VIRUSMYTH HOMEPAGE
Int Arch Allergy Immunol
1994; 103: 118-126
Infectious AIDS -
Stretching the Germ Theory Beyond Its Limits
Peter Duesberg
Department of Molecular and Cell Biology, University of
California, Berkeley, Calif., USA
Abstract
The hypothesis that human immunodeficiency virus (HIV)
causes AIDS was advanced in 1984, based only on circumstantial evidence.
To this date, the primary evidence are correlations between the presence
of antibody against HIV and AIDS. But these correlations are biased by
proponents of the HIV hypothesis in favour of HIV. They ignore HIV-free
AIDS and they base correlations on selected studies because there are no
national HIV-AIDS statistics. The HIV-AIDS hypothesis has made the following
predictions: (1) AIDS would 'explode' from the original risk groups into
the general population via sexual transmission of HIV. (2) Health care
workers would contract AIDS from their patients, scientists from propagating
HIV, and prostitutes from their clients. (3) The 150 chimpanzees that have
been experimentally inoculated with HIV, and the 15,000 American hemophiliacs
who have been iatrogenically inoculated before 1984, would develop AIDS.
(4) immunity and vaccines would protect against AIDS. (5) HIV would cause
AIDS by killing T-cells. (6) AIDS would occur only in people infected by
HIV. But none of these predictions proved to be correct. Recent studies
show that HIV is a passenger virus instead of the cause of AIDS: (1) AIDS
occurs at unpredictable intervals after infection; (2) HIV may be active,
passive, or totally absent from otherwise identical AIDS cases. Indeed,
AIDS does not meet one of the classical criteria of infectious disease:
(1) Equal distribution between the sexes; (2) disease following infection
within days or weeks, the time microbes take to become either immunogenic
or pathogenic or both; (3) the presence of a common active microbe. Therefore
it is proposed that American and European AIDS is caused by the long-term
consumption of recreational drugs and the anti-HIV drug AZT. This hypothesis
is testable and provides a rational basis for AIDS control.
Introduction
In April 1984, the retrovirologist Robert Gallo from the
National Institutes of Health in Bethesda and the American Secretary of
Health and Human Services announced, at an international press conference
in Washington, that the acquired immunodeficiency syndrome (AIDS) was caused
by a retrovirus, now termed human immunodeficiency virus (HIV) [1]. The
announcement was made before even one American study on HIV had appeared
in the scientific literature. Gallo and his collaborators cited antibodies
against the virus in "about 85% of patients with AIDS" as the
only evidence for their hypothesis [1]. Although AIDS occurred despite
antiviral antibodies, the researchers expressed "hope that a vaccine
would be ... ready in about two years" [1]. In the scientific papers
that followed the next month, HIV was said to cause AIDS by depleting T-cells
[2, 3]. The hypothesis proposed that HIV would cause all of the 30 heterogenous
AIDS diseases [4], including those that are not consequences of immunodeficiency,
such as cancer, weight loss and dementia (Table 1) [5].
Infectious AIDS: From Hypothesis to Dogma
In 1986, the American Academy of Sciences and the Institute
of Medicine assembled a blue ribbon committee of medical scientists to
confront the growing AIDS epidemic. The committee, chaired by David Baltimore,
concluded that the isolation of HIV by Montagnier et al. [6] and Gallo
et al. [2] "led to its definitive identification as the cause of AIDS"
[7]. Without mention of dissent [8, 9], a derivative committee declared
in 1988: "The committee believes that the evidence that HIV causes
AIDS is scientifically conclusive" [boldface in original] and proposed
to rename AIDS "HIV disease" [10]. The committees had sealed
the hypothesis into national dogma. However, the committee's conclusion
was based only on circumstantial evidence including five questionable assumptions:
(1) The primary assumption was that, " ... close
to 100 percent of the affected individuals can be found to harbor the virus"
and "The probability that this distribution might have occurred by
chance is less than one in a million" [10].
However, since no national HIV-AIDS statistics exist [11],
the committee had to rely on selected individual studies and unpublished
observations. For example, the committee selected a Science News
& Comment article entitled "A rebel without a cause of AIDS"
[9], an unpublished speech of the epidemiologist Winkelstein and the papers
of Montagnier and Gallo as the source for the "close to 100%"
correlation [10]. But the original paper by Montagnier et al. [6] only
reported a single isolation of HIV from the lymph node of a person who
did not have AIDS, and Gallo's isolate proved to be Montagnier's virus
[12]. And the authenticity of the HIV-AIDS correlations from Gallo's group
has since been questioned on several accounts [12].
