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Human immunodeficiency virus and acquired immunodeficiency syndrome:
Correlation but not causation

by PETER H. DUESBERG


ABSTRACT        AIDS is an acquired immunodeficiency syndrome defined by a
severe depletion of T cells and over 20 conventional degenerative and
neoplastic diseases. In the U.S. and Europe, AIDS correlates to 95% with risk
factors, such as about 8 years of promiscuous male homosexuality, intravenous
drug use, or hemophilia. Since AIDS also correlates with antibody to a
retrovirus, confirmed in about 40% of American cases, it has been hypothesized
that this virus causes AIDS by killing T cells. Consequently, the virus was
termed human immunodeficiency virus (HIV), and antibody to HIV became part of
the definition of AIDS. The hypothesis that HIV causes AIDS is examined in
terms of Koch's postulates and epidemiological, biochemical, genetic and
evolutionary conditions of viral pathology. HIV does not fulfill Koch's
postulates: (i) free virus is not detectable in most cases of AIDS;
(ii) virus can only be isolated by reactivating virus in vitro from a few
latently infected lymphocytes among millions of uninfected ones; (iii) pure
HIV does not cause AIDS upon experimental infection of chimpanzees or
accidental infection of healthy humans. Further, HIV violates classical
conditions of viral pathology. (i) Epidemiological surveys indicate that the
annual incidence of AIDS among antibody-positive persons varies from nearly 0
to over 10%, depending critically on nonviral risk factors. (ii) HIV is
expressed in < [or =] 1 of every 10 [to the fourth power] T cells it
supposedly kills in AIDS, whereas about 5% of all T cells are regenerated
during the 2 days it takes the virus to infect a cell. (iii) If HIV were the
cause of AIDS, it would be the first virus to cause a disease only after the
onset of antiviral immunity, as detected by a positive "AIDS test." (iv) AIDS
follows the onset of antiviral immunity only after long and unpredictable
asymptomatic intervals averaging 8 years, although HIV replicates within 1 to
2 days and induces immunity within 1 to 2 months.(v) HIV supposedly causes
AIDS by killing T cells, although retroviruses can only replicate in viable
cells. In fact, infected T cells grown in culture continue to divide. (vi)
HIV is isogenic with all other retroviruses and does not express a late,
AIDS-specific gene. (vii) If HIV were to cause AIDS, it would have a
paradoxical, country-specific pathology, causing over 90% Pneumocystis
pneumonia and Kaposi sarcoma in the U.S. but over 90% slim disease, fever,
and diarrhea in Africa. (viii) It is highly improbable that within the last
few years two viruses (HIV-1 and HIV-2) that are only 40% sequence-related
would have evolved that could both cause the newly defined syndrome AIDS.
Also, viruses are improbable that kill their only natural host with
efficiencies of 50-100%, as is claimed for HIVs. It is concluded that HIV is
not sufficient for AIDS and that it may not even be necessary for AIDS
because its activity is just as low in symptomatic carriers as in
asymptomatic carriers. The corellation between antibody to HIV and AIDS does
not prove causation, because otherwise indistinguishable diseases are now set
apart only on the basis of this antibody. I propose that AIDS is not a
contagious syndrome caused by one conventional virus or microbe. No such
virus or microbe would require almost a decade to cause primary disease, nor
could it cause the diverse collection of AIDS diseases. Neither would its
host range be as selective as that of AIDS, nor could it survive  if it were
as inefficiently transmitted as AIDS. Since AIDS is defined by new
combinations of conventional diseases, it may be caused by new combinations
of conventional pathogens, including acute viral or microbial infections and
chronic drug use and malnutrition. The long and unpredictable intervals
between infection with HIV and AIDS would then reflect the thresholds for
these pathogenic factors to cause AIDS diseases, instead of an unlikely
mechanism of HIV pathogenesis.


--from PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCE U.S.A., Vol. 86,
       pp. 755-764, Feb. 1989
       by Peter H. Duesberg, Dept. of Molecular and Cell Biology, Univ. of
       California, Berkeley CA 94720