1990, 141, 511
TIMES AND TRENDS
Research in Immunology, and prior to that, the Annales de
l'lnstitut Fasteur, have traditionally offered a significant part of
the journal space to scientific exchanges and discussions, as, for example,
the Forums. The journal is open to many types of exchange, and various
forms can be adopted. Here we open our columns to Dr. P. Duesberg and Dr.
L. Montagnier, who have agreed to discuss the matter of whether HIV is
the causative agent of AIDS. Below is Dr. P. Duesberg's starting contribution.
We shall later publish that of Dr. L. Montagnier, and invite other contributions
on this topic. In particular, we hope that the question of autoimmune disease
in AIDS will be further discussed. Contributions should be sent to the
Editor inChief, and publication will be very rapid.
AIDS: NONINFECTIOUS DEFICIENCIES
ACQUIRED BY DRUG CONSUMPTION AND OTHER RISK FACTORS
Dept. of Molecular and Cell Biology;
University of California,
Berkeley, CA 94720 (USA)
The first 5 AIDS cases, described in 1981, were all male homosexual drug
users with pneumocystis pneumonia and acute cytomegalovirus infections
(Gottlieb et al., 1981). Since then, over 100,000 cases of about 25 conventional
diseases including predominantly pneumonia, Kaposi's sarcoma, lymphoma,
dementia, tuberculosis, candidiasis and diarrhoea have been recorded as
AIDS diseases in the US (CDC, 1990). Over 90 % occurred in two major risk
groups (CDC, 1990), namely in 20 to 40year old intravenous drug
users and male homosexuals who also consume drugs (Gottlieb et al., 1981;
Lauritsen and Wilson, 1986; CDC, 1 987; Darrow et al., 1987; Haverkos and
Dougherty, 1988; Rappoport, 1988; Adams, 1989; Chaisson et al., 1989; Weiss,
S., 1989; FriedmanKien et a/., 1990). Because acquired immune deficiency
is thought to be the common cause of these vastly disparate diseases, they
were grouped together as the AIDS syndrome.
There are two competing hypotheses as to what causes AIDS, the virusAIDS
and the riskAIDS hypothesis.
The virusAIDS hypothesis, currently held by most medical scientists,
in particular virologists, proposes that the retrovirus HIV (human immunodeficiency
virus) causes AIDS by killing billions of T cells but only on average 8
to 10 years after infection (Institute of Medicine, Natl. Acad. Sci., 1986,
1988; Coffin et al., 1986; Gallo and Montagnier, 1988; Blattner et al.,
1988; Duesberg, 1989a). HIV was originally discovered by Montagnier and
coworkers in 1983 as a latent retrovirus in AIDS patients (BarreSinoussi
et. al., 1983). Tracking latent viruses, like HIV, depends largely on technology
that was only developed in the 70's and 80's. Prior to that time, a latent
virus such as HIV was practically undetectable. It is for this reason that
the virus is perceived as "new" (Gallo and Montagnier, 1988;
Blattner et al., 1988). On the basis of the virusAIDS hypothesis,
about 25 conventional diseases are now defined as AIDS if they occur in
the presence of antibody to HIV (Institute of Medicine, Natl. Acad. Sci.,
1986, 1988; CDC, 1987, 1990; Duesberg, 1989a). However, except for antibody
to HIV or rare elements of the latent virus, there is no known distinction
between conventional Kaposi's sarcoma (FriedmanKien et al., 1990),
Iymphoma, dementia, tuberculosis, candidiasis, diarrhoea, etc. and their
The fact that antibody to HIV is found in the US predominantly in AIDS
risk groups, and that about 1.5 % of the 1 to 1.5 million antibodypositive
Americans develop AIDS diseases annually (Duesberg, 1989a), are cited as
the primary arguments for the virusAIDS hypothesis (Coffin et al.,
1986; Institute of Medicine, Natl. Acad. Sci., 1986, 1988; Gallo and Montagnier,
1988; Blattner et al., 1988). Yet a correlation, in particular one with
antibody to a virus, is not an unambiguous argument for viral causation
of a disease (Duesberg, 1989a). Moreover, the relevance of this correlation
to the aetiology of AIDS is questionable because it is 100 % by definition
(Institute of Medicine, Natl. Acad. Sci., 1986, 1988; Duesberg, 1989a)
rather than by natural coincidence between the diseases and HIV.
