The Failure of"New
Victories Against HIV"
A rebuttal to Scientific American's
report on AIDS
David Rasnick submitted the following letter to the Editor of
The special 27-page report entitled "New Victories Against HIV" that appeared in the
July, 1998 issue of Scientific American
is very misleading on several counts, starting with the title. The question is whether
the virus called HIV causes AIDS, as is commonly believed.
The first paragraph of page 81 falsely claims that, "Ten years
ago scientists knew that the disease [AIDS] was caused by HIV."
I am a scientist and the President of The Group for the Scientific
Reappraisal of the HIV Hypothesis of AIDS (The Group for short). I
and my colleagues, numbering in the thousands, are unable to identify
any documents that show AIDS to be a contagious disease and HIV to
be the cause of AIDS. We would appreciate you providing us with the
references to such documentation. Below, I draw your attention to
additional examples of the numerous, unsupported assertions made in
your July 1998 special report.
The section entitled "How HIV Harms," by Bartlett and Moore, begins by stating that
"The virus spreads from one person to another usually through sexual intercourse"
among other ways. This statement is blatantly false since it takes, on average, over
1,000 sexual contacts with an HIV-positive individual for a person to develop antibodies
to HIV (Peterman, 1988; Jacquez, 1994; Padian, 1997). The inefficiency of transmission
reflects the absence of infectious virus, and the tiny percentage of even latently
infected cells (about 1 per 1,000) in antibody-positive persons (Duesberg, 1989; Duesberg,
1992; Duesberg and Bialy, 1996). From 1985 to 1995, the Centers for Disease Control
and Prevention (CDC) estimated a constant level of one million Americans with antibodies to HIV (Curran, 1985;
Duesberg, 1992; Duesberg, 1996; Krieger, 1996). That
means, on average, 260,000 random sexual contacts would be required for the average
American to develop antibodies against HIV.
However, the figures and statistics from the CDC are generally unreliable and contain
contradictions, both internally and also with the orthodoxy, of which the CDC is
a part. According to the CDC, HIV, the putative cause of AIDS, remained constant
in the population during a period when the annual number of new cases of AIDS increased,
reached a peak, and declined. In 1996, the estimated number of HIV positive Americans
was lowered to 650,000-900,000 (Centers for Disease Control and Prevention, 1996).
This new figure was taken from a 1996 publication that estimated the number of people with
antibodies to HIV in the U.S. up to 1992 (Karon et al., 1996). Surprisingly, this
1992 estimate, which the CDC still uses today (Centers for Disease Control and Prevention, 1997), was not based on
the results of the many tens of millions of HIV antibody
tests performed in the U.S. since 1985. In fact, the 1992 estimate conflicts with
the CDC's published results based on the HIV antibody tests. The data from the CDC's
National HIV serosurveillance summary based on over 50 million blood samples tested show
that the number of Americans with antibodies to HIV was 62,000 in 1985 and had declined
steadily to 13,000 by 1993, the last year reported (Centers for Disease Control,
1995). Thus, the CDC continues to use the six-year-old estimate of 650,000-900,000 HIV
positive Americans, which was not based on the results of HIV antibody testing, instead
of the much lower, five-year-old figure based on the results of tens of millions
of antibody tests.
Returning to Scientific American's
special report, in the second paragraph of page 85, Bartlett and Moore state that
HIV kills CD4 T-cells. In the middle of page 86, they say that, "At the cellular
level, scientists also know how HIV invades and destroys CD4 T lymphocytes." No justification is given for these
assertions. Such claims have been made previously, most famously
in articles by Ho and Wei that appeared in a 1995 issue of Nature
(Ho et al., 1995; Wei et al., 1995). But they were immediately criticized on multiple
counts in letters to the editor. For instance, referring to the extremely low levels
of HIV-infected cells of AIDS patients, the HIV researchers Ascher and his associates wrote to
: "The central paradox of HIV pathogenesis remains. It is a murder scene with far
more bodies than bullets" (Ascher, 1995). The viral dynamics presented in the Ho
and Wei papers continue to be criticized, for instance, in Nature Medicine
(Grossman and Herberman, 1997; Gorochov, 1998; Pakker, 1998; Roederer, 1998). According
to Roederer, the two papers by Pakker and Gorochov "provide the final nails in the
coffin for models of T cell dynamics [including Ho and Wei's] in which a major reason for changes in T cell numbers is
the death of HIV-infected cells" (Roederer, 1998).
Moving on to the assertions regarding viral load, the authors state in the middle
of page 87 that, "at any stage, viral levels correlate with prognosis." In March
1997, I attended a conference in Southern California on the Chemotherapy of AIDS
where David Ho introduced the session he was chairing with the words: "High levels of viremia
are not predictive of clinical outcome." Because of this, Ho went on to propose that
the so-called viral set point may better correlate with future disease progression.
However, according to the NIH's "1998 Guidelines to Physicians for the Use of Antiretroviral
Agents in HIV-Infected Adults and Adolescents," the viral set point can only be determined
in asymptomatic individuals who are not taking drugs in order to prevent erroneously high viral load results. This
requirement puts into doubt the reliability
of the viral load test in symptomatic AIDS patients since we don't know what the
test is measuring.
