A Brief History of AIDS: The Signatures and The Syndrome

In 1981, on June 5, “Pneumocystis Pneumonia–Los Angeles,” by Dr. Michael Gottlieb and colleagues of University of California at Los Angeles, appeared in Morbidity and Mortality Weekly Report (vol. 30, pp. 250-52), a Centers for Disease Control and Prevention (CDC) publication. This was the first article about AIDS in the medical literature. In July of that same year, a Task Force on Kaposi’s Sarcoma and Opportunistic Infections was established at the CDC under the direction of Dr. James Curran [1].

According to Dr. Gallo and Dr. Montagnier, their work together was open and collaborative and established that AIDS or pre-AIDS exhibited a consistent molecular signature [2]. This signature was first called lymphadenopathy-associated virus (LAV) and Human T-cell-lymphotropic virus type III (HTLV-III), and then, Human Immunodeficiency Virus (HIV). Because of the significance of these initial observations, I include here several paragraphs from a recent NEJM article written jointly by Gallo and Montagnier [2]. I will then review nine other hypotheses regarding the pathogenesis of AIDS, and then review some of the successes that the “HIV=AIDS” hypothesis has achieved:

“The story began in an unfavorable environment: during the late 1970’s, many people thought that epidemic diseases caused by microbes, including viruses, no longer posed a threat in industrialized countries. Other prevailing beliefs were that viruses did not cause any human cancer and that there was no such thing as a retrovirus that infected humans. Some of these beliefs were justified, since attempts to find tumor viruses and, in particular, retroviruses in cancers and other diseases in humans had a troubled history, and many of the groups that had the greatest expertise in the study of retroviruses had turned their efforts toward research on oncogenes. Luckily, and rather amazingly, however, the conceptual and technical tools arrived in our hands just before the first patients with AIDS were identified in 1981. In addition, there remained a few heretical or “old-fashioned” groups-among which were our two laboratories-that persisted in searching for retroviruses in human cancers, particularly breast cancers and leukemias. This search finally paid off with the discovery of human T-cell leukemia virus types 1 and 2 (HTLV-1 and HTLV-2), the first of which was shown to cause an unusual T-cell leukemia. This discovery was made possible by 15 years of basic research on leukemogenic retroviruses in animals, including the design and development of highly sensitive biochemical assays that were based on reverse transcriptase-the enzyme that is present in all retroviruses, which was discovered in 1970 by Temin and Baltimore.”

“An additional important contributor was the development of methods for growing T lymphocytes in culture for a period sufficient to allow the expression of putative latent retroviruses. This effort was helped greatly by the isolation of specific factors-in particular, the T-cell growth factor (now called interleukin 2) in Bethesda, Maryland. The role of interferon in repressing the production of retroviruses in mouse cells was demonstrated in Paris, and this discovery led to the use of anti-interferon serum in the search for human retroviruses. Thus, at the beginning of the 1980’s, we had the essential tools required to search for a retrovirus in this new and menacing disease called AIDS. But why search for a virus, and specifically a retrovirus, in AIDS? The answer was far from obvious in 1982.”

“At that time, AIDS had already appeared as a long-lasting disease, with an extremely long lag time between exposure to the agent (through blood or sexual activity) and the profound state of immune suppression characterized by the occurrence of opportunistic infections or cancers. Many factors-fungi, chemicals, and even an autoimmunity to leukocytes-were invoked at that time as possible causes. However for us, there were clues. First, the various manifestations of AIDS were unified by a biologic marker: a decrease in the levels of a specific subgroup of T cells that harbored the CD4 surface antigen. CD4 and other CDs had been identified only a few years earlier with the use of specific monoclonal antibodies, thanks to the work of Milstein and Kohler. The findings regarding the T cell subgroup suggested an agent that specifically targeted CD4+ T cells, and HTLV (the putative cancer causing virus) was one such agent. Moreover there were animal models in which lymphotropic retroviruses caused not only leukemias or lymphomas, but also an AIDS-like wasting syndrome. Furthermore, HTLV was transmitted through blood and sexual activity, as well as from mother to infant, which was consistent with some of what we learned early on about the epidemiology of AIDS. Finally, the Centers for Disease Control and Prevention (CDC) reported cases of AIDS in patients with hemophilia who had received only filtered clotting factors, which seemed to eliminate the possibility that the agent was a microorganism larger than a virus.”

“This set of arguments convinced us, as well as Max Essex in Boston, each independently to start a search for an HTLV-like virus in patients with AIDS. We began conducting this research at the National Institutes of Health in Bethesda and at the Pasteur Institute in Paris. The theory that a retrovirus caused AIDS was correct, but the hypothesis that it was a close relative of HTLV proved to be wrong. In Bethesda, an earlier survey involving the use of molecular and immunologic probes seemed to favor a variant similar to HTLV-1 (the putative cancer virus). In fact, some patients with AIDS were doubly infected with HTLV-1 and the new agent, which complicated the interpretation of the nature of the virus causing AIDS.”

In January of 1983, the CDC met with blood banking organizations in Atlanta to discuss proposals to screen out individuals at high risk for AIDS from the blood donor pool. Self-identification through questionnaires or interviews was proposed. In March of 1983, the CDC published guidelines adopted by the PHS requesting members of groups having increased risk for AIDS to refrain from donating blood [1].

By May of 1983, the research group of Luc Montagnier published that LAV’s signature was associated with lymphadenopathy [3]. The Sinnousi et al., paper was at first rejected. However, the paper was accepted and published with the help of Robert Gallo, who shepherded the paper through to publication (personal communication), and who as a collaborator maintained close contact with the Montagnier group both before and after the rejection of the paper, as they shared samples, technical training (Barre-Sinoussi received training in Gallo’s lab), and hypotheses regarding AIDS and retroviruses.

Gallo and Montagnier also claimed in the 2003 NEJM article that [2]:

“In early 1983, a clear-cut isolate was obtained in Paris, with the help of interleukin-2 and anti-interferon serum, from cultured T-lymphocytes derived from a lymph-node-biopsy specimen from a patient with lymphadenopathy, a syndrome that was considered to be a precursor of AIDS. This virus proved to be different from HTLV in terms of antigenicity and morphology, but it could be propagated only in fresh cultures of T lymphocytes and not in permanent T-cell lines, which impeded its full characterization. The idea that the causative agent of AIDS should be sought in swollen lymph nodes was partly right, since we now know that lymph nodes are the main site where the virus hides during the presymptomatic phase. At this early stage, it seemed more likely that the isolate was causative than that it was opportunistic, since the immunosuppression was very mild. In some ways, however, it was also a misleading idea that delayed the full characterization of the virus and its mass production for seroepidemiologic studies, because only some viral isolates from patients with fully developed AIDS grow quickly in permanent cell lines, as we would soon learn.”

“This technical breakthrough was first achieved in late 1983 in Bethesda. Among a few strains in the Bethesda laboratory that grew in continuous cell lines, one came, unbeknownst to both of us, from the third isolate from a patient with Kaposi’s sarcoma in Paris. The origin of the HIV strain with a very high capacity for growth that could readily overcome other HIV strains in culture-and which contaminated cell cultures in several laboratories, beginning with both of ours-was unraveled only in 1991, thanks to the use of the polymerase-chain reaction-technique.”

However, The Pasteur Institute’s Patient One didn’t have AIDS. Patient One had sought medical consultation for swollen lymph nodes, muscle weakness without fever or weight loss, and for at least two episodes of gonorrhea. The year before, he was treated for syphilis, which for decades, has been known as “the great imitator:”

“The patient will complain of rashes, fever, itching, sore throat, headache, malaise, vertigo, sweating, insomnia, nausea, prostration, weight loss, loss of hair, or aching in the bones and joints. Some have hypertension, kidney disease, swollen liver, or swollen spleen; others have a subacute meningitis with cranial nerve involvement. This stage of syphilis is often confused with such conditions as infectious mononucleosis, iritis, neuroretinitis, lichen planus, cancer, nephritis, dementia, lymphomas, psoriasis and other skin eruptions, and even drug reaction. For this reason secondary syphilis is called the great imitator” [4].

“The Treponema pallidum acts specifically against the thymus gland. The thymus dependent parts of the lymphatic system deteriorate, and there is consequent decrease in the numbers of T-lymphocytes. The T-helper cells are particularly affected by this: there is a decline in their number and the ratio with the T-suppressor cells is reversed. Consequently, a long-term effect of syphilis is loss of, or decline in, the system of immunity, and lowering of the individuals capacity to defend himself against other infectious conditions” [4].