In addition, a viral aetiology of AIDS is claimed based on anecdotal
cases of transmission (Institute of Medicine, Natl. Acad. Sci., 1986, 1988;
Gallo and Montagnier, 1988; Blattner et al., 1988). It is claimed that
because of infection with HIV, antibodypositive haemophiliacs or other
antibodypositive recipients of transfusions have developed diseases
otherwise typical of their various conditions, although these diseases
appear on average only 8 to 10 years after antiviral immunity and only
in 13 % of them per year (Duesberg, 1989a). Likewise it is claimed
that HIV transmission from mother to child is the reason some antibodypositive
babies have developed typical pediatric diseases on the average 2 years
after perinatal infection (Duesberg, 1989a) (but not the diseases typical
of the major AIDS risk groups such as Kaposi's sarcoma) (Duesberg, 1988;
Beral et al., 1990; CDC, 1990). Yet there is not a single controlled epidemiological
study to confirm the postulated viral aetiologv of AIDS transmission, comparing
for example the incidence of AlDSlike diseases in two groups of matched
haemophiliacs that differ only in antibody to HIV (Duesberg, 1989a).
Moreover, the virusAIDS hypothesis is not compatible with orthodox
viral pathology. It is paradoxical that:
a) Unlike all other pathogenic viruses, HIV hardly infects any cells
when it is claimed to be pathogenic (Duesberg, 1987, 1988, i989a). During
AIDS, < 1 in 500 lymphocytes contain a latent HIV provirus and only
1 in 10,000 to 100,000 contain an active provirus-just as in millions of
asymptomatic carriers (Duesberg, 1987, 1989a, 1989b; Schnittman et al.,
1989). Therefore, it is difficult to explain the loss of billions of T
cells said to be the hallmark of AIDS (Institute of Medicine, Natl. Acad.
Sci., 1986, 1988; CDC, 1987). Like the rest of us, even viruses need to
do something to get something done.
b) In view of the claims that in vivo HIV kills T cells directly (Baltimore
and Feinberg, 1989; Ho et al., 1989) over 99 % of the few T cells that
ever become infected survive infection to become "reservoirs"
of latent HIV (Schnittman et al., 1989).
c) In view of recent claims that viraemia is necessary for AIDS (Baltimore
and Feinberg, 1989; Coombs et al., 1989; Ho et al., 1989), the number of
infected cells remains low in all AIDS cases (Duesberg, 1990).
d) AIDS diseases-by definition (Institute of Medicine, Natl. Acad. Sci.,
1986; Coffin et al., 1986)-only occur after the onset of antiviral immunity,
a "positive" AIDS test (Duesberg, 1987, 1988, 1989a). All other
viruses cause diseases primarily before antiviral immunity when they are
biochemically most active (Evans, 1989).
e) AIDS diseases only occur after long, unpredictable latent periods,
averaging 8 to 10 years with a minimum of 2 years in adults (Duesberg,
1989a), while all other viruses including pathogenic retroviruses cause
primary disease within weeks after infection. Such long latent periods
are particularly paradoxical if one argues that antiviral immunity is essential
for pathogenicity (Duesberg, 1989a).
f) The same virus would take an average of 2 years to cause diseases
in children and an average of 8 to 10 years in adults (Institute of Medicine,
Natl. Acad. Sci., 1988; Duesberg, 1989a).
g) The same virus is proposed to cause neoplastic diseases such as Kaposi's
sarcomas and AIDS lymphomas as well as necrogenic diseases such as Tcell
death or AIDS dementia (Duesberg, 1989a). This, in particular, is implausible,
since neither Kaposi's cells nor neurons are even infected by HIV (Duesberg,
1989a). Indeed, neurons cannot be infected by HIV because retroviruses
depend on mitosis to initiate infection (Rubin and Temin, 1958), and neurons
h) Immune deficiency should cause neoplasms such as Kaposi's sarcoma
and lymphoma (Duesberg, 1989a). Tcelldeficient humans or animals
such as nude mice have no more tumours than immune competent counterparts
(Kinlen, 1982; Sharkey and Fogh, 1984).