(2) The committee also believed that "The virus is
not found in persons who are not at risk for infection"-assuming that
infection was restricted to AIDS risk groups, e.g. male homosexuals, intravenous
drug users and recipients of transfusions [7]. However, HIV has since been
found in 1 million healthy Americans, 0.5 million healthy Europeans, 1.5
million healthy South Americans, 1.5 million healthy Asians and 8 million
healthy Africans [13].
(3) The committee further believed that " ... AIDS
is unknown in populations that are free of HIV antibodies," i.e. that
there is no HIV-free AIDS [10]. However, many HIV-free AIDS cases had already
been reported by 1986 and 1988, when the committees confronted AIDS [11].
(4) The committee accepted without questioning the unique
practice of the HIV researchers to present antibodies against HIV as pathogenic
powers of HIV. Proponents of the HIV-AIDS hypothesis interpret these antibodies
as indicators of current and future HIV disease. However, antibodies against
all other microbes are signs of rejection of the microbe and protection
against future disease.
(5) The committee accepted uncontrolled statistics as
evidence for AIDS from transfusion of HIV [10]. For example, AIDS researchers
blame HIV for pneumonia and other opportunistic infections that occur in
about 2% of HIV-positive hemophiliacs per year [5, 10]. However, controlled
studies have since shown that the incidence of immunodeficiency in matched
groups of HIV-positive and negative hemophiliacs is the same [5].
Thus the committee had adopted the virus-AIDS hypothesis
on the basis of questionable assumptions, primarily the assumption that
all AIDS correlates with HIV.
How Good is the Correlation between HIV and AIDS?
The natural coincidence between HIV and AIDS can only
be determined by first diagnosing AIDS clinically and then testing for
HIV. However, since the HIV-AIDS hypothesis has been accepted in 1986,
the definition of AIDS by clinical criteria alone has been abandoned in
America and Europe in favor of an HIV-based definition [10]. Moreover all
HIV-AIDS correlations are based on selected individual studies, because
to date no national and international AIDS statistics reporting HIV tests
exist [11]. As a result, proponents of the HIV-AIDS hypothesis bias HIV-AIDS
correlations in several ways:
(1) They cite HIV-AIDS correlations from selected, individual
studies which are frequently based on non-standardized and unconfirmed
HIV antibody tests [11, 14].
(2) They present antibodies against HIV, instead of activities
and titers of HIV, as a rational cause of AIDS.
(3) They exclude clinically diagnosed, HIV-free AIDS defining
diseases from their statistics, e.g., the 4,621 cases cited below [11],
because the HIV-AIDS hypothesis postulates that HIV causes AIDS. Therefore
HIV-free AIDS cases are either diagnosed by their old names, e.g. Kaposi
sarcoma, pneumonia, etc., or renamed "idiopathic CD4 lymphocytopenia,"
or ICL [15].
But the effort to set apart HIV-positive from HIV-negative
AIDS cases is not based on any clinical or convincing epidemiological criteria
[11, 16]. According to an editorial by Fauci: "Given the heterogeneity
of the [ICL] syndrome, it is highly likely that there is no common cause"
[15]. Yet at the same time the proponents of the HIV hypothesis, including
Fauci, insist that HIV must be the common cause of the 30 heterogenous
AIDS diseases.
The editorial also argues that the HIV-free AIDS or ICL
cases are unlike the HIV-positive cases because "Approximately one
third of the patients are women, as compared with 11% among those with
HIV ..." (in America). But proponents of the HIV-AIDS hypothesis,
including Fauci, insist that HIV also causes African AIDS, despite about
50% of the African patients being women [10].
Indeed, other retroviruses have been proposed as causes
of HIV-free AIDS, particularly at the VIII International AIDS Conference
in 1992 in Amsterdam [17, 18], because these cases were clinically indistinguishable
from HIV-positive AIDS. Following the HIV precedent, these retroviruses
were considered "new" AIDS causes simply because of their presence
in these cases.
It follows that the primary argument for the HIV-AIDS
hypothesis, the HIV-AIDS correlation, is a circular argument. It is in
reality an artefact of the HIV-based AIDS definition, which is a restatement
of the HIV hypothesis.
To date the virus-AIDS hypothesis has been a complete
failure in terms of public health benefits: no vaccine has been developed,
AIDS continues to spread despite efforts to stop the spread of HIV, and
nobody has ever been cured from AIDS. However the acid test of a hypothesis
is not to produce useful results, but to make accurate predictions.