The Pasteur Institute’s Patient One also tested positive for antibodies to three different viruses: cytomegalovirus (CMV), Epstein-Barr virus, and Herpes [3]. Because of these symptoms, Patient One was diagnosed with pre-AIDS or ARC, and not what would be described later as classic, full-blown AIDS. The 1983 paper describing the characterization of Patient One’s sera was thus derived from biochemical data, in vitro culturing data using stimulated primary lymphocytes exposed to Patient One’s serum, electron microscopy of cultures exhibiting the molecular signature of “HIV,” and serology from the sera derived from Patient One and several other potential AIDS patients. The characterization of the sera from this ARC patient (as well as several other patients) was principally carried out using PHA and IL-2-stimulated primary lymphocyte cultures to which were serially added fresh, “uninfected” lymphocytes. This strategy was employed in order to propagate the production of a possible lymphocyte-tropic virus that may be present. However, this method was “inefficient,” and it was believed and later shown by the Gallo group that permanently growing infected cell lines would be a more efficient way to amplify the minute molecular signature that Montagnier’s group associated with LAV’s molecular signature.

By November of 1983, the CDC published formal recommendations for the protection of laboratory and clinical personnel having contact with AIDS patients and clinical specimens. The recommendations were based on those for hepatitis B [1].

In April of 1984, amidst a climate of extreme urgency and fear, and to assure the public that government scientists were attempting to protect the blood supply from spreading a potential causative microbe in 1984, HTLV-III (later called “HIV-1”) was introduced at a press conference given by Margaret Heckler, as being “a variant of a known human cancer virus,” and it was announced that “HTLV-III” was “the probable cause” of AIDS. In May, four papers from Dr. Gallo’s laboratory demonstrating that the HTLV-III retrovirus was the cause of AIDS were published in Science. These are the 4 papers that established that “HIV’s” signature was present in at least 48 “bona-fide AIDS patients”, and constituted the experimental basis of the hypothesis that “HIV” causes “AIDS.”

The initial description and press release by Margaret Heckler of “HIV” as a known variant of a cancer virus was unfortunate, because as stated by Gallo and Montagnier [1], the molecular signature that was associated with “HIV” had been distinguished from Gallo’s early characterizations of the leukemia-associated retroviral signatures of HTLV-I and HTLV-II. The patent and intellectual property issues of the U.S. and French governments surrounding the creation of an “AIDS” blood test to protect the blood supply also proved to be an unfortunate series of confusing and hateful events that made possible accusations against the American-French collaboration that virtually insured suspicion of the “HIV=AIDS” hypothesis, and served to derail progress toward defining AIDS.

Despite the presence of the “HIV” signature in 48 isolates from what were then defined as AIDS patients, the contaminating isolates sent from The Pasteur Institute that infected the cultures of the Gallo group, Robin Weiss’s group in England, and at least several other laboratories, and despite the fact that Gallo shepherded through the 1983 Barre-Sinnousi et al. paper through to publication, the American-French collaboration and patent on the blood test was to be plagued by numerous accusations of stealing, deception, misconduct, and fraud. In a series of investigations lasting more that 5 years, the following kinds of investigations and reports swarmed about the heads of the scientists, particularly the heads of Gallo and his principal researcher, Papovic:

1. The legal records from the patent dispute, before the Board of Patent Appeals and Interferences, Montagnier et al. v. Gallo et al., Interference No. 101, 574;

2. The extensive documentary record from the Office of Scientific Integrity investigation into the Laboratory of Tumor Cell Biology at the National Cancer Institute;

3. The extensive documentary record from the House Subcommittee on Oversight and Investigations Committee on Energy and Commerce, chaired by the Honorable John Dingell (D-Mich);

4. The investigation by the U.S. Attorney for District of Maryland into the case, where she wrote:

“..we recognize that this case transcends the normal type of criminal case in that the conduct of these two scientists [Gallo and Popovic] reflects upon the integrity of the scientific process, the National Cancer Institute, and indeed the conduct of the government as a whole.” (Battaglia Letter, dated 1/10/94).

5. The articles in Science: (Culliton, Inside the Gallo Probe, Science. 1990 Jun
22;248(4962):1494-8); (Hamilton, What next in the Gallo case, Science 1991 Nov

6. The numerous articles by John Crewdson in the Chicago Tribune on this issue (“Researchers Dismiss an AIDS Virus Discovery,” Crewdson 2/18/88; “Rival Scientists Question Research on AIDS Lesions,” Crewdson 6/9/94; “U.S. Inquiry Discredits Gallo on AIDS Patent,” Crewdson 6/19/94; “U.S. May Yield on AIDS Royalties,” Crewdson 6/26/94,) that claimed such things as:

(From John Crewdson: Gallo Case, Truth Termed A Casualty Report: Science Subverted in AIDS Dispute; Chicago Tribune (CT) – SUNDAY, January 1, 1992 from the Dingell Report):

“The violence to principles of responsible, ethical science was just as profound. At a crucial point early in the (Gallo laboratory’s) HIV research, international politics and the technocrats committed to those politics virtually took over that research, claiming the laboratory’s putative accomplishments as accomplishments of the United States administration and by extension, the United States itself.”

“Once done, the (Gallo laboratory’s) interests became the government’s interests; defending the (Gallo laboratory) scientists’ reputations and claimed accomplishments became necessary for defending the honor of the United States. The defense thus became a consuming effort for significant portions of the U.S. government.”

“The result was a costly, prolonged defense of the indefensible in which the (Gallo laboratory’s) “science” became an integral element of the U.S. government’s public relations/advocacy efforts. The consequences for HIV research were severely damaging, leading, in part, to a corpus of scientific papers polluted with systematic exaggerations and outright falsehoods of unprecedented proportions.”

7. The book by John Crewdson, entitled “Science Fictions” (Littler Brown, 2002);

8. The numerous articles in the New York Times (“American Co-Discoverer of H.I.V. is Investigated Anew,” Hilts 3/2/92; “Federal Inquiry Finds Misconduct by a Discoverer of the AIDS Virus,” Hilts 12/31/92; “Science and Law Clash Over Fraud-Case Appeals,” Hilts 11/8/93; “Key Patent on AIDS to Favor French,” Hilts 7/12/94).

However, the subterfuge and accusations of misconduct surrounding the Laboratory of Tumor Virology and the Pasteur institute’s collaboration(s) were later dismissed, as described in the following documents:

1. The final HHS Office of Research Integrity ruling which began with the statement “After all the sound and fury?[there was no wrong doing on the part of Gallo, or his collaborators];”

2. Dingell’s own disavowal to the wild report of one non-scientist;

3. The New England Journal of Medicine article I have quoted from above on the history of the finding written jointly by Gallo and Montagnier;

4. Evidence that Gallo’s group had obtained 48 bona-fide isolates of bona-fide AIDS patients that exhibited the molecular signature they believed was “HIV” (as opposed to only the several isolates from ill-defined or ARC patients (with pre-AIDS) as was characterized by the Pasteur group using primary cultures in their 1983 paper.

Thus, the interests of the U.S. and French governments regarding the patenting of the blood test, fear of contagion, religious views regarding morality, sex, and drugs, and politics began the war that was perhaps to become known as the most politicized disease in history. Even though it was concluded that there was no misconduct found in either the Gallo or Papovic cases, the numerous accusations, and the lengthy and costly investigations of misconduct and blame only served to polarize those involved and those critical of them, and the charges of wrong doing only fueled bitter rivalry and criticism that has lasted for more than two decades. The 48 consistent molecular signatures that became known as “HIV” in isolates that Gallo’s group tied to a clinical syndrome in bone-fide AIDS patients (not only a putative ARC patient as the Pasteur had studied), constituted a strong motive to pursue in depth, the nature and meaning of that molecular signature, and In November, of 1984, the Pasteur Institute investigators published the genetic sequence of LAV [1].

By 1985, it was published that transmission of AIDS amongst health care workers was not a major public health concern because no transmission of AIDS was reported [5].

Also, in 1985, after a year of “HIV” testing, it was published that “68% to 89% of all repeatedly reactive ELISA (HIV antibody) tests represent false positive results among sperm donors [6].