i) The most common AIDS disease in the US is pneumocystis pneumonia
while the most common AIDS diseases in Africa are slim disease, diarrhoea
and fever, although Pneumocystis carinii is ubiquitous in all humans, including
Africans (Duesberg, 1989a).
j) AIDS diseases would occur in the US to over 90 % in males, but would
be equally distributed between the sexes in Africa if they were caused
by a sexually transmitted virus introduced into each country about 1020
years ago (Duesberg, 1989a).
k) Among all risk groups in the US, HIV would cause Kaposi's sarcoma
almost exclusively in homosexuals (Duesberg, 1988, 1989a; Beral et al.,
1990). It is also incompatible with viral aetiology that Kaposi's sarcomas
in American homosexuals with HIV are indistinguishable from those without
(FriedmanKien et al., 1990).
The virusAIDS hypothesis is unproven, because (1) HIV as the hypothetical
cause of AIDS fails to meet many classical criteria of viral pathology,
(2) HIV has not been shown to have any unconventional properties to resolve
the above paradoxa (Duesberg, 1989a), and (3) there are no controlled epidemiological
studies showing a role for HIV in AIDS. The view that HIV is not sufficient
or even not proven to be necessary for AIDS (Duesberg, 1987, 1988, 1989a)
have been voiced by a number of scientists including: Bialy (1988); Eigen
(1989); Evans (1989; Duesberg, 1989c); Gilbert (Hall, 1988; Liversidge,
1989); Griffin (1989); Haas (1989); Holub (1988); RootBernstein (1990);
Rubin (1988a,b); Schwartz (1989); Sonnabend (1989); Stewart (1989); Weiss,
R. (1989) and at least one nonscientist, Fauci's sister Denise (Fauci,
1989; Duesberg, 1989d). Moreover, FriedmanKien et al. (1990) and Beral
et al. (1990) have now called HIV into question as a cause of Kaposi's
sarcoma, which used to be the hallmark of AIDS in the early 80's (Beral
et al., 1990) for the same reasons I have cited above and previously (Duesberg,
The riskAIDS hypothesis suggests that AIDS is caused primarily
by noninfectious agents. These include psychoactive drugs, overmedication
with antibiotics (Rappoport, 1988; Rubin, 1988a; Adams, 1989; Sonnabend,
1989) and above all AZT, a chain terminator of DNA synthesis administered
to treat HIV infection since 1987 (Duesberg, 1989a; Farber, 1989; Lauritsen,
1989). Consumption of psychoactive drugs is often associated with traditional
causes for immune deficiency such as protein malnutrition and parasitic
infections (Seligman et al., 1984) and AZT is directly immunosuppressive
because it is designed to kill lymphocytes (Duesberg, 1989a; Farber, 1989;
Lauritsen, 1989). This hypothesis is compatible with views stated by RootBernstein
(1990; Rubin (1988a,b); Sonnabend (1989); and Stewart (1989). The risk
a) Why AIDS is limited to risk groups rather than random in the population,
as would be expected from an infectious agent.
b) Why natural vaccination against HIV (a "positive AIDS test")
does not protect against AIDS.
c) The long and unpredictable latent periods between HIV infection and
AIDS, averaging 8 to 10 years in adults, as the individual reaches a pathogenic
threshold of AIDS risks. The shorter latent periods in children averaging
about 2 years would reflect prenatal and postnatal risk factors, as 90
% of babies with AIDS are either, born to mothers who are drug addicts
or prostitutes or both, or are haemophiliacs (Duesberg, 1988; CDC,
d) The enormous diversity and riskgroupspecificity of AIDS
diseases in terms of the diversity of risk factors. For example, the incidence
of Kaposi's sarcoma exclusively in homosexuals correlates and declines
directly with their groupspecific use of nitrite inhalants (Lauritsen
and Wilson, 1986; Haverkos and Dougherty, 1988; Rappoport, 1988; Duesberg,
1989a; Beral et al., 1990) regardless of the presence of HIV (FriedmanKien
et al., 1990). The nearly complete difference between the major AIDS diseases
in the US and Africa could be explained as a consequence of drug consumption
in the US and of malnutrition and conventional parasitic infections in
e) The paradox as to why HIV, unless an innocent bystander, can afford
to infect actively 1 in 10,000 and latently < 1 in 500 susceptible lymphocytes
even in those dying from AIDS (Duesberg, 1989a; Coombs et al., 1989; Ho
et al., 1989; Schnittman el a/., 1989).
