epidemiology: Inconsistencies with human immunodeficiency virus
and with infectious disease
Acad. Sci. USA
Vol. 88, pp.
1575-1579, February 1991
of Molecular and Cell Biology,
229 Stanley Hall
University of California, Berkeley, CA 94720
by Peter H. Duesberg, October 11, 1990
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.
is like a bikini:
is revealed is interesting;
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
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
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-AlDS hypothesis
for over 2 billion dollars annually, have failed to contain or cure
AIDS (32 33).
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.
Between AIDS and HIV
of HIV-infected Persons Differ 10- to 65-Fold Depending on Their
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.
Among HIV-lnfected Americans Differ About 10-Fold Based on Gender.
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 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
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.
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.
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 1989 (1).
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
(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.
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
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).
Diseases Occur Without HIV in All Risk Groups.
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
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).
Between AIDS and Infectious Disease
That Are Not Male-Specific Show a 10-Fold Preference for Males.
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).
of 10 Years Are Not Compatible with Infectious Disease.
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 substances.
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
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
Evidence That HIV Is Not Pathogenic
HIV Is Epidemiologically
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.
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-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.
to HIV Is a Marker for American AIDS Risks.
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 (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.
for Disease Control (1990) HIV/AIDS Surveillance (Centers for Disease
Control, Atlanta), Jan issue.
for Disease Control (1987) J. Am. Med. Assoc. 258, 1143-1154.
J. & Wilson, H. (1986) Death Rush, Poppers and AIDS (Pagan,
H. W. & Dougheny, J. A., eds. (1988) Health Hazards of Nitrite
Inhalants (Natl. Inst. Drug Abuse, Bethesda. MD), NIDA Res. Monogr.
J. (1988) AIDS Inc. (Human Energy, San Bruno, CA).
6. Adams, J.
(1989) AIDS: The HIV Myth (St. Martin's, New York).
P. H. (1990) Res. Immunol. 141, 5-11.
for Disease Comrol (1982) Morbid. Mortal. Wkly. Rep. 31 (43), 577-580.
9. Center for
Disease Control (1982) Morbid. Mortal. Wkly. Rep. 31 (23), 305-307.
J. A., Witkin, S. S. & Punillo, D. T. (1983) Ann. N. Y. Acad.
Sci. 437, 177-183.
F., Chermann, J. C., Rey, F., Nugeyre, M. T., Chamaret, S., Gruest.
J., Dauget, C., Axler-Blin, C., Vezinet-Brun, F., Rouzioux, C.,
Rosenbaum, W. & Montagnier, L. (1983) Science 220, 868-870.
R. C., Sarin, P. S., Gelmann, E. P., Roben-Gurofl, M. & Richardson,
E. (1983) Science 220 865-867.
S. (1987) New Sci. l13, 49-58.
B. J. (1990) Science 248, 1494-1498.
E. (1990) Science 248, 1499-1507.
of Medicine (1986) Confronting AIDS (Natl. Acad. Press, Washington).
R. C. & Montagnier, L. (1988) Sci. Am. 259 (4), 41-48.
of Medicine (1988) Confronting AIDS - Update 1988 (Natl. Acad. Press,
J . W., Jaffe, H . W., Hardy, A. M., Morgan, W. M., Selik, R. M.
& Dondero, T. J. (1988) Science 239, 610-616.
20. Piot P.,
Plummer, F. A., Mhalu, F. S., Lamboray. J.-L., Chin, J. & Mann,
J. M. (1988) Science 239, 573-579.
21. Lemp. G.
F., Payne, S. F., Ruthetford, G. W., Hessol, N. A., Winkelstein.
W., Jr., Wiley, J. A., Moss, A. R., Chaisson, R. E., Chen, R. T
Feigal, D. W., Thomas, P. A. & Werdegar, D. (l990) J. Am. Med
. Assoc . 263, 1497-1501.
R., Woelfel, B. M., Stoneburner, R., Milberg, J., Parker, R. &
Truman, B. (1987) N. Engl. J. Med. 317, 1297-1302.
Z., Bratzke, B., Stadler, R. & Otfanos, C. E. (1990) Med. Klin.
(Munich) 85, 224-225.
S. M ., Belenko, M., Fazzini, E. & Schinella, R. (1987) Chest
25. Gill, P.
S., Akli, B., Coletb, P., Ranck, M., Louriero, C., Bemstein-Singer,
M., Krailo, M. & Levine, A. M. (1989) Am. J. Med. 87, 57-61.
