, was registered as a patent by Gallo and collaborators (13-15).
This happened before even one American study on HIV had been published
(13). According to this view HIV is a lymphotropic retrovirus that
is sexually transmitted (16-20). On average 10-11 years after infection
and appearance of neutralizing antibodies, HIV is postulated to
cause immunodeficiency by killing billions of T cells (16-21). Only
then, indicator diseases are said to develop from which patients
die on average within 1 year (21-26). Thus HIV became the first
virus for which a positive antibody test is interpreted as an indicator
for primary diseases that have yet to come. Antibodies against conventional
viruses typically signal protection against disease and those against
some persistent viruses also signal a small risk of secondary disease
upon virus reactivation (27, 28). Although no retrovirus has ever
been shown to be pathogenic in humans (29), HIV is thought to be
50-100% fatal, more than any other human virus (16-21). The novelty
of AIDS is postulated to reflect the novelty of HIV. The large variety
of indicator diseases are postulated to reflect underlying immunodeficiency,
and the almost exclusive concentration of AIDS in 20- to 40-year-olds
(1) is postulated to reflect sexual or parenteral transmission of
hypothesis was accepted by most medical scientists, in particular
virologists, by 1986 (16-18, 30). Accordingly, the virus was named
HIV by an international committee of retrovirologists (30) and became
the only basis for the definition of AIDS: "Regardless of the
presence of other causes of immunodeficiency, in the presence of
laboratory evidence for HIV, any disease listed ... indicates a
diagnosis of AIDS" (2). AIDS is now diagnosed whenever antibody
to HIV is detectable along with any of the 25 indicator diseases,
even if no immunodeficiency or opportunistic infections are detected,
as in cases of Kaposi sarcoma, lymphoma, dementia, and wasting syndrome
(2, 18, 23-26, 31). Moreover, infection in the absence of any clinical
symptoms is now termed, and often treated as, "HIV disease"
(18). However, all efforts directed by the virus-AIDS hypothesis,
for over 2 billion dollars annually, have failed to contain or cure
AIDS (32, 33).
I have challenged the virus-AIDS hypothesis because HIV is latent
and is present in only 1 out of 500 T cells during AIDS, because
retroviruses typically do not kill cells, and because AIDS appears
on average 10 years after the virus has been neutralized by antibodies
(7, 29, 34). In response to this challenge it was agreed that the
hypothesis cannot be defended in terms of orthodox virology, based
on known genetic and biochemical properties of HIV (35-47). However,
it was claimed that epidemiological evidence supports the virus-AIDS
hypothesis (35, 36, 38-41, 44-47) and that Gallo (48), Montagnier
(editorial comment in ref. 7, p. 5), and possibly others (editorial
footnote in ref. 34, p. 755) would prove it. Here this epidemiological
evidence is called into question.
Between AIDS and HIV
Risks of HIV-Infected Persons Differ 10- to 65-Fold Depending on
Their Country. If AIDS is caused by HIV,
the ratio of infected to diseased carriers should be similar in
different countries. However, in the United States about 10% (or
100,000) (1) of 1 million HIV-positives (16, 18, 49, 50) have developed
AIDS since 1985, but in Uganda only 0.8% (or 8000) of 1 million
(51), and in Zaire only 0.15% (4636) (52) of 3 million HIV-positives
(34). Although AIDS surveillance by some African countries has been
questioned, surveillance by Uganda is reported as "highly successful,"
providing "the highest number ... of cases ... in Africa"
(51). Since the HIV epidemics of both the United States and Africa
are said to be new and to have an African origin (17, 20, 36, 45),
but the AIDS risks of infected Americans are 10- to 65-fold higher
than those of Africans, country-specific pathogens are necessary
for AIDS. Moreover, if AIDS equaled opportunistic infections resulting
from immunodeficiency, more, instead of less, AIDS per HIV carrier
would be expected in Africa than in the United States.