f) The recent emergence of AIDS diseases in the US as a function of
the enormous increase during the last 10 to 20 years in the consumption
of psychoactive drugs (NNICC Reports, 19781988; Rappoport, 1988; Adams,
1989). For instance, cocaine consumption alone has increased 5fold
during the last 10 years in the US (NNICC Reports, 19781988). Indeed,
about a third of the American AIDS patients are confirmed intravenous drug
users (CDC, 1990). In addition many, perhaps most, of the male homosexuals
with AIDS appear to have used various psychoactive drugs (Gottlieb et al.,
1981; Lauritsen and Wilson, 1986; Darrow et al., 1987; Haverkos and Dougherty,
1988; Rappoport, 1988; CDC, 1990; Adams, 1989; FriedmanKien et al.,
1990). Together, these two risk groups represent 90 % of the US AIDS cases
(CDC, 1990). Moreover, since 1987, 20,000 antibodypositive symptomatic
and asymptomatic persons in the US (Marx, 1989) and 50,000 worldwide (Deer,
1989) have been treated with the DNA chain terminator AZT, which is directly
immunosuppressive (Duesberg, 1989a). Thus, the use of drugs appears to
be a common denominator of most AIDS cases in the US.
g) The preferential occurrence in the US of HIV in AIDS risk groups
can also be reconciled with the risk hypothesis. Since HIV is not widespread
in the US and also very hard to transmit due to its chronic latency (Duesberg,
1989a), only those who have intimate contacts with many others are likely
to be infected, as for example promiscuous homosexuals, drug addicts sharing
needles or practicing prostitution, and haemophiliacs. Thus HIV would serve
as an outstanding, but not an absolute (FriedmanKien et al., 1990)
surrogate marker for AIDS risks (Darrow et al., 1987; Duesberg, 1989a;
Weiss, S., 1989).
It is concluded that in the US and probably in Europe, AIDS is a collection
of noninfectious deficiencies of which about 90 % are acquired by
drug consumption associated with malnutrition and parasitic infections
and other specific risks, such as chronic transfusions for treatment of
haemophilia. The 10 % of AIDS cases occurring outside the risk groups in
the US. (CDC, 1990) are consequences of the clinical definition of AIDS,
namely conventional diseases occurring in persons accidentally infected
by HIV. The African AIDS epidemic would also appear to be the product of
the allembracing AIDS definition, namely a widespread heterosexual
distribution of the newly detectable, dormant HIV together with old African
diseases like slim disease, fever and diarrhoea. For example, about 1020
% of the 30 million Zairens carry latent HIV in Africa, but only 335 developed
AIDS in the period from 1985 to 1988 (Duesberg, 1989a). Like nearly all
retroviruses in wild animals endemic human retroviruses are probably transmitted
perinatally (Duesberg, 1989a). This would more convincingly explain the
heterosexual distribution in Africa of HIV, and hence diseases now termed
AIDS because of HIV, than theories about peculiar sexual practices (G.
Klein, 1988; Institute of Medicine, Natl. Acad. Sci., 1988).
I thank Harry Rubin and Bryan Ellison for cutical comments.
I am supported by Outstanding Investigator Grant #5R35CA39915
04 from the National Cancer Institute
ADAMS, J. (1989), AIDS: the HIV Myth. St. Martin's Press,
New York; Macmillan Press, London.
BALTIMORE, D. & FEINBERG, M.B. (1989), HIV revealed.
New Engl. J. Med., 321, 1673.
BERAL, V., PETERMAN, T.A., BERKELMAN, R.L. & JAFFE,
H.W. (1990), Kaposi s sarcoma among persons with AIDS: a sexually transmitted
infection? Lancet, 1, 123.
