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Section 6. The common debates.

Q6.1	What are Strecker and Segal's theories that HIV is manmade?
Q6.2	Other conspiracy theories.
Q6.3	Duesberg
-----------------------------------------------------------------------
Question 6.1. What are Strecker and Segal's theories that HIV is
manmade? 

Jakob Segal's theory is that HIV was formed from visna (a sheep virus)
and HTLV-I (Human T-cell Leukemia Virus) by US army biological research
labs in 1977 or 1978. The virus supposedly escaped accidentally after
being tested on prisoners.

Robert Strecker's theory is that HIV was formed from visna and BLV
(Bovine Leukemia Virus) by the US in the 1970's after 30-40 years of
work. The virus was supposedly tested on populations in Africa and was
deliberately introduced into the US homosexual community through the
hepatitis B vaccination program.

The alleged evidence to support this theory: 

* Visna is very similar to HIV. HIV can be formed by combining the
genes 
of visna and BLV or HTLV. HIV is not similar to primate viruses. The
government was interested in biological warfare and was planning to
make an immune-system destroying virus. In particular, the DOD
Appropriations for 1970 Hearings, 91st Congress, Part 6, p 129 states: 

There are two things about the biological agent field I would like to
mention. One is the possibility of technological surprise. Molecular
biology is a field that is advancing very rapidly, and eminent
biologists believe that within a period of 5 to 10 years it would be
possible to produce a synthetic biological agent, an agent that does
not naturally exist and for which no natural immunity could have been
acquired.

Mr. Sikes. Are we doing any work in that field? 

Dr. MacArthur. We are not.

Mr. Sikes. Why not? Lack of money or lack of interest? 

Dr. MacArthur. Certainly not lack of interest. 

[MacArthur provides the following information:] 

The dramatic progress being made in the field of molecular biology led
us to investigate the relevance of this field of science to biological
warfare. A small group of experts considered this matter and provided
the following observations:

* All biological agents up to the present time are representatives of 
naturally occurring disease, and are thus known by scientists
throughout the world. They are easily available to qualified scientists
for research, either for offensive or defensive purposes. 

* Within the next 5 to 10 years, it would probably be possible to make
a 
new infective microorganism which could differ in certain important
aspects from any known disease-causing organisms. Most important of
these is that it might be refractory to the immunological and
therapeutic processes upon which we depend to maintain our relative
freedom from infectious disease.

* A research program to explore the feasibility of this could be 
completed in approximately 5 years at a total cost of $10 million.'' 

* HIV is a new disease that appeared suddenly in the late 1970's
without a 
natural source.

* HIV could have been easily synthesized in a laboratory in the 1970's.

The evidence is overwhelmingly against these theories. The key problem
with these theories is they arose in the early 1980's, before SIV
(simian immunodeficiency virus) was discovered and before the relevant
viruses were sequenced. The genetic sequences clearly show: 

* HIV is much closer to SIV (simian immunodeficiency virus) than HIV is
to 
visna, BLV, HTLV or any other known virus. 

* HIV can't be formed from splicing together parts of other known
viruses. 

Viral genetic sequences can be ftp'd from ncbi.nlm.nih.gov in
repository/aids-db.

To summarize the other arguments against Strecker and Segal's theories:

* The military testimony described a future study to see if making a
new agents was feasible, not to actually produce it. More importantly,
they are looking for an agent refractory to immunological processes;
this means something resisting immunological processes. The quoted
testimony and other parts of the testimony state they are looking for a
new agent for which people do not have natural immunity; this is
entirely different from an agent that destroys the immune system. It is
also much easier than producing something like HIV. 

* Most scientists believe HIV evolved from SIV or a close relative. HIV
did not suddenly appear in the late 1970's, but has been found in
preserved blood samples from the 1950's. 

* Biotechnology was not sufficently advanced in the 1970's to produce
something like HIV, and it is debatable that it would be possible even
now. Since the details of HIV are not understood even now, it is
inconceivable that someone could have deliberately designed HIV in the
1970's.

