Proc. Natl. Acad. Sci. USA
Vol. 88, pp. 1575-1579, February 1991
AIDS epidemiology: Inconsistencies with human immunodeficiency
virus and with infectious disease
PETER H. DUESBERG
Department of Molecular and Cell Biology, 229 Stanley
Hall University of California, Berkeley, CA 94720
Contributed by Peter H. Duesberg, October 11, 1990
ABSTRACT The newly defined syndrome AIDS includes 25 unrelated parasitic,
neoplastic, and noninfectious indicator diseases. Based on epidemiological
correlations, the syndrome s 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.
Epidemiology is like a bikini:
what is revealed is interesting;
what is concealed is crucial.
AIDS is a newly defined syndrome of 25 old parasitic neoplastic, and
noninfectious diseases, including in the United States 53% pneumonia, 19%
wasting disease 13% 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
drugs 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 (1).
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 immunodeiiciency 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 (3-7,
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 HIV (16-20).
This virus-AlDS 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-AlDS hypothesis
for over 2 billion dollars annually, have failed to contain or cure AIDS
Since 1987 I have challenged the virus-AlDS 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-AlDS 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.
Noncorrelations Between AIDS and HIV
AIDS 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.
AIDS Risks Among HIV-lnfected Americans Differ About 10-Fold Based
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).
Abnormal Health Risks Correlate Directly with the Incidence of AIDS
Since 97% of the American AIDS patients come from behavioral or clinical
health-risk groups and since the incidence of AIDS indicator diseases in
riskmatched, 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
In response 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
Further it 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
(i) 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
AlDS-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.
Surprisingly, 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 Vlll
(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
The low annual incidence of AlDS-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 (16, 59).
(ii) 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.
(iii) 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.
(iv) 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 drugs (95).
Since the 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).
AIDS 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).
A prospective 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 (68, 69).
Among intravenous 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 (16).
Since all 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).
Inconsistencies Between AIDS and Infectious Disease
AIDS Diseases That Are Not Male-Specific Show a 10-Fold Preference
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).
Latent 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
Specific AIDS Diseases Are Not Transmissible Among Different Risk
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.
Unlike 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 currrent definition in 1987
(2), AIDS has spread very slowly, claiming among >100 million sexually
active Americans only 20,000-30,000 cases annually (1).
Epidemiological Evidence That HIV Is Not Pathogenic
HIV 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 l9-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.
HIV 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
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).
Since perinatal 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-AlDS hypothesis. This provides the only
plausible explanation for the random distribution of HIV in even as few
as 0.03% of 17- to l9-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.
Antibody 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.
Because AIDS 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).
A consistent 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, 67-69).
However, not 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).
An Alternative Hypothesis
Numerous correlations have linked American AIDS with the consumption
of drugs. The CDC reports that 30% are intravenous drug users (l) 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-AlDS
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
S-R35-CA39915-06 from the National Cancer Institute.
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