Ho et al. (1),
and Feinberg and Baltimore (2) suggest that "residual"
(1) or "lingering doubts" (2) about the virus-AIDS hypothesis
are now resolved by new evidence for viremia in AIDS patients, published
in NEJM (1-3). A paper by myself (4) is quoted as the source of
these doubts. For the following reasons my doubts remain unresolved:
1) The data
of Ho et al. (1) and Coombs et al. (3) both include AIDS cases with
very low or no titers of HIV, varying from 0-10 infectious units/ml,
just as low as in aysmptomatic carriers. It follows that HIV viremia
is not necessary for AIDS.
2) Ho et al.
(1) and Feinberg and Baltimore (3) now propose that HIV causes AIDS
by killing T-cells directly. This is unlikely for several reasons:
Despite the newly described viremia, the percentage of infected
lymphocytes in AIDS is reported to be only 0.25% (1), far less than
the 5% that is regenerated by the host during the 2 days it takes
a retrovirus to replicate (4,5). Since over 99% of infected T-cells
survive infection and restrict the virus to latency (4,6), at most
1% of .025% or 0.0025% of lymphocytes could be killed every 2 days.
Further HIV, like all retroviruses is not cytocidal (4). It is produced
for "AIDS-testing" in chronically infected, immortal T-cell
lines at much higher titers than are observed in vivo-even now (4).
that all latent parasites, pathogenic or not, are activated by immunodeficiency,
HIV viremia may well be the consequence rather than the cause of
acquired immunodeficiency. Take for example Herpes virus reactivation
upon immunosuppression in humans or radiation induced retroviruses
in animals (4,7). Moreover immunodeficiency occurring only after
extremely long asymptomatic periods, averaging 8-10 years since
infection, cannot be explained in terms of orthodox viral pathology.
All orthodox viruses are most pathogenic soon after infection and
prior to antiviral immunity when they are at the highest rates of
plausible causes for pathogenicity after long asymptomatic periods
are evident in over 90% of those who develop AIDS in the U.S. (8),
namely the intravenous consumption of psychoactive drugs, often
associated with malnutrition and parasitic infections, which is
confirmed in 30% (4,8). Many, perhaps most of the homosexuals who
developed AIDS also have been using drugs (4,8) such as alkyl nitrite
inhalants, which have been directly correlated with the exclusive
incidence of Kaposi sarcomas in homosexuals (4,9,10). Individual
thresholds for intoxication directly explain the long and variable
asymptomatic periods, said to be the latent periods of HIV (4).
Indeed the annual consumption of cocaine alone increased over 5-fold
in the 10 years during which AIDS emerged (11). The most directly
immuno-suppressive drug is the cytotoxic DNA chain terminator AZT,
which is administered since 1987 to 20,000 antibody-positive Amerericans
(12) and to 50,000 world wide (13).
in symptomatic and asymptomatic carriers raises a number of new
a) Why did
numerous prior studies (4) using the methods described now (4,14)
fail to reveal HIV viremia?
b) How can
persons with a positive AIDS-test, which measures neutralizing antibody
(4), have at the same time relatively high titers of HIV?
c) Where would
the relatively high titers of HIV come from, if only <0.0025%
of all lymphocytes are expressing HIV?
d) How can
there be HIV-viremia without p24 antigenemia if p24 is part of HIV?
e) Why only
20 sero-conversions and not one case of AIDS in 2000 healthcare
workers stuck by hypodermic needles used on AIDS patients (4)?
Last it is
reassuring that based on the new data HIV joins the long list of
viruses and other microbes which increase in titer in immunodeficient
patients (4). One paradox resolved!
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T, Alam M. Quantitation of human immunodeficiency virus Type 1 in
the blood of infected persons. N Engl J Med 1989; 321: 1621-1625.
MB, Baltimore D. (editorial) HIV revealed. N Engl J Med 1989;321:
3. Coombs RW,
Collier AC, Allain J-P, Nikora B, Leuther M, Gjerset GF, Corey L.
Plasma viremia in human immunodeficiency virus infection. N Engl
J Med 1989;321: 1626-1631.
PH. Human immunodeficiency virus and acquired immuno-defiency syndrome:
correlation but not causation. Proc Natlk Acad Sci U S A 1989;86:
5. Levy M,
Bandiera A, Forni L and Couthino A. A phenotypic and functional
analysis of longlived B and T lymphocytes. Cell Immun. 1988;117:
SM, Psallidopoulos MC, Lane HC, Thompson L, Baseler M, Massari F,
Fox CH, Salzman NP & Fauci A. The reservoir for HIV-1 in human
peripheral blood is a T-cell that maintains expression of CD-4.
Science 1989;245: 203-208.
7. Gross L.
Oncogenic Viruses (2nd edition) Pergamon Press, New York.
for Disease Control. HIV/AIDS Surveillance. CDC, October 1989.
J and Wilson H. Death Rush, Poppers and AIDS. Pagan Press, New York,
HW, Dougherty JA. Epidemiologic studies-Kaposi's sarcoma vs. opportunistic
infections among homosexual men with AIDS, in Health Hazards of
Nitrite Inhalants, (eds.) Haverkos, HW & Dougherty, JA. National
Institute on Drug Abuse, NIDA Research Monograph 1988;83: 96-105.
11. The National
Narcotics Intelligence Consumers Committee: NNICC Reports 1978-1988.
Office of National Drug Control policy (Executive Office of the
President, Washington DC 20500).
12. Marx, JL.
Drug-resistant strains of AIDS virus found. Science. 1989;243: 1551-1552.
13. Deer, B.
Revealed: fatal flaw of drug that gave hope. Sunday Times (London)
p. 18A, April 16, 1989.
14. Falk LA,
Paul D, Landay A, Kessler H. HIV isolation from plasma of HIV-infected
persons. N Engl J Med 1987;316: 1547-1548.