Strecker's claim that HIV was introduced via hepatitis B vaccinations
is extremely doubtful. McDonald et al, Lancet, 1983 Oct 15,
2(8355):882-4 state the incidence of AIDS in unvaccinated sexually
active homosexual men was _higher_ than in vaccinated men, although the
rates were too low for statistical significance. Stevens et al, JAMA,
1986 April 25, 255(16):2167-2172 tested blood samples from the
beginning of the vaccination program and found that 6.6% were already
HIV-positive. Therefore, HIV couldn't have been introduced via the
vaccinations. 

While evaluating these theories, I recommend treating Segal's and
Strecker's literature citations with extreme skepticism, as they are
both rather casual about the connection between their claims and the
contents of the papers. In particular, Strecker provides quotes that do
not appear in the cited papers.

Finally, since both theories allege a coverup of the connection between
visna and HIV, a clear explanation of their relationships may be
helpful. The viruses described above are all retroviruses. Retroviruses
have three subfamilies: Oncoviruses, Lentiviruses, and Spumaviruses.
HTLV is a oncovirus, while the remainder are lentiviruses. The analysis
of genetic sequences gives strong evidence for the evolution of
lentiviruses. They apparently branched into the primate lentiviruses
(HIV-1, HIV-2, and SIV), and the nonprimate lentiviruses (visna, BLV,
EIAV, FIV, CAEV, etc.) Thus, HIV and visna have many similarities since
they are both lentiviruses, but HIV and SIV are much more similar. (See
Fields Virology for more information on retrovirus classification and
"The Emergence of Simian Human Immunodeficiency Viruses", Myers et al,
AIDS Research and Human Retroviruses, 8(3), 1992 373-386 for more
information on lentivirus evolution.)
---------------------------------------------------------------------
Question 6.2. Other conspiracy theories. 

One school of thought holds that the "AIDS was a U.S. biological
warfare experiment" myth was extensively spread as part of a
disinformation campaign by Department V of the Soviet KGB (their
`active measures' group). They may not have invented the premise
(Soviet disinformation doctrine favored legends originated by third
parties), but they added a number of signature details such as the name
of the supposed development site (usually Fort Meade in Maryland) which
still show up in most retellings.

According to a defector who was once the KGB chief resident in Great
Britain, the KGB promulgated this legend through controlled sources in
Europe and the Third World. The Third World version (only) included the
claim that HIV was the result of an attempt to build a "race bomb", a
plague that would kill only non-whites.

From the CDC AIDS Clearinghouse:

"Soviets Secretly Tried to Blame U.S. for AIDS--CIA" Reuters (09/30/93)

Langley, Va.--For more than five years, the former Soviet Union
attempted to blame the AIDS virus on a plot by U.S. military
scientists, according to newly declassified CIA documents. The papers
reported that the Soviets launched a campaign in 1983 aiming to tie the
emergence of AIDS to American biological weapons research. The
disinformation was circulated in 25 different languages in over 200
publications, as well as in posters, leaflets, and radio broadcasts, in
more than 80 countries before the campaign was finally abandoned by the
Soviets, according to a study cited by the CIA in the documents. The
Soviets dropped the campaign in 1988 when the United States refused to
cooperate with them on a research program on AIDS, which was by then
spreading in the U.S.S.R., said the CIA article. The Soviet campaign
was apparently retaliation for the Reagan administration's claims of
Soviet-produced "yellow rain," or yellow traces found on vegetation due
to a Soviet biological weapon. 

Reproduction of the above excerpt is encouraged; however, copies may
not be sold, and the CDC Clearinghouse should be cited as the source of
this information. Copyright 1993, Information, Inc., Bethesda, MD 
---------------------------------------------------------------------
Question 6.3. Is HIV the cause of AIDS?

The following discussion is excerpted from the sci.skeptic ``Frequently
Questioned Answers'' posting.