Predictions of the HIV-AIDS Hypothesis
The HIV-AIDS hypothesis makes the following testable predictions,
none of which proved to be correct [5, 19]:
The failure to make valid predictions is the hallmark
of a flawed hypothesis. It raises two fundamental questions: (1) Is HIV
a passenger virus rather than the cause of AIDS? (2) Is AIDS infectious?
Is HIV a Passenger Virus Rather than the Cause of AIDS?
The correlation argument assumes that the presence of
a virus in a disease is sufficient proof of causation. But the presence
of a virus in a disease is by no means proof of causation. Particularly
since HIV does not cause AIDS if inoculated into chimpanzees or if iatrogenically
introduced into hemophiliacs, it could be just a harmless passenger virus.
Passenger viruses are "widely distributed ... in mammals, causing
no obvious disease" [37]. In the absence of functional proof, the
distinction between a causative and a passenger virus can be made by the
temporal relations between infection and disease, by the consistency of
its presence, and by the biochemical activity of the virus during the course
of the disease as follows:
HIV meets all criteria of a harmless passenger virus in
AIDS:
(1) HIV infection precedes AIDS by unpredictable intervals
that average about 10 years. This time is referred to as latent period
of HIV by proponents of the HIV-AIDS hypothesis, although HIV typically
remains latent even when AIDS occurs [5]. Several groups report that HIV
may reach high titers during the primary infection [40-42]. According to
Piatak et al., these titers range from 10 to 104 infectious units per milliliter
[42]. Despite these relatively high HIV titers in some people, and despite
the absence of antiviral immunity in all, there is no AIDS during the primary
infection [40-42]. In addition, the T-cell counts are normal [42, 43].
When the primary infection is terminated by antiviral
immunity, no infectious HIV remains, the T-cell are normal and there is
also no AIDS [42]. In the face of antiviral immunity, the virus persists
as a latent provirus in healthy hosts (fig. 2).
(2) HIV also meets one of the most telling criteria of
a passenger virus in relation to a disease: HIV-free AIDS (see above, fig.
2). At least 4,621 AIDS cases have been documented in the literature since
1984 in whom there is no HIV [11]. About a third of these, 1,691, were
recorded in the US, 475 in Europe and 2,555 in Africa [11]. Since Africa
uses the clinical, rather than the HIV-based AIDS definition, most of these
cases were observed in Africa. The US and Europe bias AIDS statistics against
HIV-free AIDS, because they use the HIV-based AIDS definition (see above).
(3) Several groups have documented that HIV may be either
active or passive once immunodeficiency is acquired and AIDS appears [42,
44, 45]: Piatak et al. observe either no infectious HIV, e.g. 0
infectious units per milliliter plasma in 5 out of 27 HIV-antibody-positive
AIDS cases, or fewer than 25 infectious HIVs per milliliter in 6 out of
27 cases, or 102-105 in 16 out of 27 otherwise identical AIDS cases [42,
43]. Others have reported similar noncorrelations between virus titers
and AIDS [44-46].
Likewise, there is no correlation between AIDS and the
number of HIV-infected cells. Simmonds et al. report that there
are from 1 to 700 to 1 in 83,000 HIV-infected leukocytes in healthy HIV
carriers and from 1 in 900 to 1 in 30,000 in AIDS patients [47]. Bagasra
et al. report that there are from 1 in 30 to 1 in 1,000 infected
leukocytes in healthy carriers and from 1 in 10 to 1 in 1,000 in patients
with fatal AIDS. [48] Thus there are healthy persons with 43 times (30,000:700)
and 33 times (1,000:30) more HIV-infected cells than in AIDS patients.
It follows that there is neither a correlation between
HIV titers, nor between the number of HIV-infected cells and AIDS-the hallmark
of a passenger virus. (4) Even as an active passenger,
HIV does not aggravate the course of AIDS by any HIV-specific symptom,
as some other passenger viruses or microbes do. For example, cytomegalovirus,
herpes virus, Pneumocystis carinii and Candida each cause
corresponding opportunistic infections if they are activated by acquired
immunodeficiency (table 1). By contrast, the AIDS cases with active or
passive HIV appear to be identical, according to several groups of investigators
[42, 44, 45, 48]. Indeed no HIV-specific AIDS symptom has ever been described,
as all AIDS-defining diseases have been known previously [10, 49] and occur
in HIV-free AIDS patients [11]. Thus HIV is not even a cofactor for AIDS.