BARRESINOUSSI, F., CHERMANN, J.C., REY, F., NUGEYRE,
M.T., CHAMARET, S., GREUST J., DANGUET, C., AXLERBLIN, C., VEZINETBRUN,
F., ROUZIOUX, C., ROSENBAUM, W. & MONTAGNIER, L. (1983), Isolation
of Tlymphotropic retrovirus from a patient at risk for acquired immune
deficiency syndrome (AIDS). Science, 220, 868.
BIALY, H. (1988), Where is the virus? And where is the
press? Bio/Technology, 6, 121.
BLATTNER, W., GALLO, R.C. & TEMIN, H. (1988), HIV
Causes AIDS. Science, 241, 5141.
CENTERS FOR DISEASE CONTROL (1987), Revision of the CDC
surveillance case definition for acquired immunodeficiency syndrome. J.
Amer. med. Assor., 258, 1143.
CENTERS FOR DISEASE CONTROL (1990), HIV/AIDS Surveillance:
AIDS cases reported through December 1989. Centers for Disease Control,
CHAISSON, R.E., BACCHETTl, P., OSMOND, D., BRODIE, B.,
SANDE, M.A. & Moss, A.R. (1989), Cocaine use and HIV infection in intravenous
drug users in San Francisco. J. Amer. med. Ass., 261, 561.
COFFIN, J., HAASE, A., LEW, J.A., MONTAGNIER, L., OROSZLAN,
S., TEICH, N., TEMIN, H., TOYOSHIMA, K., VARMUS, H., VOGT, P. & WEISS,
R. (1986), Human immunodeficiency viruses. Science, 232, 697.
COOMBS, R.W., COLLIER, A.C., ALLAIN, J.P., NIKORA,
B., LEUTHER; M., GJERSET, G.F. & COREY, L. (1989), Plasma viremia in
human immunodeficiency virus infection. New Engt. J. Med., 321, 1626.
DARROW, W.W., ECHENBERG, D.F., JAFFE, H.W., O MALLEY,
P.M., BYERS, R.H., GETCHELL, J.P. & CURRANT J.W. (1987), Risk factors
for human immunodeficiency virus (HIV) infections in homosexual men. Amer.
J. Publ. Hlth, 77, 479.
DEER, B. (1989), Revealed: fatal flaw of drug that gave
hope. Sunday Times, London, April 16 (p. 18A).
DUESBERG, P.H. (1987), Retroviruses as carcinogens and
pathogens: expectations and reality. Cancer Res., 47, 1199.
DUESBERG, P.H. (1988), HIV is not the cause of AIDS. Science,
DUESBERG, P.H. (1989a), Human immunodeficiency virus and
acquired immunodeficiency syndrome: correlation but not causation. Proc.
Nat. Acad. Sci. (Wash.), 86, 755.
DUESBERG, P.H. (1989b), Questioning AIDS findings. Science
News, 136, 131.
DUESBERG, P.H (19S9c), Does HIV cause AIDS? (letter).
J. Acq. Immun. Def. Synd., 2, 514.
DUESBERG, P.H. (1989d), Duesberg responds (letter). The
AAAS Observer, November 3, Supplement to Science, 8, 2.
DUESBERG, P.H. (1990), Letter to the editor. New Engl.
J. Med. 1990, in press.
EIGEN, M. (1989), The AIDS debate. Naturwissenschaften,
EVANS, A.S. (1989), Does HIV cause AIDS? an historical
perspective. J. Acq. Immun. Def. Synd., 2, 107.
FARBER, C. (1989), Sins of omission: the AZT scandal.
Spin, New York, November, pp. 40, 42, 44, 115117.
FAUCI, A. (1989), Writing for my sister Denise. The AAAS
Observer, September 1, Supplement to Science, 7, 4.
FRIEDMANKIEN, A.E., SALTZMAN, B.R., CAO, Y., NESTOR,
M.S., MIRABILE, M., LI, J.J. & PETERMAN, T.A. (1990), Kaposi's sarcoma
in HlVnegative homosexual men. Lancet, I, 168.
GALLO, R.C. & MONTAGNIER, L. (1988), AIDS in 1988.
Sci. Amer., 259, 41.