The generally accepted theory is that AIDS is caused by the Human
Immunodeficiency Virus (HIV). There are two different versions of HIV:
HIV-1 and HIV-2. These viruses are believed, on the basis of their
genetic sequences, to have evolved from the Simian Immunodeficiency
Virus (SIV), with HIV-2 being much more similar to SIV. Several years
after the initial HIV infection, the immune system is weakened to the
point where opportunistic infections occur, resulting in the syndrome
of AIDS. A good reference for more information on the "mainstream" view
of AIDS is: 

The Science of AIDS: readings from Scientific American magazine. New
York: W.H. Freeman, c1989.

Peter Duesberg has promulgated this theory: HIV is a harmless
retrovirus that may serve as a marker for people in AIDS high-risk
groups. AIDS is not a contagious syndrome caused by one conventional
virus or microbe. AIDS is probably caused by conventional pathogenic
factors: administration of blood transfusions or drugs, promiscuous
male homosexual activity associated with drugs, acute parasitic
infections, and malnutrition. Drugs such as AZT promote AIDS, rather
than fight it. His theory is explained in detail in "Human
Immunodeficiency Virus and Acquired Immunodeficiency Syndrome:
Correlation but not Causation", Proc. Natl. Acad. Sci. USA V86
pp.755-764, (Feb. 1989). 

Other references to Duesberg's theory: 

Kolata, Gina, Debunking Doubts That H.I.V. Causes AIDS, New York Times
(03/11/93), P. B13.

A team of California researchers has disproved a theory claiming that
recreational drug use, and not HIV, is the cause of AIDS. The
scientists reported in a commentary published today in Nature that
their research shows no relationship between recreational drug use,
excluding IV-drugs, and the development of AIDS. The research team was
led by Dr. Michael S. Ascher, an immunologist at the California
Department of Health Services, and Dr. Warren Winklestein Jr., an
epidemiologist at the University of California--Berkeley. Dr. Ascher
and colleagues wrote their paper in response to a challenge by Tom
Bethell, a media fellow at the Hoover Institution at Stanford
University, to compare people who used drugs with those who didn't and
to determine whether those who took drugs had a higher incidence of
AIDS. Bethell wrote in an article in the San Francisco Chronicle of the
theory proposed six years ago by Dr. Peter H. Duesberg, a molecular
biologist at the University of California--Berkeley. Duesberg argues
that HIV is not the cause of AIDS and that the drug AZT speeds, rather
than slows, the depletion of the immune system. Bethell asked why no
research had been done on this hypothesis. Therefore, Dr. Ascher et al.
retested their hypothesis of the analysis of the San Francisco Men's
Study, a group of 1,034 randomly selected single men who lived in San
Francisco and were 25-54 years old in 1984, when the study began. The
researchers found that homosexuals and heterosexuals in the study were
equally likely to use drugs. However, 26 percent of homosexuals
developed AIDS, whereas none of the heterosexuals did. All of the men
were infected with HIV, but there was no link between drug use and
AIDS. Related Story: Wall Street Journal (03/11) P. B5 

Ascher, M.S. et al., Does Drug Use Cause AIDS?, Nature (03/11/93) Vol.
362, No. 6416, P. 103.

Although Peter Duesberg, a professor of molecular biology at the
University of California--Berkeley, believes that AIDS and drug use are
related, they are not, writes M.S. Ascher et al. of the California
Department of Health Services in Berkeley, Calif. Duesberg has
maintained since 1987 that HIV is not the infectious aetiological agent
for AIDS and has recently stated that either drug consumption or
conventional clinical deficiencies and their treatments cause
AIDS-related illnesses. However, the researchers found this untrue.
They analyzed data from a unique population-based cohort study, the San
Francisco Men's Health Study (SFMHS). It is based on a randomly
selected cohort of 1,027 single men 25-54 years old. The researchers
examined the cohort at 6-month intervals for 96 months, and obtained
drug-use data and determined HIV serostatus at each examination. The
researchers compared heavy drug use for the 25-months period before
entry into the study among 215 heterosexual and 812 homosexual/bisexual
cohort members. Except for amyl nitrate, with 18 percent heavy use in
homosexuals versus no heavy use among heterosexuals, the percentage of
subjects reporting heavy use of each drug was similar in both sexual
preference groups: 36 versus 39 percent for marijuana; 7 versus 4
percent for cocaine; and 1 versus 5 percent for amphetamines,
respectively. During the 96 months of follow-up, 215 cases of AIDS
occurred among the homosexual/bisexual men compared with none among the
heterosexuals. It was found that if heavy use of marijuana, cocaine or
amphetamines is casually linked to AIDS, a cumulative incidence of 56
cases among the heterosexual subjects would be expected. 