Risks Among HIV-Infected Americans Differ About 10-Fold Based on
Gender. Since 1985 the U.S. Army has tested
1.15 x 106 male and female 17- to 19-year-old recruits for antibodies
to HIV. Every year 0.03% of the males and females in this age group
were found to be HIV-positive (53). Although HIV has been distributed
equally between the sexes among 17- to 24-year-old Americans for
the last 5 years, about 10 times more AIDS cases have occurred in
males (1, 53). Ninety-five percent of these were either intravenous
drug users or homosexuals (1, 53).
Health Risks Correlate Directly with the Incidence of AIDS Diseases.
Since 97% of the American AIDS patients come from behavioral or
clinical health-risk groups and since the incidence of AIDS indicator
diseases in risk-matched, HIV-free control groups is never reported
(1), it may be argued that pathogens associated with abnormal lifestyles
are causing AIDS (3-7, 32, 34, 54)-particularly because the diseases
are risk-specific (see below).
to this, it has been pointed out that AIDS occurs outside the major
risk groups in Americans and Africans. However, to date only 3900,
or about 3%, of all American AIDS cases have come from groups without
health risk (1). These represent 25 conventional diseases that occurred
in a country of 250 million inhabitants over the last 9 years (1).
To determine whether these diseases are due to HIV, their incidence
must be compared with that in the normal, HIV-free population. However,
this has not been done, because these diseases are only reportable
and recorded by the CDC as AIDS if HIV is present (1). Thus there
is no controlled epidemiological evidence that HIV is pathogenic
in the normal United States population. The same is true for Africa.
The cumulative incidence of AIDS from 1986 to 1989 in Uganda was
only 8000 (0.8%) out of 1 million HIV-positives (51), or about 0.2%
annually. (Most AIDS statistics are cumulative and thus always increasing.)
Since >90% of these cases are common African diseases like slim
disease, fever, diarrhea, and tuberculosis (34, 51) and their incidence
in HIV-free controls is not reported, it is uncertain whether HIV
is pathogenic in Africa.
has been argued based on anecdotal cases that AIDS did not exist
prior to HIV in clinical health-risk groups such as (i) hemophiliacs,
(ii) other recipients of transfusions, (iii) children
of drug-addicted mothers, and (iv) drug addicts (1, 18, 35,
36, 38, 44, 45, 47). However, competing causes for AIDS diseases
have not been excluded in any of these cases.
Transfusions of blood and factor VIII and
intrinsic deficiencies associated with hemophilia, acting over the
long time periods said to be latent periods of HIV, have all been
identified as pathogenic factors for AIDS-like diseases in hemophiliacs
(55-61). To determine whether HIV or clinical deficiencies and their
treatment cause AIDS in hemophiliacs, either controlled epidemiological
studies comparing matched hemophiliacs, with and without HIV, or
epidemiological evidence that the mortality of hemophiliacs is increased
by HIV would be necessary.
in view of the many claims that HIV causes AIDS in hemophiliacs,
there is not one controlled study that has found HIV to be a health
risk. There is also no report from any country that the mortality
rate of hemophiliacs has increased due to the infection of hemophiliacs
with HIV (59). In fact, it appears to be lower than ever (56, 59).
About 75% of the 20,000 severe hemophiliacs in the United States
are reported to be HIV-positive at least since 1980 to 1982, owing
to the administration of blood or factor VIII (16, 18, 59, 61, 62).
Because the administration of plasma fractions prepared from large
numbers of donors started in 1965, many hemophiliacs may have been
HIV-positive for >10 years now (56, 59). Since 50-100% of HIV-infected
persons are postulated to develop AIDS after an average latent period
of 10 years (18, 21, 34), at least half of the 15,000 HIV-positive
hemophiliacs should have died from AIDS. Yet <2% of the 15,000
HIV-positive hemophiliacs in the United States have died with a
diagnosis of AIDS in 1988 and in 1989 (1).