G. U., Stover, D. E., Lee, M., Myskowski, P. L., Caravelli, J. F.
& Zama, M. B. (1986) Am. J. Med. 81, 11-18.
27. Mims, C.
& White, D. O. (1984) Vual Pathogenesis and Immunology (Blackwell,
A. S., ed. (1982) Viral Infection of Humans: Epidemiology and Control
(Plenum, New York).
P. H. (1987) Cancer Res. 47,1199-1220.
J., Haase, A., Levy, J. A., Montagnier, L., Oroszlan, S., Teich
N., Temin, H., Toyoshima, K., Varmus, H., Vogt, P. & Weiss,
R. (1986) Science 232, 697 (lett ).
T. C., Mann, J. M., Curran. J. W. & Piot, P. (1986) Science
234 955-963 .
P. H. & Ellison, B. (1990) Policy Rev. 53, 40-51.
D. (1990) Time 136, 42-43 (July 2 issue).
P. H. (1989) Proc. Natl. Acad. Sci. USA 86, 755-764.
W. (1988) Science 239, 1485-1488.
W., Gallo. R. C. & Temin. H. M. (1988) Science 241, 514. 515,
P. H. (1988) Science 241, 514-516.
A. S. (1989) J. Acquired Immune Defic. Syndr. 2, 107-113.
P. H. (1989) J. Acquired Immune Defic . Syndr. 2, 514-517.
M. (1989) Natunvissenschaften 76, 341-350.
P. H. (1990) Naturwissensrhaften 77, 97-102.
D. & Feinberg, M. B. (1989) N. Engl. J. Med. 321,1673-1675.
P. H. (1990) N. Engl. J. Med. 322, 1466 (lett.).
J. (1990) Br. Med. J. 300, 1596.
R. & Jaffe. H. (1990) Nature (Landon) 345, 659-660.
P. H. (1990) Nature (London) 346, 788 (lett.).
P. H. & Ellison, B. J. (1990) Policy Rev. 54, 70-83.
W. (1989) Science 243, 733.
J. W., Morgan, M. W., Hardy, A. M., Jafle, H. W., Darrow, W. W.
& Dowdle, W. R. (19851 Sciente 229, 1352-1357.
for Disease Control (1990) Morbid. Mortal. Wkly. Rep. 39, 110-119.
R. W. (1990) N. Engl. J. Med. 323, 383-389.
52. World Health
Organization (1990) World Health Organization Yearbook (W.H.O.,
D. S., Brundage, J. F., Goldenbaum, M., Gardner, I., Peterson, M.,
Visintine, R., Redfield, R. & the Walter Reed Retrovirus Research
Group (1990) J. Am. Med. Assoc. 263, 2074-2077.
G. T. (1989) Lancet i, 1325.
55. Jin, Z.,
Cleveland, R. P. & Kaufman, D. B. (1989) J. Allergy Clin. Immunol.
D. L. (1988) Am. J. Haematol. 27, 7-12.
R. (1990) Perspect. Biol. Med. 33, 480-500.
58. Ward, J.
W., Bush, T. J., Perkins, H. A. & The Study Group from the AIDS
Program, Center for Infectious Diseases, Centers for Disease Control
(1989) N. Engl. J. Med. 321, 947-952.
M. A. (1989) in AIDS Pathogenesis and Treatment, ed. Levy, J. A.
(Marcel Dekker. New York), pp. 79-95.
C. A., Tucker, J., Steel, C. M., Tedder, R. S., Cheingsong-Popov,
R., Weiss, R., McClelland, D. B. L., Phillip, I. & Prescon,
R. J. (1985) Lancet ii, 233-236.
C., Gervais, F., Shuster, J., Gold, P., O'Shaughnessy, M. &
Robert-Gurofl, M. (1984) N. Engl. J. Med. 311, 1514-1515.
C. F., Miller, H. G. & Moses, L. E., eds. (1989) AIDS, Sexual
Behavior and Intravenous Drug Use (Natl. Acad. Press, Washington).
63. Bove, J.
R., Rigney, P. R., Kehoe, P. M. & Campbell, J. (1987) Transfusion
(Philadelphia) 27, 201-202.