Other important events that occurred in 1985 include the fact that in January, NCI scientists and their collaborators published the genome of HTLV-III in Nature, and in March, the first AIDS antibody test, an ELISA-type test, was released. In June, the CDC revised the case definition of AIDS to include additional specific disease conditions and to exclude people as AIDS cases if they had a negative result on testing for serum antibody to HTLV-III/LAV. In July, United Press International reported that actor Rock Hudson had AIDS, and in September, Indiana teen Ryan White, a hemophiliac suffering from “AIDS,” was refused entry to school. Also in September, the U.S. military services began testing for the AIDS virus among its personnel, and in October, Rock Hudson died. He was the first major public figure to die of AIDS, and Public fear about AIDS increased dramatically. That December, the publication of a finding that the AIDS virus is present in saliva increased public fears about AIDS [1].

By 1986, CDC and other agencies were concluding how infectious the molecular signature thought to be “HIV” could be-if it could be transmitted casually, through insect bites, or through saliva, or simply from a drop on a kitchen table. From all of these studies it was concluded that even huge amounts of “HIV” are very fragile, and it’s activity is completely abrogated by detergent exposure for a few seconds, even:

“?with an initial infectious titer of approximately 7 log10 tissue culture infectious
dose (TCID50) per milliliter?is undetectable and reduced more than 7 log10TCID50
within one minute 0.5% solution of nonidet-P40” [7].

Nonidet-P40 is a weak detergent used widely in many laboratories, and this implied that simple methods of sterility and precautions could be used so as to not become infected in laboratories, or in nosocomial (hospital) situations.

These observations raised issue with factor concentrates for Hemophiliacs. As Gallo and Montagnier had hypothesized earlier:

“the Centers for Disease Control and Prevention (CDC) reported cases of AIDS in patients with hemophilia who had received only filtered clotting factors, which seemed to eliminate the possibility that the agent was a microorganism larger than a virus.”

However, it was not clear how “HIV” could survive the freezing and thawing and lyophilization procedures used to make Factor VIII and IX concentrates. The “HIV=AIDS” proponents suggested that the reason these concentrates can still be infectious after months or years of drying, freezing, and thawing, is because “HIV” is so concentrated in them (Robert Gallo, personal communication). However, factor concentrates were pooled from thousands of blood donations, in which perhaps, if we assume one “HIV-positive” blood sample to be present with “high viral load” amongst several thousand negatives, then by pooling the blood, “HIV” is diluted, rather than concentrated. This hypothesis needs to be addressed in order to explain how hemophiliacs who were said to become “HIV-positive through factor concentrates, actually acquired “HIV.” In addition, a cogent point Gallo and Montagnier made in the NEMJ article, is that, the filtering of the concentrate assumes that only particles the size of viruses can pass through these filters. But one must also consider that whatever the agent was, it could survive freezing and drying in a vacuum, and it was small enough, like viruses OR proteins, to pass through the filters during the clotting factor preparation process.

Also by 1986 another key paper appeared in the prestigious journal, Cell, suggesting that “HIV” tropism wasn’t directed only at CD4 lymphocytes, as Gallo and Montagnier had proposed. Instead, it was suggested that the expression of the cellular protein, T4, by any and all human cells, was exploited by “HIV” as a receptor molecule that enabled entry of the virus into any cell expressing the normal endogenous Human T4 protein. This included brain cells and epithelial cells (skin cells) that expressed the T4 protein, and this molecular species was suggested to explain such diverse effects as immune suppression and AIDS dementia. As stated by Paul Jay Maddon, Angus G. Dalgleish, J. Steven McDougal, Paul R. Clapham, Robin A. Weiss, and Richard Axel (Cell, Vol 47, 333-348, 7 November 1986):

“The T4 gene encodes the AIDS virus receptor and is expressed in the immune system and the brain

The isolation of clones encoding the human surface protein T4, and the expression of the T4 gene in new cellular environments, have enabled us to examine the role of this protein in the pathogenesis of AIDS. Our studies support a mechanism of AIDS virus infection that initially involves the specific interaction of the AIDS virus with T4 molecules on the cell surface. This association can be demonstrated on T4+ transformed T and B lymphocytes as well as epithelial cells. Furthermore, the presence of T4 on the surface of all human cells examined is sufficient to render these cells susceptible to AIDS virus infection. Our data suggest that the T4-AIDS virus complex is then internalized by receptor-mediated endocytosis. Finally, we find that the T4 gene is expressed in the brain as well as in lymphoid cells, providing an explanation for the dual neurotropic and lymphotropic character of the AIDS virus. In this manner, a T lymphocyte surface protein important in mediating effector cell-target cell interactions has been exploited by a human retrovirus to specifically target the AIDS virus to populations of T4+ cells.”

Also by 1987, it wasn’t only the previously highly regarded oncogene and retrovirus work that has assured Peter Duesberg’s place in the history of molecular biology, virology, and cancer research. In 1987, Duesberg wrote a encyclopedic review article in which a series of clear and logical proofs was presented, in an attempt to help determine if indeed a virus actually could be associated with an illness, or not [9]. In this review article, which portrayed retroviruses as carcinogens and pathogens, and because of his previous studies with retroviruses and cancer, Duesberg argued for the retroviral reality of “HIV’s” molecular signature as advanced by the Gallo and Montagnier groups. However, in the article, Duesberg also theorized that the presence of “HIV’s” molecular signature in AIDS patients, in people who had received transfusions, or IV drug addicts, or non-human primates, constituted a harmless passenger virus, challenging Gallo’s and Montagnier’s hypothesis that (note above what Gallo and Montagnier wrote in 2003):

“it seemed more likely that the isolate was causative than that it was opportunistic?”

Duesberg’s absolute faith in the reality of the molecular signature that had become tto be known as “HIV,” but doubt about its pathogenicity in the development of AIDS, can best be seen in a statement he made later in the 1990’s, when he tried to claim an award offered to find “the missing [HIV] virus” (http://www.virusmyth.net/aids/award.htm). In all the literature, it is a statement, perhaps, that stands as the most persuasive argument that the molecular signature of “HIV” corresponds to a unique retrovirus (http://www.virusmyth.net/aids/award.htm):

“Here I take up these challenges. I will argue that HIV exists, and has been properly identified as a unique retrovirus on the grounds that (i) it has been isolated – even from its own virion structure – in the form of an infectious, molecularly cloned HIV DNA that is able to induce the synthesis of a reverse transcriptase containing virion, and (ii) that HIV-specific, viral DNA can be identified only in infected, but not in uninfected human cells. In view of this I can base my claim for the isolation of HIV on the most rigorous method available to date, i.e. molecular cloning of infectious HIV DNA, rather than only on the much less stringent, traditional “rules for isolation of a retrovirus … discussed at the Pasteur Institute, Paris, in 1973” that were stated criteria of isolation in Continuum’s missing virus reward. Indeed I will show that molecular cloning of infectious HIV DNA exceeds the criteria of the old “Pasteur rules.”

(I) Isolation of HIV

“The existence of the retrovirus HIV predicts that HIV DNA can be isolated from the chromosomal DNA of infected cells. This prediction has been confirmed as follows: Full-length HIV-1 and HIV-2 DNAs have been prepared from virus-infected cells and cloned in bacterial plasmids (13-15). Such clones are totally free of all viral and cellular proteins, and cellular contaminants that co-purify with virus. These clones produce infectious virus that is neutralized by specific antisera from AIDS patients. For example, virus produced by infectious HIV-2 DNA is neutralized by antiserum from HIV-2 but not from HIV-1-infected people.”

“Since infectious HIV DNA has been isolated from infected human cells that is free of HIV’s own proteins and RNA as well as from all cellular macromolecules, HIV isolation has passed the most vigorous standards available today. In other words these infectious DNA clones meet and exceed the isolation standards of the traditional “Pasteur rules.” Isolation of infectious HIV DNAs is theoretically the most absolute form of isolation – it is the equivalent of isolating the virus’ soul, its genetic code, from the virus’ body, the virus particle. Thus HIV isolation based on molecular cloning exceeds the old standards defined as “Pasteur rules” by Continuum.”

(II) Identification of HIV

“The existence of HIV predicts that infected cells contain a unique, virus-specific DNA of 9150 nucleotides that cannot be detected in DNA of uninfected human cells. The probabilities that cellular DNA and other viral DNAs would contain the same sequence of 9150 nucleotides is 1 in 4E9150, or 1 in 10E4500 – extremely close to zero! Since the odds that a given nucleotide of any DNA is either A, G, C or T are in 1 in 4, the odds that any DNA has the same sequence of 9150 nucleotides as HIV-1 or HIV-2 are only 1 in 4E9150.”

“Thanks to the outrageous interest in HIV as the hypothetical cause of AIDS, many investigators have sought specific HIV DNA in humans with and without AIDS in an effort to confirm that rather unreliable HIV antibody-test.”