The low annual
incidence of AIDS-like diseases among hemophiliacs in the United
States is likely to reflect hemophilia-related morbidity and mortality
under a new name. Indeed, among American hemophiliacs infected for
an average of at least 10 years with HIV, elapsed time as a hemophiliac
stands out as the critical determinant for AIDS diseases. The median
age of hemophiliac AIDS patients is 34 years, or 14 years higher
(59) than that of their asymptomatic peers, which is 20-22 years
The thesis that HIV transfusions cause AIDS in other patients is
also entirely uncontrolled (36). Indeed, a controlled study might
be difficult because 50% of American patients (other than hemophiliacs)
die within 1 year (58) and 60% within 3 years (63) after a transfusion-long
before the average 10 years that HIV is said to require for pathogenicity
have elapsed. The pathogenic conditions that necessitated the transfusions
are obviously deadlier than the hypothetical pathogen HIV.
About 95% of the children with AIDS in the United States were subject
to pathogenic conditions other than the putative pathogen HIV, either
drug addiction of the mother or deficiencies of their own that required
blood transfusions (1). The remainder probably reflects normal morbidity
of infants born to healthy mothers who are perinatally (see below)
or iatrogenically infected by HIV.
A rare controlled study showed that among 297 asymptomatic, HIV-positive
intravenous drug users the AIDS risk over 16 months was 3 times
higher in those who persisted than in those who stopped injecting
incidence of AIDS diseases in non-risk groups appears normal, and
since the abnormal incidence of AIDS diseases in risk groups correlates
directly with their abnormal health risks, there is no epidemiological
evidence that HIV is pathogenic. Although longitudinal studies of
selected risk groups claim, some even without published data or
references (64), that HIV-positives have more AIDS, none of these
studies have controlled the negatives for all health risks and selection
biases (18, 47, 62, 65).
Indicator Diseases Occur Without HIV in All Risk Groups. Tsoukas
et al. (61) observed severe immunodeficiency in 6 of 14 HIV-free
and 9 of 15 HIV-positive hemophiliacs. Ludlam et al. (60) described
a group of 15 hemophiliacs who had acquired immunodeficiency before
they were infected by HIV. Others observed HIV in only 7 of 19 (55)
or 10 of 19 (66) hemophiliacs who had very similar immunodeficiencies.
However, direct correlations were observed between the degree of
immunodeficiency and the amount of clotting factor consumed, in
both HIV-negatives and HIV-positives (60, 66).
study from Canada identified immunodeficiency in 33 of 161 HIV-free
homosexual men. Nine of these became subsequently infected by HIV
(65). Further, a recent study identified initially 6 and now 12
HIV-free Kaposi sarcoma cases in male American homosexuals, some
of which occurred in the absence of immunodeficiency (67, 68). Others
recorded the occurrence of Kaposi sarcoma in AIDS risk groups long
before AIDS (57). And recently, CDC workers have postulated a Kaposi
agent other than HIV, because of the almost exclusive occurrence
of Kaposi sarcoma in homosexuals among AIDS risk groups (69). Moreover,
there is no trace of HIV even in the Kaposi sarcomas of patients
in which antibody to HIV is confirmed (34). Thus HIV is necessary
neither for immunodeficiency nor for Kaposi sarcoma in homosexuals,
although their association is perceived as the hallmark of AIDS
drug users in New York representing a "spectrum of HIV-related
diseases," HIV was not observed in 26 of 50 pneumonia deaths,
15 of 22 endocarditis deaths, and 5 of 16 tuberculosis deaths (70).
Likewise, no HIV was observed in 24 of 54 prisoners with tuberculosis
in New York State, of whom 47 were street-drug users (71). Similar
neurological deficiencies were recently observed in 12 HIV-infected
and 16 uninfected infants from drug-addicted mothers (72). In a
group of 21 heroin addicts, of whom only 2 were infected by HIV,
the ratio of helper to suppressor T cells was found to decline within
13 years from a normal of 2 to <1 (73), which is typical of AIDS
AIDS indicator diseases occur in AIDS risk groups in the absence
of HIV, HIV is not a necessary cause for these diseases (except
for their diagnosis as AIDS). Current AIDS statistics probably include
additional HIV-free cases because HIV was confirmed up to 1989 in
only about 73% of all American AIDS cases, and in only 39% of the
AIDS cases from New York and 61% from California (74). Moreover,
statistics are biased in favor of HIV-positive cases because AIDS
is reportable whereas most HIV-free indicator diseases are not (57).
and Infectious Disease
Diseases That Are Not Male-Specific Show a 10-Fold Preference for
Males. The distribution of conventional
sexually transmitted diseases is almost even between the sexes (75).
