Reply By Duesberg

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).

3) Considering 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 multiplication.

However biochemically 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).

Further viremia in symptomatic and asymptomatic carriers raises a number of new questions:

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!

Sincerely,

Peter Duesberg

References Cited:

1. Ho DD, Mougdil T, Alam M. Quantitation of human immunodeficiency virus Type 1 in the blood of infected persons. N Engl J Med 1989; 321: 1621-1625.

2. Feinberg MB, Baltimore D. (editorial) HIV revealed. N Engl J Med 1989;321: 1673-1675.

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.

4. Duesberg PH. Human immunodeficiency virus and acquired immuno-defiency syndrome: correlation but not causation. Proc Natlk Acad Sci U S A 1989;86: 755-764.

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: 327-338.

6. Schnittman 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 (2^nd edition) Pergamon Press, New York. 1970.

8. Centers for Disease Control. HIV/AIDS Surveillance. CDC, October 1989.

9. Lauritsen J and Wilson H. Death Rush, Poppers and AIDS. Pagan Press, New York, 1986.

10. Haverkos 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.