“But because only 1 in 100 T-cells are ever infected in humans, virtually all such studies use Kary Mullis’ polymerase chain reaction, a technique that is designed to amplify a DNA-needle into a DNA-haystack. Such efforts have confirmed the existence of HIV-specific DNA in most (not all) antibody-positive persons with and without AIDS – but not in the DNA of antibody-negative people. For example, Jackson et al have tested blood of 409 antibody-positives including 144 AIDS patients and 265 healthy people. In addition 131 antibody-negatives were tested. HIV-specific DNA subsets – defined in size and sequence by HIV-specific primers (start signals for the selective amplification) – were found in 403 of the 409 antibody-positives, but in none of the 131 antibody-negative people.”

“The high sequence specificity of HIV DNAs is translated into the specificity of their proteins, eg. antibodies against HIV-1 do not neutralize HIV-1 (sic) and vice versa.”

In Conclusion

“HIV has been isolated by the most rigorous method science has to offer. An infectious DNA of 9.15 kilo bases (kb) has been cloned from the cells of HIV-antibody-positive persons, that – upon transfection – induces the synthesis of an unique retrovirus. This DNA “isolates” HIV from all cellular molecules, even from viral proteins and RNA. Having cloned infectious DNA of HIV is as much isolation of HIV as one could possibly get. The retrovirus encoded by this infectious DNA reacts with the same antibodies that cross-react with Montagnier’s global HIV standard, produced by immortal cell lines in many labs and companies around the world for the HIV-test. This confirms the existence of the retrovirus HIV.”

“The uniqueness of HIV is confirmed by the detection of HIV-specific DNA sequences in the DNA of most antibody positive people. The same DNA is not found in uninfected humans, and the probability to find such a sequence in any DNA sample is 1 in 4E9500 – which is much less likely than to encounter the same water molecule twice by swimming in the Pacific ocean every day of your life.”

These statements serve to show only that Duesberg’s believed in the reality of retroviruses and “HIV” in particular, and also felt that the tools of molecular virological reductionism were and are unequivocal, with statements such as:

“Such clones are totally free of all viral and cellular proteins, and cellular contaminants that co-purify with virus; “Since infectious HIV DNA has been isolated from infected human cells that is free of HIV’s own proteins and RNA as well as from all cellular macromolecules, HIV isolation has passed the most vigorous standards available today?”

Therefore, his principal contributions to the AIDS era were to argue for “HIV” constituting a unique exogenous retroviral signature that Gallo and Montagnier believed they had isolated from AIDS patients. However, as mentioned, in that same 1987 Cancer Research paper [9], and with his careful and painstakingly difficult to read logic, Duesberg, perhaps more than anyone else, raised issue that as a retrovirus, “HIV” could not cause AIDS. Duesberg’s objection to the fact that “HIV” causes AIDS” emerged from a comparison of associations of non-specific viral molecular signatures in natural populations, and disease. As necessary evidence for “infectious cancers,” for example, Duesberg demonstrated how it was possible to go beyond Koch’s postulates with respect to viruses (Koch’s postulates are applicable to bacteria and other free-living exogenously-derived pathogens because they are free-living organisms, and only problematically with viruses, because every molecule of a virus ultimately is made by cells and viruses are non-living supramolecular assemblages made without exception by the cells they infect), by confirming if molecular markers associated with disease seen under experimental circumstances in genetically weakened animals or highly inbred animals, also occurs among wild, or natural populations of animals (and humans). Thus, because of Deusberg’s comparison of observable disease to disease markers in wild populations compared to weakened laboratory or highly inbred domestic animals, we are able to ask if a pathogen or microbe might have some biochemical activity, and thus a role in pathogenesis of a disease in natural populations, and exclude the frequently encountered situation where natural populations of animals or humans only express markers associated with a particular disease, but do not ever (or rarely) develop disease.

Duesberg’s analysis presented in the Cancer Research article [9], detailed a century or more of virological research and cancer, and described in great detail the dynamics, speculative mechanisms of genetic integration, and timing of virological infections that do cause cytotoxic and cytocidal damage associated with some types of neoplastic transformation seen in laboratory Petri dishes, and in some genetically weakened species of animals. A few examples might convey a small part of Duesberg’s contribution (Italic references are from the Cancer Research paper):

“Avian lymphomotosis virus was originally isolated from leukemic chickens (29). However subsequent studies proved that latent infection by avian lymphomatosis viruses occurs in all chicken flocks and that by sexual maturity most birds are infected (30-32). Statistics report an annual incidence of 2-3% lymphomatoses in some flocks. Yet these statistics include the more common lymphomas caused by Marek’s virus (a herpes virus) (33,34).”

“Viremia has a fast proliferative effect on hemopoietic cells and generates lympohoblast hyperplasia (Fig.1) (32,36,37). Hyperplasia appears to be necessary but not sufficient for later leukemogenesis because it does not lead to leukemia in tumor-resistant birds (36).”

“The murine leukemia viruses were also originally isolated from leukemic inbred mice (9) and subsequently detected as latent infections in most healthy mice (8,13,16,17, 38). Indeed, about 0.5% of the DNA of a normal mouse is estimated to be proviral DNA of endogenous retroviruses, corresponding to 500 proviral equivalents per cell (18). Nevertheless, leukemia in feral mice is apparently very rare. For instance low virus expression, but not a single leukemia was recorded in 20% of wild mice (38) probably because wild mice restrict virus expression and thus never become viremic and leukemic. However in an inbred stock of feral mice predisposed to lymphoma and paralysis, 90% were viremic from an early age, of which 5% developed lymphomas at about 18 months (3).”

“Experimental infections of newborn, inbred mice with appropriate strains of murine leukemia viruses induce chronic viremias. Such viremic mice develop leukemias with probablilities of 0-90% depending on the mouse strain. However, if mice that are susceptible to leukemogenesis are infected by the time they are immunocompetent or are protected by maternal antibodies if infected as neonates, no chronic viremia and essentially no leukemia are observed (although a latent infection is established) (41).”

“The evidence that mammary carcinomas are transmissible by a milk-borne virus, MMTV, indicates that the virus is an etiological factor (51,52). However, the same virus is also endogenous but not expressed in most healthy mice (16, 53). Since no mammary tumors have been reported in wild mice, the natural incidence must be very low, but in mice bread for high incidence of mammary carcinomas it may rise to 90% (13,16,54,55).”

“Feline leukemia virus was originally isolated from cats with lymphosarcoma (59) and subsequently from many healthy cats. It is estimated that at least 50-60% of all cats become naturally infected with by feline leukemia viruses at some time during their lives (60,61).”

“The bovine and human retroviruses associated with acute leukemias are always biochemically inactive or latent. Viremia, which is frequently associated with a leukemia of congenitally or experimentally infected domestic chickens, cats, or inbred mice, has never been observed in the bovine or human system. Accordingly, bovine and human leukemia viruses could be isolated form certain leukemic cells only after cultivation in vitro away from the suppressive immune system of the host (71,72).”

“HTLV-I or ATLV was originally isolated from a human cell line derived from a patient with T-cell leukemia (71). It replicates in (cycling-emphasis mine) T-cells (27) and also in endothelial cells (76) or fibroblasts (77).” The virus was subsequently shown, using antiviral antibody for detection, to be endemic as latent, asymptomatic infections in Japan and the Caribbean (27). Since virus expression is undetectably low not only in healthy but also in leukemic virus carriers, infections must be diagnosed by antiviral antibody or biochemically by searching for latent proviral DNA. Due to the complete and consistent latency, the virus can be isolated from infected cells only after activation in vitro when it is no longer controlled by the host’s antiviral immunity and suppressors. Therefore the virus is not naturally transmitted as a cell-free agent like other pathogenic viruses, but only congenitally, sexually, or by blood transfusion, that is, by contacts that involve exchange of infected cells (13, 27).”

“It is often pointed out that functional evidence for the virus cancer hypothesis is difficult to obtain in humans because experimental infection is not possible and thus Koch’s third postulate cannot be tested. However, this argument does not apply here since naturally and chronically infected, asymptomatic human carriers are abundant. Yet most infections never lead to leukemias and none have been observed to cause viremias. Moreover, not a single adult T-cell leukemia was observed in recipients of blood transfusions from a virus-positive donor (13, 78, 79), although recipients developed antiviral antibody (81).”

“The incidence of adult T-cell leukemia among Japanese with antiviral immunity is estimated to be only 0.06% based on 339 cases of T-cell leukemia among 600,000 antibody-positive subjects (78).”