GOTTLIEB, M.S., SCHANKER, H.M., FAN, P.T., SAXSON, A.,
WEISMAN, J.D. & POZALSKI, I. (1981), Pneurnocvstis pneumoniaLos
Angeles, MMWR, in "Reports on AIDS Published in the MMWR" 30
(pp. 250252). (US Department of Health & Human Services, Public
Health Service) Centers for Disease Control, Atlanta, Georgia.
GRIFFIN, B. (1989), Burden of proof. Nature (Lond.), 338,
HAAS, M. (1989), The need for a search for a proximal
principle of human AIDS. Cancer Res., 49, 2184.
HALL, S. (1988), Gadfly in the ointment. Hippocrates,
HAVEKKOS, H.W. & DOUGHERTY, J.A. (1988), Epidemiologic
studies - Kaposi's sarcoma vs. Opportunistic infections among homosexual
men with AIDS, in "Health hazards of nitrite inhalants" (Haverkos,
H.W. & Dougherty, J.A.) (pp. 96105). National Institute on Drug
Abuse Monograph 83.
Ho, D.D., MOUGDIL, T. & ALAM, M. (1989), Quantitation
of human immunodeficiency virus Type I in the blood of infected persons.
New Engl. J. Med., 321, 1621.
HOLUB, W.R. (1988), AIDS: a new disease? Amer. Clin. Prod.
Rev., 7, 28.
INSTITUTE 0F MEDICINE (1986) Confronting AIDS. Natl. Acad.
Sci., Washington, D.C.
INSTITUTE or MEDICINE (1988) Confronting AIDS - update.
Natl. Acad. Sci., Washington, D.C.
KINL EN, L.J. (1982), Immunosuppressive therapy and cancer.
Cancer Surv., 1, 565.
KLEIN, G. (1988), The role of science. J. Acq. Immun.
Def. Synd., 1, 611.
LAURITSEN, J. & WILS0N, H. (1986), Death Rush, Poppers
and AIDS. Pagan Press, New York.
LAURITSEN, J. (1989), Science by press release. New York
Native #331, August 21 (pp. 2021). New Yorl;.
LIVERSIDGE A. (1989), PNAS Publication of AIDS Article
Spurs Debate Over Peer Review, in "The Scientist" April 3 (pp.
I, 45, 19), Philadelphia.
MARX, J.L. (1989), Drugresistant strains of AIDS
virus found. Science, 243, 1551.
NNICC REPORTS (19781988), The National Narcotics
Intelligence Consumers Committee. Office of National Drug Control Policy
(Executive Office of the President) Washington, D.C. 20500.
RAPPOPORT, J. (1988), AIDS Inc. Human Energy Press, San
ROOTBERNSTEIN, R. (1990), Do we know the cause(s)
of AIDS? Perspectives Biol. Med. (in press).
RUBIN, H. & TEMIN, H. (1958), A radiological study
of cellvirus interaction in the Rous sarcoma. Virology 7, 75.
RUBIN, H. (1988a), Etiology of AIDS. Science, 240, 1389.
RUBIN H. (1988b), Is HIV the causative factor in AIDS?
Nature (Lond.), 334, 201.
SCHNITTMAN, S.M., PSALLIDOPOULOS, M.C., LANE, H.C., THOMPSON,
L., BA5ELER, M., MASSARl, F., Fox, C.H., SALZMAN, N.P. & FAUCI, A.
(1989), The reservoir for HIVI in human peripheral blood is a Tcell
that maintains expression of CD4. Science, 245, 203.
SCHWARTZ, J. (1989), The politics of AIDS research. Positively
Healthy, January, pp. 1112. Richmond, Surrey, U.K.
SELIGMAN, M., CHESS, L., FAHEY, J.L., FAUCI, A.S., LACHMANN,
P.J., L AGESTEHR, J., NGU, J., PINCHING, A.J., ROSEN, F.S., SPIRA,
T.J. & W YBAN, J. (1984), AIDS An immunologic reevaluation. New
Engl. J. Med., 311, 1286.
SHARKEY, F.E. & FOGH, J. (1984), Considerations in
the use of nude mice for cancer research. Cancer Metastasis Rev., 3, 341.