By contrast American AIDS occurs almost exclusively (91%) in males,
although none of the 25 AIDS diseases is male-specific (1). However,
African AIDS appears largely compatible with infectious diseases
that strike without preference for sex, risk, and age groups (17,
18, 51) and that hardly overlap with American AIDS (see below).
Periods of 10 Years Are Not Compatible with Infectious Disease.
Viruses, retroviruses, and HIV are immunogenic and biochemically
most active within weeks or months after infection (27, 28, 34,
76, 77). There is no precedent for an infectious agent that causes
primary diseases on average only years after it is neutralized by
antibodies (27, 28, 38, 39). Yet HIV is claimed to cause AIDS on
average 10 years after transfusion in adults and only after 2 years
in children (18, 34, 62). The diversity of these latent periods
is inconsistent with one infectious agent, and their magnitude is
characteristic for diseases caused by chronic exposure to toxic
AIDS Diseases Are Not Transmissible Among Different Risk Groups.
If AIDS diseases are caused directly by HIV or are due to HIV-induced
immunodeficiencies and available parasites, all infected subjects
should have the same risk of developing those AIDS diseases that
are not associated with group- or region-specific parasites. However,
53% of American AIDS patients have Pneumocystis pneumonia
and 13% have candidiasis (1), whereas 90% of the African AIDS patients
have slim disease, fever, diarrhea, and tuberculosis but not pneumonia
and candidiasis (34, 51), although Pneumocystis carinii and
candida are ubiquitous in humans, including Africans (34, 78, 79).
In addition, the AIDS diseases of American children are different
from those of adults-namely, 50% pneumonia, 16% wasting disease,
12% dementia, and 20% bacterial infections, which are exclusively
diagnosed in children (1). Further, in the United States, Kaposi
sarcoma occurs 20 times more often in homosexuals than in hemophiliacs
and intravenous drug users (69), often in the absence of immunodeficiency
(23-26, 67). Thus, specific AIDS diseases are not transmissible
among different risk groups, suggesting that distinct, nontransmissible
pathogens must be primary causes.
New Infectious Diseases, AIDS Does Not Spread Exponentially.
AIDS is said to be a new sexually transmitted disease (17, 18, 36,
45). The epidemiological hallmark of a new transmissible disease
is that it spreads exponentially until it has saturated a susceptible
pool of the population, a process described by Farr's law (80).
Therefore AIDS would be expected to increase in the sexually active
population at an exponential rate, provided there is at least some
promiscuity. Yet since the AIDS test has been established and AIDS
was given its current definition in 1987 (2), AIDS has spread very
slowly, claiming among >100 million sexually active Americans
only 20,000-30,000 cases annually (1).
That HIV Is Not Pathogenic
Is Epidemiologically Not New. Since 1985,
when HIV infection became detectable with the "AIDS test,"
the number of infected Americans has remained constant at about
1 million, or 0.4% of the population (16, 18, 49, 50). Likewise,
the percentage of HIV-positive male and female U.S. Army recruits
has remained constant at 0.03% for 5 years, although >70% of
17- to 19-year-olds are sexually active and about 50% are promiscuous
(53, 62). The strikingly constant incidence of HIV indicates that
it is epidemiologically not new in the United States and thus not
a plausible cause for the new epidemic AIDS.