In conclusion, the tumor risk of the statistically most relevant group of retovirus infections, namely the latent natural infections with antivial immunity, is very low. It averages less that 0.1% in different species, as it is less than 1% in domestic chickens, undetectably low in wild mice, 0.04% in domestic cats on an annual basis, 0.01 to 0.4% in cattle, and 0.06% in humans. Thus the virus is not sufficient to cause cancer.”

Duesberg’s 1987 Cancer Research review article also discusses integration sites of viruses, tumor resistance genes, mathematically calculated probabilities of transformation, the evidence of chromosomal abnormalities being the only transformation-specific markers of retrovirus–infected tumor cells, how heterogeneity among the karyotypes (chromosome numbers) of individual human or murine leukemias of the same lineage suggest that chromosome abnormalities are coincidental with rather than causal for transformation, the oncogene hypothesis of Huebner is discussed and dismissed because the hypothesis was based on viral studies only in highly inbred strains of mice and domestic chickens, the hypothesis that latent cellular cancer genes are activated by provirus integrations is discussed and challenged because of the monoclonality Duesberg believed is the hallmark of tumors induced by onc genes. The hypothesis that latent cellular cancer genes are transactivated by viral proteins is discussed and challenged, and an argument is made that these viruses might indirectly cause cancer through hyperplasia that may be induced by the carcinogenic or irritant properties of these “viruses,” and that understanding the initiation of cancer will result when a better understanding of hyperplasia and host resistance genes are forthcoming-a valid point that is still awaiting clarification by the cancer establishment today.

Then, using similar kinds of considerations, a relatively short section entitled “Retroviruses and AIDS” was presented by Duesberg toward the end of the 1987 Cancer Research paper, and the information was subjected to the same kind of considerations as the “cancer viruses” discussed above, and it is in this context of cancer viruses and onc genes that his arguments should be considered. Moreover, reading the “HIV-AIDS” section of this paper in the context of his extensive examination of “cancer viruses” and their behavior, is a subject that has never been addressed by his many critics, yet considering “HIV” in this context generates a completely different view of what Duesberg actually was criticizing about the “HIV=AIDS” hypothesis.

The first section of the Retroviruses and AIDS section is a synopsis of the epidemiology of “AIDS” and “HIV” as it was typically presented by The Public Health Service in the year 1987 and several years before he wrote this paper. Duesberg made no claims that weren’t widely disseminated in CDC official records, and other available surveys of the time. However, in retrospect, it is interesting to note that Duesberg presented the following statements after his extensive treatment of cancer-associated viruses:

“Because of the nearly complete correlation between AIDS and immunity against the virus, the virus is generally assumed to be the cause of AIDS (13, 27). Accordingly, detection of antiviral antibody, rather than virus, is now most frequently used to diagnose AIDS and those at risk for AIDS (27, 217-224). This is paradoxical, since serum antibody from AIDS patients neutralizes AIDS virus (225-227) and since antiviral immunity or vaccination typically protects against viral disease. It is even more paradoxical that a low antibody titer is equated with a low risk for AIDS (228, 229).”

Here, Duesberg raised issue with what he considered to be paradoxical viral effects: namely that if testing positive for “HIV” with antibody detection kits are accurate, and if this antibody has been shown by McDougal et al., Gallo et al., Weiss et al., (references 225-227 in the Cancer Research Paper) to neutralize “HIV,” then how could this virus possibly cause disease once anti-viral immunity was established? This question still goes unanswered today, and is still a good question that goes unanswered in the context of other microbial diseases (Hepatitis B, C, HPV, syphilis, etc), if not ignored completely.

Duesberg continued his argument by stating:

“Unlike all other retroviruses, AIDS viruses are thought to be direct pathogens that kill their host cells, namely T-lymphocytes (13, 27), and possibly cells of the brain (230, 255). This view is compatible with the phenotype of AIDS, the hallmark of which is a defect in T-cells (13, 27, 215), and with experimental evidence that many but not all viral isolates induce cytopathic fusion of T-lymphocytes under certain conditions in vitro (Section D). Further it is incompatible with neurological disease (231, 232, 255). However, cell killing is incompatible with the obligatory requirement of mitosis for retrovirus replication (16, 25) and with the complete absence of cytocidal effects in all asymptomatic infections in vivo (Section D).”

Duesberg presented other concerns about “HIV’s” molecular signature and AIDS as well:

“Infections with no risk and low risk for AIDS indicate that the virus is not sufficient to cause AIDS.”

“On the basis of this particular epidemiology, it was concluded that the virus is not transmitted as cell-free agent like pathogenic viruses but only by contacts that involve exchange of cells (13, 27).”

“In these virus-infected groups the annual incidence of AIDS was found to average 0.3% (224) and to reach peak values of 2 to 5% (218, 223, 233). However even in these groups there are many more asymptomatic than symptomatic virus carriers.”

“Other infected groups appear to be at no risk for AIDS. In Haiti and in certain countries in Africa antibody-positive individuals range from 4 to 20% of the population, whereas the incidence of AIDS is estimated at less than 0.01% (223, 229, 234). Several reports describe large samples of children from Africa who were 20 (228) to 60% (221) antibody positive and of female prostitutes who were 66 to 80% antibody positive (221, 235), yet none of these had AIDS. Among male homosexuals and hemophiliacs of Hungary about 5% are AIDS virus positive, yet no symptoms of AIDS were recorded (161). Among native male and female Indians of Venezuela 3.3 to 13.3% have antiviral immunity, but none have symptoms of AIDS (236). Since these Indians are totally isolated from the rest of the country, in which only one hemophiliac was reported to be virus positive (236), the asymptomatic nature of their infections is not likely to be a consequence of a recent introduction of the virus into their population. Thus it is not probable that these infections will produce AIDS after the average latent period of 5 years (Section B).”

Again, the references and data Duesberg gives were not disputed. In fact, many of these quoted references were produced by key AIDS officials including Montagnier, Curran, Weiss, Biggar, Gallo, and others, and were published in Science, The Lancet, Cancer Research, JAMA, and in other journals of some notariety.

Each of the issues in the AIDS section of the paper that Duesberg raised, was simply a rehashing of arguments he raised concerning the non-compatibility of long latent periods and cancer initiation among the so-called onc or non-onc gene-containing viruses (as seen in cell culture dishes in transformation experiments, or in genetically weakened animals given toxic carcinogenic infusions before their immune systems have been given a chance to develop). What is perhaps most striking about Duesberg’s Retroviruses and AIDS section in retrospect, is that he advocated that “HIV” might generate a mononucleosis like illness for all the same reasons that timing of replication and biochemical activity of high virus titres may play a role in oncogenic and non-oncogenic viruses. In other words, through his knowledge of the so-called and supposed retroviral cancer virus induced effects in genetically weakened animal strains, he separated the immediate short-term effects of viral replication before antibody immunity becomes established, from long latency viral diseases such as those induced by what he believed constituted a hyperplastic (overstimulated) augmentation of cell proliferation and aneuploidy, that is typically associated with cancers that form in genetically weakened strains of animals who harbor the molecular signature of viruses that do not contain onc genes.

“The eclipse period of AIDS virus replication in cell culture is on the order of several days, very much like that of other retroviruses (238). In humans virus infection of a sufficient number of cells to elicit an antibody response appears to take less than 4 to 7 weeks. This estimate is based on an accidental needle-stick infection of a nurse, who developed antibody 7 weeks later (239), and on reports describing 12 (240) and 1 (232) cases of male homosexuals who developed antibody 1 to 8 weeks after infection. During this period a mononucleosis-like illness associated with transient lymphoadenopathy was observed. In contrast to AIDS (see below), this illness appeared 1 to 8 weeks after infection and lasted only 1 to 2 weeks until antiviral immunity was established. The same early mononucleosis-like disease, associated with lymphocyte hyperplasia, was observed by others in primary AIDS virus infections (234). This is reminiscent of the direct, early pathogenic effects observed in animals infected with retroviruses prior to the onset of antiviral immunity (Part I, Section B).”