It follows that HIV is a harmless passenger virus that
does neither cause AIDS nor even contribute an HIV-specific symptom to
AIDS. Since AIDS is not caused by HIV nor consistently associated with
another active infectious agent [5], it may not be infectious.
AIDS Fails All Criteria of Infectious Disease
Proponents of the HIV-AIDS hypothesis acknowledge that
"AIDS does not have the characteristics of an ordinary infectious
disease. This view is incontrovertible" [50]. More specifically, the
epidemiologists Eggers and Weyer [51] state that "the spread of AIDS
does not behave like the spread of a disease that is caused by a single
sexually transmitted agent." To reconcile AIDS with infectious disease
they "simulated a cofactor [that] cannot be identified with any known
infectious agent" [52]. The epidemiologists Anderson and May [53]
had to invent "assortative scenarios" for different AIDS risk
groups to match AIDS with infectious disease. Indeed, AIDS does not meet
even one of the common criteria of all known infectious diseases:
Thus AIDS does not fit even one of the classical criteria
of an infectious disease.
The Drug-AIDS Hypothesis
The paradoxa of the virus-AIDS hypothesis are all readily
resolved by postulating noninfectious AIDS. In view of this I have proposed
that AIDS in America and Europe is caused by the long-term consumption
of recreational drugs and AZT [5, 59]. African AIDS has been proposed to
be an unrelated epidemic caused by malnutrition, parasitic infections and
poor sanitation [5].
Indeed, AIDS in America and Europe fits all classical criteria of a
drug-induced disease syndrome. AIDS correlates epidemiologically and chronologically
with the drug epidemics that started in America and Europe after the Vietnam
war:
(1) About 30% of all American and European AIDS patients
are intravenous drug users [4, 5]. This group includes nearly all heterosexuals
with AIDS [4, 5]. It also includes 80% of all American and European babies
with AIDS who were intrauterine drug users, because their mothers injected
drugs during pregnancy [5].
It is known since 1982 that virtually 100% of homosexual
males with AIDS or at risk for AIDS have been longterm users of oral, aphrodisiac
drugs, particularly nitrite inhalants, that confer euphoria and facilitate
anal intercourse [60-69]. Epidemiological studies from San Francisco and
Vancouver have just confirmed, in 1993, that 100% of several hundred male
homosexuals with AIDS had used multiple recreational drugs [70, 71, 81].
In addition some had also used the cytotoxic DNA chain terminator AZT as
antiviral drug [72-75, 81]. The immunotoxicity of these recreational drugs
has been documented in the literature since 1909 [5, 76].
About 200,000 HIV-positive healthy people and AIDS patients
are currently treated four times daily with AZT and other DNA chain terminators
as anti-HIV drugs. These drugs kill all growing cells, particularly those
of the highly proliferative immune system [5]. Thus AZT is AIDS by prescription.
(2) In the US recreational drug use increased over the
last years at about the same rate as AIDS [5]. For example, cocaine consumption
increased 200-fold from 1980 to 1990 based on cocaine seizures that increased
from 500 kg in 1980 to 100,000 kg in 1990 [5]. During the same time cocaine-related
hospital emergencies increased 24-fold from 3,296 cases in 1981 to 80,355
cases in 1990 [5] (fig. 1b). Note the parallelisms between the spreads
of AIDS (fig. 1a) and the spreads of cocaine and cocaine-related hospital
emergencies since 1981, and the contrast with the non-spread of HIV since
1984 (fig. la).
(3) 90% of the American AIDS patients are male, because
according to the US Bureau of Justice Statistics males consume about 75%
of all illicit injected drugs, and because homosexual males are virtually
the only consistent users of aphrodisiac drugs like alkyl nitrites [5,
59].
(4) AIDS occurs on average 10 years after initiation of
risk behavior, because it takes years of recreational drug consumption
to cause disease [5, 63, 77], e.g., 20 years of smoking to get lung cancer
[78] or emphysema, or years of alcoholism to develop liver cirrhosis. The
great variations in "latent periods" from HIV to AIDS that currently
average 10 years [10] are euphemisms for the time required by individuals
to accumulate sufficient drug toxicity to generate AIDS diseases [5].
(5) Different risk groups have risk-group-specific AIDS
diseases, e.g., Kaposi sarcoma is observed almost exclusively in homosexuals
[79], because homosexuals are the almost-exclusive users of aphrodisiac
nitrite inhalants [5, 65]; tuberculosis and weight loss is observed in
intravenous drug users, because intravenous drugs cause those symptoms
[5]; anemia and lymphocytopenia is observed in recipients of AZT which
kills proliferating bone marrow cells [5, 80]; and hemophiliacs get pneumonias
and candidiases almost exclusively, because long-term transfusion of foreign
proteins is immunosuppressive [5].