Depends on Perinatal Transmission for Survival and Is Thus Not Likely
to Be Fatally Pathogenic. Due to the absence
of HIV in the semen of 24 of 25 HIV-positive men, with one provirus
detected per 106 cells (81), and due to the chronic latency and
presence of HIV provirus in only 1 of 500 susceptible lymphocytes
(34, 82), HIV depends on an average of about 500 sexual contacts
to be transmitted (83, 84). Perhaps even more contacts are necessary,
because only about 15% of the wives of hemophiliacs are HIV-positive
(20), although about 75% of severe hemophiliacs in the United States
have been positive for 8-10 years. Therefore it is unlikely that
HIV could survive by sexual transmission. Further, it is unlikely
to be preferentially transmitted by homosexual males, since about
10% of both males and females frequently practice anal intercourse
Based on animal
and human models, retroviruses depend almost exclusively on perinatal
transmission for survival. They are very difficult to transmit horizontally
by immune competent animals and humans, because they are chronically
suppressed, first by maternal antibody and then by the baby's own
(76, 77), and possibly also by cellular suppressors (34). Even retroviruses
with sarcomagenic or leukemogenic oncogenes have never spread horizontally
in breeding colonies (29, 85). Therefore, specific strains of mice,
chickens, or humans from geographically distinct regions are often
marked for generations by distinct strains of perinatally transmitted,
latent retroviruses (85, 86). For example, HTLV is endemic in certain
islands of Japan and marks specific ethnic groups among mixed populations
in the Caribbean (86). Wild animals (29, 85, 86) or humans (42,
43, 86) with an acute retrovirus infection are virtually never observed.
Acute retrovirus infections result from experimental infection or
horizontal infections among mass-bred animals, typically prior to
immune competence with virus strains not covered by maternal antibodies
(76, 77, 85).
transmission of HIV is at least 50% efficient (18, 20, 34, 62),
and sexual transmission is <0.2% efficient, it appears that HIV,
like other retroviruses, depends on perinatal transmission for survival.
Therefore, it cannot be fatally pathogenic in most infections within
2-10 years, as postulated by the virus-AIDS hypothesis. This provides
the only plausible explanation for the random distribution of HIV
in even as few as 0.03% of 17- to 19-year-old healthy Americans
(53) and in about 10% of Africans of all ages (31, 34, 49, 51).
This explains why no more than 2456 AIDS cases have been recorded
among about 75 million Americans under the age of 19 in the last
9 years (1), although at least 0.03%, or 25,000, can be estimated
to be perinatally infected (53). It appears that >90% of perinatally
infected Americans are asymptomatic for at least 19 years.
to HIV Is a Marker for American AIDS Risks.
American AIDS risk groups and patients are marked by antibodies
not only to HIV but also to many other viruses and microbes, such
as cytomegalovirus, hepatitis virus, herpes simplex virus, HTLV,
parvovirus, Epstein-Barr virus, genital papilloma virus, Treponema,
Neisseria, amoebae, candida, and mycoplasma (1, 5, 6, 10,
12, 54, 57, 67, 75, 78, 87, 88). Among these, antibodies to HIV
and HTLV are perhaps the most specific markers because their prevalence
in AIDS patients is 73% (74) and 25% (87), respectively, but only
0.03% (53) and 0.025% (86) in the general United States population.
patients carry antibodies to many more viruses and microbes, in
particular, rare ones such as HTLV, than the general population,
it is arbitrary to delineate HIV as an etiologic agent of AIDS by
the presence or titer of antibody alone. In addition, this hypothesis
is inconsistent with the typical sequence of events in which antibodies
follow rather than precede viral pathogenicity (27, 38, 39), incompatible
with HIV-free indicator diseases, and implausible in the absence
of HIV activity (34, 82). As tens of thousands of positive tests
for antibody and hundreds of negative tests for free virus have
shown (34), HIV remains typically dormant in "T-cell reservoirs"
even during AIDS (82). The simultaneous occurrence of HIV viremia
and antiviral antibodies was reported in some AIDS patients in 1989,
but this observation has not been replicated by others (42, 43).
More and more of the AIDS-associated parasites are now named as
AIDS cofactors of HIV, most recently HTLV and mycoplasma (45, 88).
alternative explanation for the high prevalence of antibody to HIV
(and other microbes) in AIDS risk groups and AIDS patients proposes
that HIV is a marker for American AIDS risks (34). The probability
of becoming HIV antibody-positive correlates directly with the frequency
of injecting unsterile drugs (34, 62, 70, 89-91), with the frequency
of transfusions (59-61), and with promiscuity (62, 65, 89, 92).