Maddox, John, Where the AIDS Virus Hides Away, Nature (03/25/93) Vol.
362, No. 6418, P. 287.

Because of the new findings that HIV replicates in the lymph nodes
while in the so-called latent period, Professor Peter Duesberg of the
University of California--Berkeley may want to change his position,
writes John Maddox of Nature. Duesberg has held that drug taking is
responsible for AIDS, and not HIV. Most viruses are DNA viruses, which
ordinarily replicate within cells by hijacking the preexisting
machinery of DNA transcription and translation. But the genomes of
retroviruses, like HIV, by contrast, consist of RNA. Those of the
lentiviruses, of which HIV is one, come equipped with a gene specifying
a reverse transcriptase (for converting RNA into the complementary
DNA). While the RNA genome may be used, as if it were one of the
infected cell's own messenger molecules, to generate the proteins that
would allow an intact virus particle to be regenerated, by far the more
efficient means of replication is that DNA complementary to the viral
RNA should be incorporated in the genome of the cell, where it will
serve as a template for the production of its own genomic RNA and thus
for intact viral particles. Duesberg claims that it is difficult to
recover from helper T lymphocytes, whose attrition for many patients
indicates the onset of overt AIDS, virus particles that might plausibly
infect others. The new findings show that the virus is alive and well
in the lymph nodes, among other locations, of those infected with HIV.
The recent revelations suggest that, nevertheless, the alternatives for
AIDS patients are even less justifiable than seemed likely a few years
ago. Duesberg should now admit the possibility that he has been
mistaken, concludes Maddox.

Q: What is AIDS?
by Robert Holzman and David Mertz
--------------------------------------------------------- 

The immune system is responsible for defending the body against
bacteria, parasites, viruses and cells identified as foreign such as
virally infected, transplanted, and (many believe) malignant cells. The
Acquired Immune Deficiency Syndrome (AIDS) is a condition in which a
person's immune system is so weakened that s/he becomes susceptible to
conditions that occur rarely in those with intact function. The formal
case definition includes a large number of indicator diseases deemed,
in the words of the original: "at least moderately predictive of
cellular immune deficiency". This original definition, free of
assumptions regarding etiology, has been modified in accordance with
the general acceptance of HIV as the causal agent responsible for the
vast majority of AIDS cases. The revised definition also includes
certain conditions believed ascribable to advanced HIV infection itself
(e.g. wasting). A concise summary of the 1993 case definition may be
found in the textbook, Scientific American Medicine section 7, chapter
XI, page 2.

Q: Why is HIV considered to be the cause of AIDS? 

The epidemic occurrence, in 1980, of Kaposi's Sarcoma in homosexual men
and, in 1981, of certain unusual infections in intravenous drug users,
were unprecedented events. While all of the initially recognized
diseases were previously known, and most were occasionally seen in
persons who were ostensibly immunologically normal, the risk of
developing them was strongly associated with the presence of an
immunosuppressed state, generally due to therapy for cancer or
suppression of graft rejection. In order to identify cases for study
and comparison with noncases, an operational definition was developed
(see the FAQ question What is AIDS?) The issue for investigators was
why so many homosexual men and intravenous drug users were developing
such severe immune suppression now, while previously only subtle
defects in immunity had been seen in such individuals. 