The drug-AIDS hypothesis is experimentally and epidemiologically
testable and provides a rational basis for AIDS prevention and control.
*
This article is the first of two in "Controversy: HIV and AIDS,"
sponsored by Georg Wick, editor-in-chief of International Archives of
Allergy and Immunology.
Acknowledgements
I thank Jody Schwartz for a critical review and Bryan
Ellison for discussions. Supported in part by the Council for Tobacco Research,
USA, and private donations from Glenn Braswell (Los Angeles, Calif., USA),
Dr. Richard Fischer (Annandale, Va., USA), Dr. Fabio Franchi (Trieste,
Italy) and Dr. Friedrich Luft (Berlin, FRG).
References
1. Altman, L.K.: Researchers believe AIDS virus is found.
New York Times, April 24, 1984, pp. C1, C3.
2. Gallo, R.C., Salahuddin, S.Z., Popovic, M., Shearer,
G.M., Kaplan, M., Haynes, B.F., Palker, T.J., Redfield, R., Oleske, J.,
Safai, B., White, G., Foster, P., Markham, P.D.: Frequent detection and
isolation of cytopathic retrovirus (HTLV-III) from patients with AIDS and
at risk for AIDS. Science 1984; 224: 500-503.
3. Popovic, M., Sarngadharan, MG., Read, E., Gallo, R.C.:
Detection, isolation, and continuous production of cytopathic retroviruses
(HTLV-III) from patients with AIDS and pre-AIDS. Science 1984; 224:
497-500.
4. Centers for Disease Control: HIV/AIDS Surveillance;
year-end edition. February 1993, pp. 1-23.
5. Duesberg, P.H.: AIDS acquired by drug consumption and
other noncontagious risk factors. Pharmacol Ther 1992; 55: 201-277.
6. Barré-Sinoussi, F., Chermann, J.C., Rey, F.,
Nugeyre, M.T/, Chamaret, S., Gruest, C., Dauget, C., Axler-Blin, C., Vezinet-Brun,
F., Rouzioux, C., Rozenbaum, W., Montagnier, L.: Isolation of a T-lymphotropic
retrovirus from a patient at risk for acquired immune deficiency syndrome
(AIDS). Science 1983; 220: 868-871.
7. Institute of Medicine: Confronting AIDS. Washington,
National Academy Press, 1986.
8. Duesberg, P.H.: Retroviruses as carcinogens and pathogens:
Expectations and reality. Cancer Res 1987; 47: 1199-1220.
9. Booth, W.: A rebel without a cause for AIDS. Science
1988; 239: 1485-1488.
10. Institute of Medicine: Confronting AIDS-Update
1988. Washington, National Academy Press, 1988.
11. Duesberg, P.: The HIV gap in national AIDS statistics.
Biotechnology 1993; 11: 955-956.
12. Cohen, J.: H.H.S.-Gallo guilty of misconduct. Science
1993; 259: 168-170.
13. Merson, M.H.: Slowing the spread of HIV: Agenda for
the 1990s. Science 1993; 260: 1266-1268.
14. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou,
J.M.: Is a positive Western blot proof of HIV infection? Biotechnology
1993; 11: 696-707.
15. Fauci, A.S.: CD+ T-lymphocytopenia without HIV infection-No
lights, no camera, just facts. N Engl J Med 1993; 328: 429-431.
16. Editorial: AIDS minus HIV? Lancet 1992; 340:
280.
17. Cohen, J.: New Virus Reports Roil AIDS Meeting. Science
1992; 257: 604-605.
18. Cowley, G.: Is a new AIDS virus emerging? Newsweek,
July 27, 1992, p 41.
19. Benditt, J., Jasny, B.: AIDS the unanswered questions.
Science 1993; 260: 1219, 1253-1293.
20. Okie, S.: Heterosexual AIDS may surge, Koop says.
Washington Post, April 24, 1987, p. A4.
21. Shilts, R.: And the Band Played On. New York,
St. Martin's Press, 1987.
22. Oppenheimer, G.M.: Causes, cases, and cohorts: The
role of epidemiology in the historical construction of AIDS; in Fee, E.,
Fox, D.M. (eds): AIDS: The Making of a Chronic Disease. Berkeley,
University of California Press, 1992, pp. 49-83.