However, in America, only promiscuity aided by aphrodisiac and psychoactive
drugs, practiced mostly by 20 to 40-year-old male homosexuals and
some heterosexuals, seems to correlate with AIDS diseases (3-7,
62, 67). HIV would thus be a marker for these drugs and also for
the frequent infections by conventional venereal diseases such as
gonorrhea and syphilis (5, 6) which are not part of the AIDS definition
(2), and for the corresponding therapeutic and prophylactic medications.
In fact, HIV was named as a marker for homosexual promiscuity (92)
and recently for an "unknown sexually transmitted agent"
that is presumed to cause Kaposi sarcoma in male homosexuals (45,
all HIV antibody-positives above those expected from perinatal transmission
(e.g., 0.03% in the United States) must reflect promiscuity and
parenteral infection. Instead, perinatally infected persons may
develop antibodies only with age, as latent proviruses become activated
by transient immunosuppression or other stimuli. This predicts that
the percentage of antibody-positives among provirus-positives increases
with age. The lower incidence of antibody to HIV in 1- to 14-year-old
Zairen children (1-2%) compared with adults (4-10%) (31) is a case
in point. The incidence of antibody to HTLV also increases with
age in countries where HTLV is endemic, although HTLV is just as
difficult to transmit sexually as HIV (86).
have linked American AIDS with the consumption of drugs. The CDC
reports that 30% are intravenous drug users (1) but does not report
that another 50-60% have used oral psychoactive drugs (3-7) and
medical drugs, above all the DNA-chain terminator 3'-azido-3'deoxythymidine
(AZT) (7, 34). AZT is currently prescribed to 125,000 sick and healthy
HIV-positive persons worldwide, including about 80,000 Americans,
based on annual sales of $284 million and a wholesale price of $2200
for a year of AZT at 500 mg/day (Burroughs Wellcome Annual Report
1990 and Office of Public Affairs, personal communication). Therefore
it is proposed that either drug consumption (frequently associated
with malnutrition) by recently established behavioral groups or
conventional clinical deficiencies and their treatments are necessary
and sufficient to cause indicator diseases of AIDS. This hypothesis
resolves the many paradoxes of the virus-AIDS hypothesis. (i)
American AIDS is new because of the recent dramatic increase in
the consumption of psychoactive and medical drugs (4, 7, 70, 91).
For instance, cocaine-related hospital emergencies increased 5-fold
from 1984 to 1988 (93). (ii) American AIDS is prevalent in
20- to 40-year-old men, although not one AIDS disease is male-specific,
and this age group is the least likely to develop any diseases.
The reason is that men of this age group consume 80% of hard psychoactive
drugs (94). (iii) The vastly different AIDS diseases are
caused by different pathogens, pathogenic conditions, and their
treatments. This also explains "AIDS diseases" that do
not depend on immunodeficiency and occur without it, including Kaposi
sarcoma, lymphoma, dementia, and wasting disease (1, 2, 23-26, 34,
67). (iv) African AIDS would be old diseases caused by malnutrition
and parasitic infections under a new name, the reason why it is
equally distributed between the sexes (16, 51). (v) The long
and unpredictable latent periods between infection by HIV and specific
AIDS diseases are the product of functionally unrelated events:
the pathogenic events necessary to reach an individual's threshold
for AIDS diseases, and infection by the marker HIV.
I thank Walter
Gilbert, Howard Green, Barbara McClintock, Sheldon Penman, Robert
Root-Bernstein, and Harry Rubin for critical and constructive reviews
of the manuscript and Robert Da Prato, Bryan Ellison, Harry Haverkos,
Robert Hoffman, Marion Koerper, Anthony Liversidge, Charles Ortleb,
Claus Pierach, Russell Schoch, John Scythes, Joan Shenton, Joseph
Sonnabend, Charles Thomas, and Michael Verney-Elliott for comments
and essential information. I am supported by Outstanding Investigator
Grant 5-R35-CA39915-06 from the National Cancer Institute.
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