Among the earliest suggestions of an infectious etiology was the report
(published in Am. J. Med. 1984;76:487-492, but presented orally
earlier) that cases of AIDS among homosexuals were not occurring
randomly but were clustered among sexual contacts. 40 persons were
identified who showed linked transmission over 3 generations of
infection. At the time there were four major theories of etiology under
investigation: (1) multiple and repeated infections with
Cytomegalovirus leading to immune suppression, (2) immunologic
exhaustion from multiple previous infections, (3) alloimmunization to
lymphocytes, due to intra-rectal injection of sperm, and (4) toxic
effects of components of inhalant drugs or genital lubricants. Theories
2-4 were incompatible with the observed pattern of transmission. No
credible evidence for theory 1 was ever produced. 

Three laboratories, Gallo's at NIH, Levy's at UCSF, and Montagnier's at
Institute Pasteur (listed alphabetically), almost simultaneously
identified a retrovirus in AIDS patients which was ultimately named the
Human Immunodeficiency Virus (HIV). The identification of infection
with this retrovirus in most (and with subsequent improvements in
technique, in almost all) persons with AIDS who were tested raised the
question whether this virus was a harmless infector, an opportunistic
pathogen, or the actual causal agent of the progressive
immunosuppression. Some of the evidence for the last role is summarized
below.

First, HIV causes a distinct acute illness (the "primary infection")
which has been characterized in otherwise healthy
(non-immunosuppressed) individuals known to have been or suspected of
having been infected at a particular time (e.g. in a laboratory
accident) or in whom the appearance of serum antibodies was detected,
indicating a recent infection. An causal role for HIV in subsequent
immune suppression is suggested by the fact that those whose symptoms
of primary infection last more than 14 days subsequently develop AIDS
more rapidly than persons who have briefer periods of illness. (Br. Med
J. 1989;299:154-157.)

Second, HIV infects cells with the CD4 receptor on their surface, cells
which are critical for immune function and which, in those with AIDS,
are abnormal in function, number, or both. (For a discussion of current
concepts of the pathogenesis of HIV-related immune suppression see
Science 1993; 262:1011-1018.)

Third, HIV infection antedates immune suppression and is the single
factor common to all AIDS risk groups. Studies of stored blood indicate
that HIV spread in the homosexual population of San Francisco a few
years before the epidemic of AIDS-indicative conditions. Moreover, in
cases where the date of infection is known exactly or approximately,
acquisition of HIV infection precedes the development of immune
suppression by substantial periods. Such situations include, for
example, transmission by transfusion to adults having cardiac surgery
or neonates with hemolytic disease, by breast milk to neonates
(including breast milk of a wet nurse to a child without familial risk
factors), by clotting factor concentrates to hemophiliacs, by
parenteral exposure of laboratory technicians or physicians to blood or
viral concentrates, and to spouses of HIV infected persons via sexual
transmission. Most telling is the observation that among infants of
HIV-infected mothers, only those that acquire HIV infection develop
progressive immune suppression and AIDS defining illnesses.

Not all accept the causal association between HIV and the immune
suppression that leads to an AIDS indicative illness. Peter Duesberg, a
retrovirologist at the University of California at Berkeley has been
the most vocal scientific critic of this hypothesis. Few of those
actively engaged in research on AIDS agree with Duesberg's analysis,
and rebuttals may be found in Nature 1990; 345:659-660 and Science
1988; 241:514-517. At least one study (M.S.Ascher, Nature, 1993;
362:103) has been designed in response to his assertions that drug use
was a major cause of AIDS associated immune suppression. In that study,
cohorts of homosexual and heterosexual men were compared, matched for
use of marijuana, cocaine or amphetamines. There was no association
between the development of AIDS and use of these drugs. The homosexual
cohort used more nitrites than did the heterosexual one, but
development of AIDS was related to the presence of HIV infection and
not to use of drugs (M.S. Ascher, Lancet, 1993; 341:1223).

Those who believe that HIV causes AIDS look to the cases associated
with transfusion, congenital infection, or sexual transmission as
coming as close to Koch's postulates as is likely to be possible in
humans. In the absence of an animal model in which HIV induces immune
suppression, it is likely to be impossible to strictly fulfill Koch's
Postulates for HIV and AIDS.