There was nothing controversial about “the eclipse period of virus replication” or any other statement in this paragraph. This short latency period was set in contrast to what Gallo and Montagnier believed was the latency for their hypothesized syndrome of the development of “AIDS’ 5, 10 or more years after infection, as Duesberg pointed out:

“By contrast the lag between infection and the appearance of AIDS is estimated from transfusion-associated AIDS to be 2 to 7 years in adults (220, 223, 241, 242) and 1 to 2 years in children from infected mothers (220, 223). The most likely mean latent period was estimated to be 5 years in adults (220, 223). Unexpectedly, most of the AIDS virus-positive blood donors identified in transfusion-associated AIDS transmission did not have AIDS when they donated blood and were reported to be in good health 6 years after the donation (220). Likewise there is evidence that individuals shown to be antibody positive since 1972 have not developed AIDS (228). Further 16 mothers of babies with AIDS did not have AIDS at the time of delivery but three of them developed AIDS years later (276). This indicates that the latent period may be longer than 5 years or that AIDS is not an obligatory consequence of infection.”

Duesberg’s principal and cogent argument therefore was that cells or viruses do not wait 5-10 or 20 years to generate their pathogenic effects, nor in humans who develop a mononucleosis like condition weeks after they exhibit the molecular signature of “HIV.”

That malnutrition, recreational drugs and prescription drugs can cause profound immune suppression and transfusions in some individuals, was not advanced by Duesberg in the Cancer Research paper. It was advanced in other papers Duesberg wrote in an attempt to explain how advanced acquired immune suppression may be caused if not with “HIV.” These ideas involving malnutrition and drug-induced immune suppression were not original with Duesberg. However, he did his best to help communicate these alternative known causes of immune suppression to the scientific community and to the general public, in an attempt to provide alternative possible reasons why a growing group of young men in Los Angeles, San Francisco, and New York appeared to be developing a strange cluster of rarely observed 3rd World-like diseases and syndromes. Instead of being caused by the molecular signatures associated with “HIV,” he argued that the fatal syndrome called AIDS probably had nothing to do with a “passenger virus,” or the molecular signature of “HIV.”

Nutritional deficiency and prescription and illicit drug reactions and their association with various immune deficiencies and other syndromes had been described in the writings of numerous scientists and physicians for more than a century, long before Duesberg was born. It was common knowledge, for example, that malnutrition or exposure to foreign proteins or exposure to extreme oxidation are all phenomena which are known to induce many of the “AIDS-defining illnesses” such as T-cell depletion, and other syndromes, as is the chronic long-term use of illicit and certain prescribed drugs, which have been the principal theories championed by Duesberg as the causes of AIDS. For instance, prescription steroids were said to iatrogenically cause of AIDS, as was published years before in 1975-6 by Anthony Fauci, who later became the NIAD Czar of AIDS funding, Doctors caused immune suppression, Fauci claimed, if they subject their patients to multiple transfusions, transplant surgery, or corticosteroid administration, as these drugs and treatments can non-specifically induce AIDS-specific drops in T-cells with high frequency [10, 11]. Fibrosis of the lung due to to heavy crack cocaine use also was considered a potent inducer of the most commonly seen AIDS-defining illness, PCP, by Fauci and others before the AIDS era. These qualifications serve to undermine the “HIV=AIDS” hypothesis, because A (“HIV”), does not generate B (immune suppression), because iatrogenically applied glucocorticoids, transfusions, blood factor concentrates in hemophiliacs, and other factors such as chronic crack cocaine use may induce a precipitous drop in B, and consequently lead to C. What this meant, “at least to those who care about patients,” Fauci warned, “is that if not careful, doctors can cause profound immune suppression through too much steroid administration.” Yet, even though these studies are in the peer-reviewed literature for all to read, the AIDS establishment kept the “HIV=AIDS” hypothesis alive, and instead of criticizing Duesberg’s work or thinking about virology, they claimed that he erected a drug-AIDS hypothesis “on the basis of no real research.” As his critics were and are so often heard to retort, “There are no published studies that show that drugs and drug effects are consistently associated with the development of AIDS.” But Anthony Fauci’s studies did! Harry Haverkos, who worked for the Public Health Service during these early days of the AIDS era, published that drug addicts should be considered by FDA scientists to be non-AIDS patients, but merely immunosuppressed, because of chronic drug abuse [12]. Duesberg was not original in his hypotheses about illicit and prescription drugs and their possible role in causing “AIDS.”

Nevertheless, “HIV=AIDS” hypothesis proponents, as well as the press and certain members of the gay community held a different view of Duesberg’s contributions. For example, despite his National Academy member status and prestigious Fogarty award for his pioneering work on oncogenes and retroviruses, Duesberg has received no federal funding since the appearance of the 1987 Cancer Research paper, and he has been repeatedly denied public debates or publication of his ideas, because his writings have been rejected by powerful journal editors such as John Madox of Nature, and others. At least once a year, it is still not unusual to see the following kinds of portrayals of Duesberg’s thinking and hypotheses by journalists:

“The Trouble with Duesberg’s Theory, By Marc B Haefele, Editor, Los Angeles Alternative Times:

“Peter Duesberg isolated the first cancer-causing gene from a virus at 33,
got tenure at Berkeley at 36, joined the National Academy of Sciences at 49.
So why is he in bad odor in the scientific and gay communities? In small
part because, on the basis of of no real experimental research, he
proclaimed in a 1988 article that AIDS wasn’t caused by the HIV virus but by
bad nutrition and recreational drugs. As the Scientific American put it “his
idea died as most failed theories do: never fully disproved but convincingly
rebutted by the National Institute for Allergic and Immune Diseases–and
ultimately ignored by nearly everyone working in the field.”

“And largely because Duesberg, a non-physician, kept peddling his theory as
fact. As the San Francisco based Project Inform noted “He offers an easy,
comforting approach to AIDS and has been able to influence people to trust
him and reject their doctor’s advice.” He fronted a “well financed” campaign
to get AIDS patients to reject medical care. Most recently, he
succeeded–temporarily–in getting South African President Thabo Mbeki to
reject the viral cause of AIDS. It’s not typical scientific procedure to
promote a debunked theory at the probable cost of thousands or millions of
lives. But that’s what Duesberg has been doing.”

Similarly, not only journalists, but scientists and physicians criticized Duesberg’s ideas and hypotheses. To quote Marc Wainberg, the 2006 Chair of The Toronto International AIDS Conference-who possesses several “HIV” drug patents such as lamivudine (3TC), and grants from GlaxoSmithKlein, Bristol-Myers Squibb and Boehringer-Ingelheim):

“As far as I’m concerned, and I hope this view is adequately represented, those who attempt to dispel the notion that HIV is the cause of AIDS are perpetrators of death. And I would very much for one like to see the Constitution of the United States and similar countries have some means in place that we can charge people who are responsible for endangering public health with charges of endangerment and bring them up on trial. I think that people like Peter Duesberg belong in jail.” (Quoted from the documentary, “The Other Side of AIDS” which won a special Jury Prize at the AFI Los Angeles International Film Festival) [13].

In 1987, an important review article appeared in Scientific American, written by Nobelist, and former NIH director, Harold Varmus, entitled Reverse transcription [8], which claimed that reverse transcriptase is a normal protein found in the uninfected cells of yeasts, insects and mammals.

Also, 1987 was the year of the publication and of the first AZT trial, and FDA approval of the drug after only 4 months of study. The Fischl Phase II trial is the trial said to have demonstrated the efficacy and safety of AZT, upon which FDA approval was obtained, and which was the only trial in US history to show in a record 4 months, that a drug (AZT) was “worthy” of FDA approval [14, 15, 16]:

“The licensing study of AZT, performed in 1987 by the NIH in collaboration with the drug’s manufacturer Burroughs Wellcome in the US, is the primary placebo-controlled study set-up to test the ability of AZT to reduce the mortality of AIDS. The study showed that, after 4 months on AZT, 1 out of 145 AIDS patients died, whereas 19 out of 139 died in the placebo group. The study interpreted this result as evidence for reduced mortality by AZT. However, this interpretation failed to consider that among the 4- month-survivors of AZT, 30 could only be kept alive with multiple blood transfusions because their red cells had been depleted by AZT below survivable levels. Thus, without lifesaving transfusions 30 more AZT-recipients would have died from anemia. In addition many AZT recipients had developed life-threatening bone marrow suppression, neutropenia, macrocytosis, headaches, insomnia and myalgia, that augured poorly for their future survival (Richman D D, et al and the AZT Collaborative Working Group 1987 The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex; N. Engl. J. Med. 317 192-197). Indeed, the low mortality of 1/145 reported for the first 4 months on AZT, could not be maintained in a follow-up study, which found the “survival benefits” of AZT rapidly declining after the original 4 month period. By 21 months, 42% of the original AZT group had died and 35% of the control group, which by then had also received AZT for 12 months on a “compassionate” basis:
Thus the placebo-controlled, licensing study did not prove that AZT reduced AIDS mortality by more than 80 compared to the untreated control.