23. Centers for Disease Control: Reports on AIDS published
in the Morbidity and Mortality Weekly Report (MMWR) June
1981 through February 1986. Springfield, Va., U.S. Dept of Health and Human
Services, National Technical Information Service, 1986.
24. Curran, J.W., Morgan, M.W., Hardy, A.M., Jaffe, H.W.,
Darrow, W.W., Dowdle, W.R.: The epidemiology of AIDS: Current status and
future prospects. Science 1985; 229: 1352-1357.
25. Centers for Disease Control: The Second 100,000 Cases
of Acquired Immunodeficiency Syndrome-United States, June 1981-December
1991. MMWR 1992; 41: 28-29.
26. Rey, S.: The good news is, the bad news is the same.
Spy, February 1993, p 19.
27. Gallo, R.C.: Virus hunting-AIDS, Cancer, and The
Human Retrovirus: A Story of Scientific Discovery. New York, Basic
Books, 1991.
28. Weiss, R., Jaffe, H.: Duesberg, HIV and AIDS. Nature
1990; 345: 659-660.
29. Rubinstein, E.: II-The untold story of HUT78. Science
1990; 248: 1499-1507.
30. Lemaitre, M., Guetard, D., Henin, Y., Montagnier,
L., Zerial, A.: Protective activity of tetracycline analogs against the
cytopathic effect of the human immunodeficiency viruses in CEM cells. Res
Virol 1990; 141: 5-16.
31. Karpas, A., Lowdell, M., Jacobson, S.K., Hill, F.:
Inhibition of human immunodeficiency virus and growth of infected T cells
by the immunosuppressive drugs cyclosporin A and FK 506. Proc Natl Acad
Sci USA 1992; 89: 8351-8355.
32. Hoxie, J.A., Haggarty, B.S., Rakowski, J.L., Pillsbury,
N., Levy, J.A.: Persistent noncytopathic infection of normal human T lymphocytes
with AIDS-associated retrovirus. Science 1985; 229: 1400-1402.
33. Anand, R., Reed, C., Forlenza, S., Siegal, F., Cheung,
T., Moore, J.: Non-cytocidal natural variants of human immunodeficiency
virus isolated from AIDS patients with neurological disorders. Lancet
1987; ii: 234-238.
34. Langhoff, E., McElrath, J., Bos, H.J., Pruett, J.,
Granelli-Piperno, A., Cohn, Z.A., Steinman, R.M.: Most CD+ T cells from
human immunodeficiency virus-l-infected patients can undergo prolonged
clonal expansion. J Clin Invest 1989; 84: 1637-1643.
35. Spornraft, P., Froschl, M., Ring, J., Meurer, M.,
Goebel, F.D., Ziegler-Heitbrock, H.W., Riethmüller, G., Braun-Falco,
O.: T4/T8 ratio and absolute T4 cell numbers in different clinical stages
of Kaposi's sarcoma in AIDS. Br J Dermatol 1988; 119: 1-9.
36. Murray, H.W., Scavuzzo, D.A., Kelly, C.D., Rubin,
B.Y., Roberts, R.B.: T4+ cell production of interferon gamma and the clinical
spectrum of patients at risk for and with acquired immunodeficiency syndrome.
Arch Intern Med 1988; 148: 1613-1616.
37. Crawford, L.: DNA viruses of the adeno, papilloma
and polyoma group; in Fraenkel-Conrat, H. (ed): Molecular Basis of Virology.
New York, Van Nostrand Reinhold Co, 1968, pp. 393-434.
38. Fenner, F., McAuslan, B.R., Mims, C.A., Sambrook,
J., White, D.O.: The Biology of Animal Viruses. New York, Academic
Press, 1974.
39. Mims, C., White, D.O.: Viral Pathogenesis and Immunology.
Oxford, Blackwell, 1984.
40. Daar, E.S., Moudgil, T., Meyer, R.D., Ho, D.D.: Transient
high levels of viremia in patients with primary human immunodeficiency
virus type 1 infection, N Engl J Med 1991; 324: 961964.
41. Clark, S.J., Saag, M.S., Decker, W.D., Campbell-Hill,
S., Roberson, J.L., Veldkamp, P.J., Kappes, J.C., Hahn, B.H., Shaw, G.M.:
High titers of cytopathic virus in plasma of patients with symptomatic
primary HIV-infection. New Engl J Med 1991; 324: 954-960.