Continuing with viral load, John Mellors' in his contribution to the July 1998 special
report entitled: "Viral load Tests Provide Valuable Answers" states in the second
paragraph of page 90: "From the start, the collective viral population in a patient
generates many billions of new HIV particles a day, resulting in destruction of millions
of CD4 T lymphocytes." This statement is based on the 1995 Nature
papers by Ho and Wei discussed above. To reiterate, there is no documented evidence
to support Mellors' statement, and available scientific literature refutes it (Sheppard,
1993; Wolthers et al., 1996; Grossman and Herberman, 1997; Gorochov, 1998; Pakker, 1998; Roederer, 1998).
Nevertheless, accepting the validity of the unproved viral
load test, Mellors made the portentous statement: "Viral-load measures have therefore
replaced assessment of clinical outcome in therapeutic trials." If Mellors is correct,
then whether patients live longer or do better when taking experimental drugs compared
to drug-free controls is no longer the basis for determining the efficacy and safety
of drugs. This is a frightening prospect.
At the top of page 91, Mellors repeats what he said at the March 1997 conference on
the Chemotherapy of AIDS: "Although the 'field' results have not matched those of
the clinical trials, a 50 percent success rate is still 100 percent better than could
be achieved just a few years ago." This is an admission, which Mellors has made before,
that mono-therapy with AZT and the other DNA chain terminators had not worked, which
he calls "the sins of the past."
A thorough critique of the errors in the July 1998 special report would require a
lengthy report in its own right. Therefore, I will end here, hoping that I have presented
sufficiently significant examples of factual errors to support my claim that the
July 1998 special report is gravely misleading and does a disservice to the general
reader. As President of The Group, I submit this letter for publication in Scientific American
. In addition, I would be happy to have Scientific American's
cooperation in providing a more extensive report from me and some other scientists,
critically reviewing where we stand scientifically with HIV/AIDS.
Sincerely, David Rasnick, PhD, President of The Group
Scientific American has yet to make a decision about publishing this letter. RA will inform readers of any feedback from
Ascher (1995) Paradox remains. Nature 375: 196.
Centers for Disease Control (1995) National HIV serosurveillance summary; update 1993.
US Dept. HHS.
Centers for Disease Control and Prevention (1996) U.S. HIV and AIDS cases reported
through December 1996. HIV/AIDS Surveillance Report: Year end edition 8: 1-39.
Centers for Disease Control and Prevention (1997) U.S. HIV and AIDS cases reported
through December 1997. HIV/AIDS Surveillance Report: Year end edition 9: 1-43.
Curran (1985) The epidemiology of AIDS: current status and future prospects. Science
Duesberg (1989) Human immunodeficiency virus and acquired immunodeficiency syndrome:
Correlation but not causation. Proc. Natl. Acad. Sci. USA 86: 755-764.
Duesberg (1992) AIDS acquired by drug consumption and other noncontagious risk factors.
Pharmacology & Therapeutics 55: 201-277.
Duesberg (1996) How much longer can we afford the AIDS virus monopoly? In: AIDS: virus
or drug-induced?, pp. 241-270, Duesberg, P. (eds.) Kluwer, Dordrecht, Netherlands.
Duesberg (1996) Duesberg and the right of reply according to Maddox-Nature. In: AIDS:
virus- or drug induced?, 5, pp. 111-125, Duesberg, P. H. (eds.) Kluwer Academic Publishers,
Gorochov (1998) Perturbation of CD4+ and CD8+ T-cell repertoires during progression
to AIDS and regulation of the CD4+ repertoire during antiviral therapy. Nature Medicine
Grossman (1997) T-cell homeostasis in HIV infection is neither failing nor blind:
modified cell counts reflect an adaptive response of the host. Nature Medicine 3:
Ho (1995) Rapid Turnover of Plasma Virions and CD4 Lymphocytes in HIV-1 Infection.
Nature (London) 373: 123-126.
Jacquez (1994) Role of the primary infection in epidemics of HIV infection in gay
cohorts. Journal of AIDS 7: 1169-1184.
Karon (1996) Prevalence of HIV Infection in the United States, 1984 to 1992. J. Am.
Med. Assoc. 276: 126-131.
Krieger (1996) 1 in 300 U.S. adults infected, says report. San Francisco Examiner,
July 7, pA8.
Padian (1997) Heterosexual transmission of human immunodeficiency virus (HIV) in Northern
California: results from a ten-year study. Am. J. Epidemiol. 146: 350-357.
Pakker (1998) Biphasic kinetics of peripheral blood T cells after triple combination
therapy in HIV-1 infection: a composite of redistribution and proliferation. Nature
Medicine 4: 208-214.
Peterman (1988) Risk of HIV transmission from heterosexual adults with transfusion-associated
infections. J. Am. Med. Assoc. 259: 55-58.
Roederer (1998) Getting to the HAART of T cell dynamics. Nature Medicine 4: 145-146.
Sheppard (1993) Viral burden and HIV disease Nature (London) 364: 291-292.
Wei (1995) Viral dynamics in human immunodeficiency virus type 1 infection. Nature
(London) 373: 117-122.
Wolthers (1996) T cell telomere length in HIV-1 infection: no evidence for increased
CD4+ T cell turnover. Science 274: 1543-1547.