Path: bloom-beacon.mit.edu!hookup!yeshua.marcam.com!zip.eecs.umich.edu!newsxfer.itd.umich.edu!gumby!wupost!wubios.wustl.edu!not-for-mail From: Michelle Murrain Newsgroups: sci.med.aids,sci.med,soc.motss,bionet.molbio.hiv,soc.answers,sci.answers,news.answers Subject: Sci.med.AIDS FAQ part 3 of 4 Followup-To: sci.med.aids Date: 5 Sep 1994 23:52:09 -0500 Organization: Hampshire College Lines: 693 Sender: sma@wubios.wustl.edu Approved: Yes: Jeff Rizzo ,jfh@netcom.com (Jack Hamilton) Distribution: world Message-ID: <17369@sci.med.aids> Reply-To: aids-request@CS.UCLA.EDU NNTP-Posting-Host: wubios.wustl.edu Xref: bloom-beacon.mit.edu sci.med.aids:6789 sci.med:53815 soc.motss:132729 bionet.molbio.hiv:498 soc.answers:1652 sci.answers:1544 news.answers:25201 ======================================================================= ======= Section 5. The common debates. Q5.1 What are Strecker and Segal's theories that HIV is manmade? Q5.2 Other conspiracy theories. Q5.3 Duesberg's Risk-Group Theory Q5.4 Contaminated polio vaccine? (please contribute) Q5.5 Who is Lorraine Day? (please contribute) ----------------------------------------------------------------------- ------- Question 5.1. 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 5.2. 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 dezinformatsiya 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 rezident 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 5.3. 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). He claims as evidence for his theory: * HIV does not meet Koch's postulates for the causative agent of an infectious disease. * The conversion rate from HIV infection to AIDS depends greatly on the country and risk group membership, so HIV isn't sufficient to cause AIDS. * The HIV virus is minimally active, does not seem to infect many cells, and is suppressed by the immune system, so how could it cause problems? * It takes between 2 and 15 years from HIV infection for AIDS to occur. HIV should cause illness right away or never. * HIV is similar to other retroviruses that don't cause AIDS. There seems to be nothing special about HIV that would cause AIDS. * AIDS patients suffer very different diseases in the US and Africa, which suggests that the cofactors are responsible, not AIDS. * How could two viruses, HIV-1 and HIV-2, evolve at the same time? It doesn't seem likely that two deadly viruses would show up together. Virtually the entire scientific community considers Duesberg's theory unsupportable, although he was a respected researcher before he came out with his theory about AIDS. There is no suggestion that his theories are the result of a political agenda or homophobia. Some of the arguments against him are: * People who receive HIV tainted blood become HIV+ and come down with AIDS. People who receive HIV-free blood don't get AIDS (unless they get HIV somewhere else). Thus, it is the HIV, not the transfusion, that causes AIDS. See also Q2.4 `How risky is a blood transfusion?' for details on how blood transfusions have become less dangerous since HIV antibody testing began. * The risk factors (homosexuality, drug use, transfusions, etc.) have been around for a very long time, but AIDS doesn't show up until HIV shows up. People who engage in homosexuality, drug use, etc. but aren't exposed to HIV don't get AIDS. On the other hand, people who aren't members of "risk groups" but are exposed to HIV get AIDS. Thus, it is the HIV, not the risk factors, that causes AIDS. * With a few recent exceptions, everyone with an AIDS-like immune deficiency tests positive for HIV. Everyone with HIV apparently gets AIDS eventually, after an average of 8 years. * Koch's postulates are more of historical interest than practical use. There are many diseases that don't satisfy the postulates. * It is not understood exactly how HIV causes AIDS, but a lack of understanding of the details isn't a reason to reject HIV. * A recent study by Ascher (see abstract below) matched up people in the same risk groups and found those with HIV got AIDS but those without HIV didn't. More information can be found in published rebuttals to Duesberg, such as in Nature V345 pp.659-660 (June 21, 1990), and in Duesberg's debate with Blattner, Gallo, Temin, Science V241 pp.514-517 (1988). Here are some recent 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. Duesberg, Peter, HIV and the Aetiology of AIDS, Lancet (04/10/93) Vol. 341, No. 8850, P. 957. Because there is no proof that HIV is the cause of AIDS, the hypothesis that drug use leads to AIDS will hopefully become a hindrance to the physiologically (AZT) and psychologically (positive AIDS test) toxic public health initiatives, writes Peter Duesberg of the University of California--Berkeley. In the Lancet's March 13 issue, Schechter et al. call Duesberg's hypothesis that injected and orally used recreational drugs and AZT lead to AIDS, "a hindrance to public health initiatives." However, their hypothesis that HIV is the cause of AIDS has not attained any public health benefits. The U.S. government spends $4 billion annually, but no vaccine, no therapy, no prevention, and no AIDS control have resulted from work on this hypothesis. Schechter et al. conclude that HIV has a key role in CD4 depletion and AIDS based on epidemiological correlations with antibodies against HIV and with self reported recreational drug use among homosexuals from Vancouver. However, their survey neglects to disprove Duesberg's drug-AIDS hypothesis, because it does not provide controls--i.e., confirmed drug-free AIDS cases--and because it does not quantify drug use and ignores AZT use altogether. To refute Duesberg's hypothesis Schechter would have to produce a controlled study demonstrating that over a period of up to 10 years HIV-positive patients who use recreational drugs or AZT or both have the same AIDS risks as positives who do not do so. The 10 year period is claimed by proponents of the HIV hypothesis to be the time needed for HIV to cause AIDS. Alternatively, they could show that HIV-free individuals who have used drugs for 10 years never get AIDS-defining illnesses, concludes Duesberg. Clayton, Julie, Duesberg's Anti-AZT Campaign Continues, Nature (06/24/93) Vol. 363, No. 6431, P. 660. The controversial American molecular biologist who claims that recreational drug use rather than HIV is the cause of AIDS has rejected as a "fabrication" the findings of a recent study designed to disprove his hypothesis. Michael Ascher and colleagues of the California Department of Health Services used data from the San Francisco Men's Health Study to demonstrate that men who were heavy drug users but showed no evidence of HIV infection did not contract the virus, whereas those in the study who were either light drug users, or did not use drugs at all, were shown to be infected with HIV. The study contradicts Peter Duesberg's idea that AIDS is a clinical development of long-term consumption of recreational drugs and of treatment with AZT. But Duesberg said at a recent meeting in London organized by a group known as the Steering Committee Against AZT Malpractice (SCAM), that he refused to accept the group's conclusion, and continued to insist that his own interpretations are sound. He continued to criticize the labeling of one table in the publication of the California study for not indicating the category of "no drug use," and that the paper was therefore invalid. He apparently ignored an explanation in the text that these subjects were represented in the table's category of "light" drug users. In addition, he said that he refused to accept the way that the results of the study were presented in a graph, claiming that "the curve is a fabrication and the conclusions are flawed." Moreover, Duesberg said that the research group's findings could be interpreted to support the opposite conclusion and suggested that there was a 100 percent correlation between AIDS and drug use. 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. THE MISSING FAQ SECTION! by Robert Holzman and David Mertz --------------------------------------------------------- Q: What is AIDS? 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 X.Y: 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. ----------------------------------------------------------------------- ------- Question 5.4. Contaminated polio vaccine? 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