A. J., Jeflnes, D. J., Harris, J. R. W., Swirsky, D. & Weber,
J. N. (1990) Nature (London) 347, 324 (lett.).
S. A., Schechter, M. T., Weaver, M. S., McLeod, W. A., Boyko, W.
J., Willoughby, B., Douglas, B., Craib, K. J. P. & O'Shaughnessy,
M. (1989) J. Acquired Immune Defic. Syndr. 2, 178-186.
R., Gracie, A., Lowe, G. D. O., Bumett, A., Froebel, K., Follett,
E. & Forbes, C. D. (1986) Br. Med. J. 293, 978-980.
A. E., Saltzman, B. R., Cao, Y., Nestor, M. S., Mirabile, M., Li,
J. J. & Peterman, T. A. (1990) Lancet 335, 168-169.
L. (1990) Discover 11 (8), 28.
V., Peterman, T. A., Berkelman, R. L. & Jafle, H. W. (1990 Lancet
R. L., Des Jarlais, D. C., Benezra, D., Gorelkin, L., Sotheran,
J. L., Friedman, S. R., Schultz, S., Mammor, M., Midvan, D. &
Maslansky, R. (1988) Science 242, 916-919.
M. M., Truman, B. I., Maguire, B., Di Ferdinando, G. T., Jr., Wormser,
G., Broaddus, R. & Morse, D. L. (1990) J. Am. Med. Assoc. 261,
72. Koch, T.,
Jeremy, R., Lewis, E., Kletter, R., Rumsey, C., Weintrub, P., Cowan,
M., Kletter, R. & Esker, S. (1990) CDC AIDS Weekly 9 (July 30
R. M., Bueso-Ramos, C., Donahoe, F., Madden, J. J., Falek. A., Nicholson,
J. K. A. & Bokos, P. (1987) Ann. N. Y. Acad. Sci. 496, 711-721.
R. M., Buehler, J. W., Karon, J. M., Chamberland, M. E. & Berkelman,
R. L. (1990) J. Acquired Immune Defic Syndr. 3, 73-82.
F. N., Penley. K. A., Robinson, M. E. & Smith, J. K. (1980)
Am. J, Epidemiol. 112, 836-843.
H. (1962) Nature (London) 195, 342-345.
H., Fanshier, L., Cornelius, A. & Hughes, W. F. (1962) Virology
J. & Masur, H. (1990) Sci. Am. 263 (2), 50-57.
B. A. (1979) Burrows Textbook of Microbiology (Saunders. Philadelphia).
D. J. & Langmuir, A. D. (1990) J. Am. Med. Assoc. 263, 1522-1525.
K. A. (1990) Sci. News 138, 286.
S. M., Psallidopoulos, M. C., Lane, H. C., Thompson. L., Baseler,
M., Massari. F., Fox, C. H., Salzman, N. P. & Fauci, A. (1989)
Science 245, 305-308.
N. & Hulley, S. (1988) J. Am. ,Med. Assoc. 259, 2428-2432.
T. A., Stonebumer, R. L., Allen, J. R., Jafle, H. W. & Curran,
J. W. (1988) J. Am. Med. Assoc. 259, 55-58.
L. (1970) Oncogenic Viruses (Pergamon, Elmsford, NY).
W. A., ed. (1990) Human Retrovirology: HTLV (Raven, New York).
M., McLane, M. F., Lee, T. H., Falk. L., Howe, C. W. S., Mullins,
J. I., Cabradilla. C. & Francis, D. P. (1983) Science 220, 859-862.
M. S. (1990) J. Am. Med. Assoc. 264, 265-266.
W. W., Echenberg, D. F., Jaffe, H. W., O'Malley, P. M., Byers,R.
H., Getchell, J. P. & Curran, J. W. (1987) Am.J. Public Health
R. E., Bacchetti, P., Osmond, D., Brodie, B., Sande, M. A. &
Moss, A. R. (1989) J. Am. Med. Assoc. 261, 561-565.
S. H. (1989) J. Am. Med. Assoc. 261, 607-609.
W. A. Biggar, R. J., Weiss, S. H. Clark, J. W. & Goeden J. J.
(1985) Cancer Res. Suppl. 45, 4598s-4601s.
of National Drug Control Policy (1988) The National Narcotics Intelligence
Consumers Committee (Exec. Off. Pres., Washington).
Institute on Drug Abuse (1987) Trends in Drug Abuse Related Hospital
Emergency Room Episodes and Medical Examiner Cases for Selected
Drugs: DAWN 1976-1985 (Natl. Inst. Drug Abuse Bethesda MD), NIDA
Ser. H, No. 3.
R., Ledergerber, W., Opravil, M., Siegenthaler, W. & Luthy R.
(1990) Br. Med. J. 301 1362-1365.