SONNABEND, J. (1989), AIDS: an explanation for its occurrence
in homosexual men, in "The acquired immunodeficiency syndrome and
infections of homosexual men" (Armstrong, D. & Ma, P.) 2nd Edit.
(pp. 449470). Butterworth, Stoneham, Massachusetts.
STEWART, G.T. (1989), Uncertainties about AIDS and HIV.
Lancet, I, 1325.
WEISS, R.A. (1989), AIDS: defective viruses to blame?
Nature (Lond.), 338, 458.
WEISS, S.H. (1989), Links Between cocaine and retroviral
infection. J. Amer. med. Ass., 261, 607.
Note added in proof:
The following new information in support of the riskAIDS hypothesis
1) Recent surveys have indicated that the incidence of AlDSlike
diseases in matched risk groups is independent of HIV up to one year after
receiving HIV in general patients (Ward et al., 1989) and probably for
over 4 years in haemophiliacs (din et al., 1989).
2) Further, it was shown that among HIVpositive mothers, drug addiction
was the only consistent risk factor for deficiencies among newborns (Blanche
et al., 1989).
3) The CDC has now retroactively revised downward the estimates of HlVinfected
persons in the US from 12 million in the period of 198589 to
0.75 million in 1986 and about I million in 1990 (CDC, 1990a). During the
same interval, the "latent" period from HIV to AIDS was increased
from initially three years to currently over ten years (Duesberg, 1989a).
These apparently are attempts to close the gaps that I have pointed out
between the number of AIDS cases predicted by the virusAIDS hypothesis
and those actually recorded (Duesberg, 1989a). Moreover, the prediction
of the virusAIDS hypothesis that, due to sexuallytransmitted
virus, AIDS would spread into the heterosexual population (Institute of
Medicine, 1988), has not materialized.
4) Finally, several defences of the virusAIDS hypothesis have failed
to refute or prove erroneous the central arguments I have raised against
it. These include defences by Blattner, Gallo and Temin (1988) / Duesberg
(1988), Eigen (1989) / Duesberg (199Oa), Evans (1989) / Duesberg (1989c),
Klein (1988),Kurth (1989) / Duesberg (1989e), Velimirovic (1989)
/ Duesberg (1989f), Fauci (1989) / Duesberg (1989d), Linz (1989) / Duesberg
(1989g), and Baltimore and Feinberg (1989) / Duesberg (1990).
BLANCHE, S., Rouzioux, C., MOSCATO, M.L.G., et al.
(1989), A prospective study of infants born to women seropositive for human
immunodeficiency virus type 1. New Eng. J. Med., 320, 1643.
CENTERS FOR DISEASE CONTROL (199Oa), Estimates of HIV
Prevalence and Projected AIDS Cases: Summarv of a Workshop. MMWR, 39 (7),
DUESBERG, P.H. (1989e), Duesberg responds. AlDSForschung
(AIFO), 10, 515.
DUESBERC, P.H. (1989f), Duesberg responds. AlDSForschung
(AIFO), 10, 521.
DUESBERG, P.H. (1989g), Noch einmal: HIV und AIDS. Nachr.
Chem. Tech. Lab., 37 (12), 1302.
DUESBERG, P.H. (199Oa), Responding to the AIDS Debate.
Naturwissenschaften, 76, 341.
KURTH, R. (1989), Is HIV the cause of AIDS? An uptodate
reply to the theories of Duesberg. AIDSForschung (AIFO), 10, 507.
LINZ, U. (1989), HIV und AIDS. Nachr. Chem. Tech. Lab.,
37 (9), 930.
VELIMIROVIC, B. (1989), What actually are the postulates
of causation? Some remarks on Duesberg's article "HIV and AIDS: correlation
but not causation". AIDSForschung (AIFO), 10, 517.
WARD, J.W., BUSH, T.J., PERKINS, H.A. et. al. (1989),
The natural history of transfusionassociated infection with human
immunodeficiency virus. New Engl. J. Med., 321, 947.
JIN, Z., CLEVELAND, R.P. & KAUFMAN, D.B. (1989), Immunodefciency
in patients with hemophilia: an underlying deficiency and lack of correlation
with factor replacement therapy or exposure to human immunodeficiency virus.
J. Allergy. Clin. Immunol., 83, 165.