42. Piatak, M., Saag, L.C., Yang, S.C., Clark, S. J.,
Kappes, J.C., Luk, K-C., Hahn, B.H., Shaw, G.M., Lifson, J.D.: High levels
of HIV-I in plasma during all stages of infection determined by competitive
PCR. Science 1993; 259: 1749-1754.
43. Duesberg, P.: HIV and AIDS. Science 1993; 260:
1705.
44. Ho, D.D., Moudgil, T., Alam, M.: Quantification of
human immunodeficiency virus type 1 in the blood of infected persons. N
Engl J Med 1989; 321: 1621-1625.
45. Coombs, R.W., Collier, A.C., Allain, J-P., Nikora,
B., Leuther, M., Gjerset, G.F., Corey, L.: Plasma viremia in human immunodeficiency
virus infection. N Engl J Med 1989; 321: 1626-1631.
46. Duesberg, P.H.: Quantification of human immunodeficiency
virus in the blood. N Engl J Med 1990; 322: 1466.
47. Simmonds, P., Balfe, P., Peutherer, J.F., Ludlam,
C.A., Bishop, J.O., Leigh-Brown, A.J.: Human immunodeficiency virus-infected
individuals contain provirus in small numbers of peripheral mononuclear
cells and at low copy numbers. J Virol 1990; 64: 864-872.
48. Bagasra, O., Hauptman, S.P., Lischner, H.W., Sachs,
M., Pomerantz, R.J.: Detection of human immunodeficiency virus type 1 provirus
in mononuclear cells by in situ polymerase chain reaction. N Engl J
Med 1992; 326: 1385-1391.
49. Centers for Disease Control and Prevention: 1993 revised
classification system for HIV infection and expanded surveillance case
definition for AIDS among adolescents and adults. MMWR 1992; 41:
1-19. 50. Goudsmit, J.: Alternative view on AIDS.
Lancet 1992; 339: 1289-1290.
51. Eggers, H.J., Weyer, J.J.: Linkage and independence
of AIDS Kaposi disease: The interaction of human immunodeficiency virus
and some coagents. Infection 1991; 19: 115-122.
52. Weyer, J., Eggers, H.J.: On the structure of the epidemic
spread of AIDS. The influence of an infectious coagent. Zentralbl Bakteriol
1990; 273: 53-67.
53. Anderson, R.M., May, R.M.: Understanding the AIDS
pandemic. Sci Am 1992; 266: 20-26.
54. Freeman, B.A.: Burrows Textbook of Microbiology.
Philadelphia, Saunders, 1979.
55. Judson, F.N., Penley, K.A., Robinson, M.E., Smith,
J.K.: Comparative prevalence rates of sexually transmitted diseases in
heterosexual and homosexual men. Am J Epidemiol 1980; 112: 836-843.
56. Duesberg, P.H., Schwartz, J.R.: Latent viruses and
mutated oncogenes: No evidence for pathogenicity. Prog Nucleic Acid
Res Mol Biol 1992; 43: 135-204.
57. Weiss, R.: Provenance of HIV strains. Nature
(London) 1991; 349: 374.
58. Duesberg, P.: The enigma of slow viruses. Lancet
1993; 342: 729.
59. Duesberg, P.H.: The role of drugs in the origin of
AIDS. Biomed Pharmacother 1992; 46: 3-15.
60. Marmor, M., Friedman-Kien, A.E., Laubenstein, L.,
Byrum, R.D., William, D.C., D'Onofrio, S., Dubin, N.: Risk factors for
Kaposi's sarcoma in homosexual men. Lancet 1982; i: 1083-1087.
61. Jaffe, H.W., Choi, K., Thomas, P.A., Haverkos, H.W.,
Auerbach, D.M., Guinan, M.E., Rogers, M.F., Spira, T.J., Darrow, W.W.,
Kramer, M.A., Friedman, S.M., Monroe, J.M., Friedman-Kien, A.E., Laubenstein,
L.J., Marmor, M., Safai, B., Dritz, S.K., Crispi, S.J., Fannin, S.L., Orkwis,
J.P., Kelter, A., Rushing, W.R., Thacker, S.B., Curran, J.W.: National
case-control study of Kaposi's sarcoma and Pneumocystis carinii pneumonia
in homosexual men. 1. Epidemiologic results. Ann Intern Med 1983;
99: 145-151.
62. Mathur-Wagh ,U., Mildvan, D., Senie, R.T.: Follow-up
of 41/2 years on homosexual men with generalized lymphadenopathy. N
Engl J Med 1985 ; 313: 1542-1543.