As the reader studies the debate on the cause of AIDS and forms his/her
own conclusions it is important to focus clearly on the arbitrary
nature of the case definition as an operational way to detect severe
immune deficiency. Even the 1993 revision of the AIDS case definition
does not require the documented presence of HIV infection. It is
logically possible for there to be more than one etiology, although
published data (New Engl. J. Med, 1993; 328:373-379.) indicate that
only 299 of 230,179 reported persons with AIDS have been HIV-negative
when testing was done (Evidence of HIV infection was sought in
approximately half the 230,179 (Duesberg, Science, 1992;257:1848)).

In summary, to assert that HIV is the cause of AIDS is to assert that
HIV was the cause of the epidemic of immune suppression that appeared
in 1980-81. To ascribe this role to HIV it is not necessary to show
that HIV is the only cause of immunosuppression in those at risk, nor
that cofactors are unimportant in the development of AIDS, nor that
every patient who meets the case definition has HIV infection. It is
only necessary to show that HIV infection can result in immune
suppression and that HIV infection occurred in the appropriate
population at an appropriate time to account for the epidemic. 

Q: What is the evidence against HIV as the cause of AIDS? 
(see also Section 7.4: The Group for the Scientific Reappraisal of the
HIV/AIDS Hypothesis)

There are many PWA's and AIDS-activists, and many in the scientific
community who remain doubtful that HIV causes AIDS. These doubts arise
both from observers of the socio-political history of HIV/AIDS, and
from some scientists knowledgeable about retroviruses, epidemiology and
immunology.

DOUBTS RELATED TO THE SOCIAL HISTORY OF HIV/AIDS Some social critics
raise questions about the circumstances in which the HIV/AIDS
hypothesis was made public: After a decade of a massively funded, but
predominantly unsuccessful, search for viral causes of cancer, in 1984
then Secretary of Health and Welfare Margaret Heckler declared to the
national press that an *American* discovery of the (probable) viral
cause of AIDS had been made -- without a single peer reviewed article
on HIV having appeared. Quickly thereafter, the word "probable" was
dropped by the press, and virtually all scientific monies for AIDS
research were directed towards HIV. Continuing this trend, suspicious
dealings between the US government and Burroughs Wellcome assured the
approval and usage of the "anti-viral" drug AZT. In an ad hoc manner,
many HIV-scientists thereafter conveniently rejected Koch's Postulates
in defense of the HIV/AIDS hypothesis. References: John Lauritsen's
1993 _The AIDS War_ (Asklepios, New York, ISBN 0-943742-08-0), Jad
Adams' 1989 _AIDS: The HIV Myth_ (St.Martin's Press, New York, ISBN
0-312-02859-8), and Jon Rappoport's _AIDS Inc._ (Human Energy Press,
San Bruno CA 94066.) 

DOUBTS ABOUT THE SCIENTIFIC VALIDITY OF THE HIV/AIDS HYPOTHESIS Were
the only doubts about HIV causation of AIDS those surrounding the
"context of discovery," these doubts would be of little interest to
anyone but historians of science. The main doubts raised by HIV-
skeptics are on the actual scientific evidence for the HIV/AIDS
hypothesis. HIV-skeptics consider this evidence to be either weak or
non-existent. Beyond the generic concern which HIV-skeptics have that
no mechanism for the alleged action of HIV has been demonstrated, the
skeptics raise several more specific problems concerning the HIV/AIDS
hypothesis. These problems fall into two major categories:
Epidemiological and Immunological/Biochemical. Two general starting
references to HIV-skeptics are: Robert Root-Bernstein's 1993,
_Rethinking AIDS_ (Free Press, New York, ISBN 0-02-926905-9), and Peter
Duesberg's article "AIDS Acquired by Drug Consumption and Other
Noncontagious Risk Factors", _Pharmoc Ther_ v.55 p.201-277, 1992. 