Fischl et al. noted a transient rise in T-cells, but by 21 months, 42% of the original AZT group had died and 35% of the control group, which by then had also received AZT for 12 months on a “compassionate” basis. Control groups were abandoned in this trial for the reasons alluded to above, which is important because it was the trial that led to the FDA approval of AZT in an unprecedented 4 months. This allegation of collusion by pharma and the CDC was unprecedented in FDA history, especially in light of accusations that the trial became unblinded after 1 week because the toxicity of AZT was apparent to everyone, especially the patients [15]. The FDA’s recommendation for the approval for AZT was also beyond all logic or common sense because it was discovered that a series of patients were switched over from the control arm to the experimental arm, and it was disclosed that 30 patients in the experimental group required life-saving transfusions to stay alive. These facts, in addition to the Boston arm of the trial being cited for fraudulent record keeping, were all obtained by the Freedom of Information Act and published by Lauritsen [16]. It is interesting to note, that, the document Lauritsen obtained through the information act and presented in his book is riddled with black deletions of text, as if the contents of the study were describing a new nuclear weapons technology rather than a new drug. The document itself is difficult to read because of so many deletions, yet creative record keeping was evident. Also, in the context of pre-maturely terminating antiretroviral human trials and switching experimental arms to placebo arms “for compassionate reasons,” one must factor in, in addition, the violations of human rights and complete lack of informed consent accompanying this practice. But these sorts of violations are legion in many AIDS clinical trials, versus the practice of conducting controlled, and complete experiments that are not changed in mid-stream, and in which patients are given full disclosure about the risks and uncertainties of an experimental drug.

Several other important events occurred in 1987. In March President Ronald Reagan and French Prime Minister Jacques Chirac announced a joint agreement settling the dispute arising from the discovery of the AIDS virus, the first international agreement relating to a biomedical research issue to be announced by heads of state. In April FDA approved the first Western blot blood test. In June NHLBI awarded a contract to maintain a colony of 50 chimpanzees for studies of post-transfusion HIV infection and AIDS, and most importantly, in August, the CDC revised its definition of AIDS to place a greater emphasis on counting AIDS patients as those who are healthy but exhibit the molecular signature of “HIV.” This “greater emphasis on HIV infection status served to dramatically increase the number of AIDS cases over night many fold, because healthy persons who presented with the molecular signature associated with “HIV” were counted as AIDS patients. In December, the CDC released the results of a study on the prevalence of HIV infection in the United States, indicating a shifting emphasis toward defining AIDS as “infection with HIV” rather than by defining particular “indicator diseases” that characterized late-stage AIDS [1].

In 1988, several important events occurred. In January, The CDC updated the International Classification of Diseases codes for HIV infection for use with U.S. morbidity and mortality data [1], and in June, the brochure “Understanding AIDS,” prepared by Surgeon General C. Everett Koop in collaboration with the CDC, was mailed to every household in the United States. In August, NIAID’s AIDS Vaccine Evaluation Units initiated their first study of an experimental AIDS vaccine. In September, NIDR investigators reported that saliva inhibits transmission of HIV, and in October, AIDS protestors, demanding a quicker approval process for drug treatments, shut down the FDA. In October, NIAID established three programs: the Centers for AIDS Research (CFARS) to improve the diagnosis, treatment, and prevention of AIDS; the Pediatric AIDS Clinical Trials Units (Pediatric ACTUs), a network of clinical sites to test experimental HIV drugs in children; and the Programs for Excellence in Basic Research (PEBRA), to develop novel strategies to determine how HIV causes disease [1].

Yet by 1988, a new hypothesis was published that attempted to explain the pathogenesis of AIDS as the result of a disturbance in cellular reduction/oxidation reactions [17]. As hypothesized by Papadopulos-Eleopulos:

“There are good reasons to doubt that HTLV-III/LAV can be regarded as the exclusive single variable in the pathogenesis of AIDS. There is therefore a spectrum of possibilities. Either it plays no role at all, is of minor significance or it contributes significantly but not exclusively to the disease. Be that as it may the one major significant variable is the concurrent exposure of the patients to oxidising agents including sperm, nitrites, opiates and factor VIII. If this is true then prevention, and possibly even cure, may be achieved with the use of appropriate antioxidants.”

Part of the basis of this hypothesis derived from the fact that Gallo and Montagnier’s groups both had used PHA (phytohemagglutinin-a plant lectin), IL-2 (interleukin-2), and other chemicals believe to oxidize and stimulate T-cells to divide several times, which was necessary to induce lymphocytes or continuous cell lines to generate the molecular signature of “HIV” after exposure to AIDS patient sera, or after exposure to supernatants from cells harboring “HIV’s” molecular signature. AIDS patients, she argued, also are highly oxidized, through exposure to various things.

Although, electron micrographs and computer-generated models of what have been identified as “HIV” viral particles can easily be found on numerous public access sites as well as in the CDC’s information websites, the Big Picture Book of Viruses, from text books, and from numerous other information sources, they look different in every picture, they either do or do not have surface projections, they either are or are not harboring a nucleic acid core, the are or are not of similar sizes, and they are always accompanied by excessive quantities of cellular debris or junk which is the most specific hallmark of viral isolation preps that claim to harbor the molecular signature of “HIV.”

But in 1998, in a short piece entitled, “Remarks on methods for retroviral isolation,” Dr. Etienne de Harven who is an emeritus Professor of Pathology, University of Toronto and who worked out the ultrastructure of retroviruses throughout his professional career of 25 years at the Sloan Kettering Institute in New York and 13 years at the University of Toronto, vociferously objected to the standards used to claim that “HIV” viral particles had been convincingly isolated. In 1956 he was the first to show electron microscope images of the Friend virus in murine (mouse) leukemia, and in 1960, to coin the word “budding” to describe steps of virus assembly on cell surfaces. He also delivered a speech at the 12th World AIDS Conference in Geneva (June 28-July 3) at the session entitled, “HIV-testing: Open Questions about Specificity”:

“The most impressive developments of molecular genetics over the past 20 years do not make Robert Koch’s postulates obsolete. The first of these postulates indicates that to be considered as pathogenic, a microorganism should be isolated in every single case of the disease. Still, according to E. Papadopulos et all and S. Lanka (Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Hedland-Thomas 1994. 13, Page B, A critical analysis of the HIV-T4-AIDS hypothesis. Genetica 95:5-24; Lanka, Stefan, 1994. Fehldiagnose AIDS? Wechselwirkung, Aachen, December, 48-53), isolation of HIV from fresh plasma of AIDS patients has never been achieved under any circumstances. Moreover, and most surprisingly, the “efficiency” of current antiviral therapeutic protocols (AZT tri-therapy) is being measured by determining “viral load” in the plasma of treated patients. “Viral load” implies viremia-i.e. the presence of circulating viral particles in the peripheral blood. The virus incriminated being allegedly a retrovirus, this would have been the time to remember that the morphology of such viruses in several animal experimental tumors and leukemias had been extensively characterised by transmission electron microscopy (EM) over the past 40 years, the viral particles having a characteristic ultrastructure and a diameter ranging between 100 and 120 nm. Some of them had been studied by methods of high resolution transmission electron microscopy (de Harven, E. 1994. Remarks on the ultrastructure of type A, B and C virus particles. Advances in Virus Research 19: 221-264, Academic Press, Inc., New York). In the 1960s, transmission electron microscopy was by far the best available method to identify viruses within or around diseased cells. Consequently, many cancer research centers all around the world, started to compete for the best equipment and training in EM, aiming at the demonstration in human malignancies of viruses similar to those which had just been recognized as significantly associated with tumors and leukemias of several laboratory animals. This approach to cancer research appeared highly justified when Lwoff, Horne and Tournier proposed to classify all viruses primarily on the basis of their morphological features demonstrated by electron microscopy (Lwoff A, Horne R, Tournier P, 1962. Cold Spring Harbour Symposium on Quantitative Biology 27:51). Identification of viruses by EM in leukemic animal tissues became unambiguous when steps in virus assembly, i.e. the ‘budding’ of complete virions from the surface of the infected cells, were described (de Harven E, and Friend C, 1960. Further electron microscope studies of a mouse leukemia induced by cell-free filtrates. J. Biophysic. and Biochem. Cytol., vol 7, 747-752. Rockefeller University Press, New York). In spite of considerable efforts, the search for similar, typical viruses in human malignancies remained entirely negative. Pleomorphic membranous microvesicles, approaching viral size, and frequently described in the literature on human malignancies as “virus-like particles” were without any pathogenic significance. As stated in 1965, typical RNA tumor viruses have never been observed in association with human neoplasia (de Harven E, 1965. Remarks on viruses, leukemia and electron microscopy. In Methodological approaches to the study of leukemias. V Defendi, edit., The Wistar Institute Press publ, Philadelphia, pp147-156).”