63. Newell, G.R., Mansell, P.W.A., Spitz, M.R., Reuben,
J.M., Hersh, E.M.: Volatile nitrites: Use and adverse effects related to
the current epidemic of the acquired immune deficiency syndrome. Am
J Med 1985; 78: 811-816.
64. Darrow, W.W., Echenberg, D.E., Jaffe, H.W., O'Malley,
P.M., Byers, R.H., Getchell, J.P., Curran, J.W.: Risk factors for human
immunodeficiency virus (HIV) infections in homosexual men. Am J Publ
Health 1987; 77: 479-483.
65. Haverkos, H.W., Dougherty, J.A.: Health Hazards
of Nitrite Inhalants; NIDA Res Monogr 83. Washington, U.S. Dept Health
& Human Services, 1988.
66. Lifson, A.R., Darrow, W.W., Hessol, N.A., O'Malley,
P.M., Barnhart, J.L., Jaffe, H.W., Rutherford, G.W.: Kaposi's sarcoma in
a cohort of homosexual and bisexual men. Am J Epidemiol 1990; 131:
221-231.
67. Ostrow, D.G., Van Raden, M.J., Fox, R., Kingsley,
L.A., Dudley, J., Kaslow, R.A., the Multicenter AIDS Cohort Study (MACS):
Recreational drug use and sexual behavior change in a cohort of homosexual
men. AIDS 1990; 4: 759-765.
68. Seage, G.R., Mayer, K.H., Horsburgh, C.R., Holmberg,
S.D., Moon, M.W., Lamb, G.A.: The relation between nitrite inhalants, unprotected
receptive anal intercourse, and the risk of human immunodeficiency virus
infection. J Am Epidemiol 1992; 135: 1-11.
69. Archibald, C.P., Schechter, M.T., Le, T.N., Craib,
K.P.J., Montaner, J.S.G., O'Shaughnessy, M.V.: Evidence for a sexually
transmitted cofactor for AIDS-related Kaposi's sarcoma in a cohort of homosexual
men. Epidemiology 1992; 3: 203-209.
70. Ascher, M.S., Sheppard, H.W., Winkelstein, W. Jr,
Vittinghoff, E.: Does drug use cause AIDS? Nature 1993; 362: 103-104.
71. Schechter, M.T., Craib, K.J.P., Gelmon, K.A., Montaner,
J.S.G., Le, T.N., O'Shaughnessy, M.V.: HIV-1 and the aetiology of AIDS.
Lancet 1993; 341: 658-659.
72. Duesberg, P.: HIV and the aetiology of AIDS. Lancet
1993; 341: 957-958.
73. Duesberg, P.:Aetiology of AIDS. Lancet 1993;
341: 1544.
74. Ascher, M.S., Sheppard, H.W., Winkelstein, W. Jr,
Vittinghoff, E.: Aetiology of AIDS. Lancet 1993; 341: 1223.
75.Schechter, M.T., Craib, K.J.P., Montaner, J.S.G., Le,
T.N., O'Shaughnessy, M.V., Gelmon, K.A.: Aetiology of AIDS. Lancet
1993 341:1222-1223.
76. Achard, C., Bernard, H., Gagneux ,C.: Action de la
morphine sur les propriétés leucocytaires; leuco-diagnostic
du morphinisme. Bull Mem Soc Méd Hôpitaux de Paris,
3rd Ser 1909; 28: 958-966.
77. Mientjes, G.H.C., van Ameijden, E.J.C., Weigel, H.M.,
van den Hoek, J.A.R., Countinho, R.A.: Clinical symptoms associated with
seroconversion for HIV-1 among misusers of intravenous drugs: Comparison
with homosexual seroconverters and infected and non-infected intravenous
drug misusers. Br Med J 1993; 306: 371-373.
78. Cooper, G.M: Oncogenes. Boston, Jones &
Bartlett, 1990.
79. Beral, V., Peterman, T.A., Berkelman, R.L., Jaffe,
H.W.: Kaposi's sarcoma among persons with AIDS: A sexually transmitted
infection? Lancet 1990; 335: 123-128.
80. Kolata, G.: Imminent marketing of AZT raises problems:
Marrow suppression hampers AZT use in AIDS victims. Science 1987;
235: 1462-1463.
81. Duesberg, P.: Can epidemiology determine whether drugs
or HIV cause AIDS? AIDS Forschung 1993; 8: 627-635
VIRUSMYTH HOMEPAGE