DOUBTS BASED ON EPIDEMIOLOGICAL DATA
First, HIV and HIV-antibodies are undetectable in a significant
percentage of AIDS cases. The exact number of such cases is disputable,
and many AIDS cases are simply never tested for HIV or HIV-antibodies:
estimates of HIV-negative AIDS cases generally range between 2% and 10%
of AIDS cases. Furthermore, Duesberg and others argue that
AIDS-defining diseases themselves occur in a large number of people who
are not defined as AIDS-cases because of their HIV- negative status.
From a philosophical point-of-view it doesn't matter what the exact
percentages are: If both AIDS itself, and AIDS- defining diseases,
occur without HIV, then HIV cannot be the sole cause of AIDS, though it
is possibly one among many contributing causes in those who are HIV+.

Second, virtually all, if not all, of those who suffer from AIDS have
been exposed to MANY immunosuppressive risks besides HIV, even if most
have, indeed, also been exposed to HIV. Many pathogens such as
Hepatitis viruses, Herpes viruses including Cytomegalovirus, Herpes
simplex, Treponema pallidum, the cause of Syphilis, Epstein-Barr Virus,
Mycobacteria, and others, are just as prevalent in AIDS- patients as is
HIV. Further, simultaneous infection with a broad spectrum of these
pathogens occurs only in those populations at high- risk for AIDS.
HIV-skeptics do not believe that any epidemiological evidence exists to
single out HIV from the other pathogens characteristic of AIDS. It is
likely, they argue, that AIDS-defining immune-suppression is caused by
the cumulative effect, or by specific synergistic interactions, of
these other pathogens. In addition, virtually all AIDS-patients have
been exposed to drugs with known immunosuppressive effects, whether
medically indicated, recreational, or both. These exposures include the
usage of opiates (medically and recreationally), nitrites, cocaine,
chronic high-dosage antibiotics, and chemotherapeutic agents. Finally,
virtually all AIDS-patients have been exposed to large amounts of
foreign antigenic tissue, whether blood products, lymphocytes or semen.
Such exposure is known to trigger auto-immunities similar to those
present in AIDS. 

DOUBTS BASED ON IMMUNOLOGICAL AND VIROLOGICAL DATA First, HIV is
non-viremic and chemically inactive in those infected, even those
suffering acute immune-suppression. Skeptics argue that the rate of
infection of T-cells by HIV is so low that even were HIV to kill every
cell it infects, the human body would have no difficulty replenishing
those cells. Even so, retroviruses, including HIV which has been
continuously grown in the same cell-line since 1984, have never been
shown consistently to kill host-cells. Estimates of the exact rate and
location of T-cell infection vary, but no estimates place the rate of
infection high enough to suggest a serious HIV threat to the immune
system, even in the lymphatic system where HIV may be present in higher
numbers than in blood. 

Second, in response to skeptics' objections about rates of T-cell
infection, HIV-scientists have proposed a pathogenesis of AIDS in HIV
triggered auto-immunities, caused by the similarity of HIV surface
proteins to those of immune system cells. However, CD4 homologies by
which HIV is alleged to cause auto-immunity or immune-system
malfunction also exist for many other pathogens/foreign tissue than HIV
-- including many pathogens common in AIDS-patients. No basis has been
demonstrated, nor plausibly hypothesized, which singles out HIV/T-cell
homologies from other homologies as a mechanism of auto- immune
reactions.

Third, the long "latency period" between HIV infection and the
development of AIDS is unlike the behavior of all other viruses, and
contradicts established retrovirology. To skeptics, this latency is
little more than an article of faith by HIV/AIDS hypothesizers. Put
simply, viruses don't cause disease after long latencies, except when
reactivation of a latent virus is triggered by external immune-
suppression. In all known viruses, production of antibodies neutralizes
the action of the virus, and the virus is eliminated or brought into
remission. Exactly the opposite is postulated for HIV; but since no
mechanism has been plausibly described for this, little can be argued
about it than one's prior convictions about HIV/AIDS causation.