“Concentrations of retroviruses from murine and avian leukemic tissue homogenates were reproducibly achieved permitting titration of infectivity into receptive laboratory animals. This was not, however, an easy approach to the problem of virus purification, large amounts of microvesicles and cell debris being usually present. As far as virus purification was concerned, it soon became evident that when viremia is present, blood plasma was far better than tissue homogenates for efficient virus isolation and purification.”

“In the case of RNA tumor viruses, now called retroviruses, the demonstration of viremia in the blood plasma of experimental leukemic animals (chickens and mice) was published more than 35 years ago. A most efficient purification method including ultrafiltration and ultracentrifugation of a 1/1 dilution of plasma in heparinized Ringer’s solution, allowed me to demonstrate packed retroviruses by transmission electron microscopy (de Harven E, 1965. Viremia in Friend leukemia: the electron microscope approach to the problem Pathologie-Biologie,13:125-134 de Harven E, 1998. Pioneer deplores “HIV”. Continuum vol 5, page 24) in thin sections of pellets obtained by high speed centrifugation of the purified virus, quite clearly establishing that the amount of contaminating cell debris was remarkably small, a conclusion which could never have been reached by using the negative staining EM method. Using this simple ultrafiltration procedure, virions were never exposed to hypertonic shock. However, sedimentation in sucrose density gradients, at the density of 1.16 gm/ml, soon became the most popular method for retrovirus purification (Sinoussi F, Mendiola L, Chermann JC, 1973. Purification and partial differentiation of the particles of murine sarcoma virus (M.MSV) according to their sedimentation rates in sucrose density gradients. Spectra 4:237-24). Interestingly, it was very well known by electron microscopists in the 1960s, that sharp bands sedimenting at the density of 1.16 frequently contained large amounts of microvesicles and cell debris of non-viral nature. These debris just happened to sediment in sucrose gradients at a density very similar to that of retroviruses clearly indicating that finding a “sharp band” at the density of 1.16 gm/ml was of little significance and was certainly far from any demonstration of retroviruses isolation.”

“But this conclusion was based on EM findings, and around 1970 the faith in retroviral oncology was assuming quasi-religious proportions! If EM cannot demonstrate viruses in the 1.16 bands, let us forget about EM and rely on other “markers”!”

“When around 1980, R. Gallo and his followers attempted to demonstrate that certain retroviruses can be suspected of representing human pathogens, to the best of my bibliographical recollection, electron microscopy was never used to demonstrate directly viremia in the studied patients. Why? Most probably, EM results were negative and swiftly ignored! But over-enthusiastic retrovirologists continued to rely on the identification of so-called “viral markers”, attempting to salvage their hypothesis.”

“When retrovirus particles are legion, the study of molecular markers can be useful, and provide an approach to quantification probably better than direct particle counting under the EM (which I always found very difficult). But when, using EM, retrovirus particles are absent relying exclusively on ‘markers’ is a methodological nonsense. ‘Markers’ of what?”

“Nevertheless, for the past ten years, HIV research and clinical therapeutic trials have been primarily based on the study of several HIV “markers”.”

“First the antibody. ELISA, then Western Blot tests were hastily developed (at sizable financial profit eagerly split between the Pasteur Institute and the US). “Seropositivity” became synonymous with the disease itself, plunging an entire generation into behavioral panic, and exposing hundreds of thousands of people to ‘preventive’ antiviral AZT therapy which actually hastened the appearance of severe or lethal immunodeficiency syndrome. Appropriate controls were apparently never carried out or were never published. Still, back in 1993 it became clear that the so-called HIV antibody tests badly lacked specificity, (Papadopulos-Eleopulos E, Turner VF and Papadimitnou JM, 1993. Is a positive Western Blot proof of HIV infection? Bio/Technology 11:696-707) cross-reactivity being observed with patients suffering from a long list of pathological conditions including malaria, leprosy, auto-immune diseases and many more.”

“Secondly, ‘viral proteins’. Several proteins have been identified as ‘HIV markers’, most frequently because they were identified in a variety of 1.16 bands. The case of the p24 “viral” antigen is a significant example and its lack of viral specificity has been well documented. (Todak C, Klein E, Lange M et al., 1991. A clinical appraisal of the p24 antigen test. International Conference on AIDS, vol 1, Florence, Italy).”

“Third, reverse transcription. If reverse transcriptase activity were a unique feature of retroviruses, it could have been an interesting molecular marker. Unfortunately, it has been shown that reverse transcriptase is found in the uninfected cells of yeasts, insects and mammals (Varmus H, 1987. Reverse transcription Sci. Am. 257:48-54) and “has nothing to do with retroviruses as such” as well referenced in a recent report from S. Lanka. Moreover, K. Mullis himself does not support the use – to amplify and quantify the “HIV genome” – which is being made of the PCR methodology he developed, which is the current method of “measuring the viral load” in AIDS patients.”

“More disturbing is the fact that some ‘markers’ are searched for in the 1.16 gradient sedimenting material which is the density where intact virions are expected to be found, but not their molecular fragments. If lysed retrovirus particles released molecular markers, the 1.16 samples should at least initially allow investigators to demonstrate virus particles by EM. They don’t. However after 15 years of most intensive HIV research, two independent groups finally decided to explore by electron microscopy the ultrastructural features of the material sedimenting at the 1.16 density. Working on “HIV-1 infected T-cell” cultures supernatants, both groups found that it contains primarily cellular debris and cell membrane vesicles which could definitely not be identified with HIV particles and rare “virus-like” particles (Gluschankof P. Mondor I, Gelderblom HR, and Sattentau QJ, 1997. Cell Membrane vesicles are a major contaminant of gradient-ennched human immunodeficiency virus type-l preparations. Virology 230:125-133; Bess JW Jr., Gorelick WJ, Bosche WJ, Henderson LE, and Arthur LO, 1997. Microvesicles are a source of contaminating cellular proteins found in purified HIV-I preparations. Virology 230:134-144).”

“Still, this is the type of sample in which “viral markers” are currently identified and used to measure the effects of anti-viral drugs in current clinical trials.”

“In conclusion, and after extensive reviewing of the current AIDS research literature, the following statement appears inescapable: neither electron microscopy nor molecular markers have so far permitted a scientifically sound demonstration of retrovirus isolation directly from AIDS patients.”

In 1989, Harold Varmus, in his Nobel lecture described the ability of scientists up until that time to distinguish between viral and cellular oncogenes, and viral versus cellular reverse transcriptases [18]. He also published a mini review in the prestigious journal, Cell, describing reverse transcriptase in bacteria [19].

Also in 1989, the investigative journalist, Celia Farber published the controversial piece, “Sins of Omission,” in Spin Magazine, which emphasized the toxicity and the rushed FDA approval of AZT with statements like:

‘But there were tremendous concerns about the new drug. It had actually been developed a quarter of a century earlier as a cancer chemotherapy, but was shelved and forgotten because it was so toxic, very expensive to produce, and totally ineffective against cancer. Powerful, but unspecific, the drug was not selective in its cell destruction.’

‘Drug companies around the world were sifting through hundreds of compounds in the race to find a cure, or at least a treatment, for AIDS. Burroughs Wellcome, a subsidiary of Wellcome, a British drug company, emerged as the winner. By chance, they sent the failed cancer drug, then known as Compound S, to the National Cancer Institute along with many others to see if it could slay the AIDS dragon, HIV. In the test tube at least, it did.’

‘At the meeting, there was a lot of uncertainty and discomfort with AZT. The doctors who had been consulted knew that the study was flawed and that the long-range effects were completely unknown. But the public was almost literally baying at the door. Understandably, there was immense pressure on the FDA to approve AZT even more quickly than they had approved thalidomide in the mid-60s, which ended up causing drastic birth defects.’

‘Everybody was worried about this one. To approve it, said Ellen Cooper, an FDA director, would represent a “significant and potentially dangerous departure from our normal toxicology requirements.”

‘Flash forward: August 17, 1989. Newspapers across America banner-headlined that AZT had been “proven to be effective in HIV antibody-positive, asymptomatic and early ARC patients,” even through one of the panel’s main concerns was that the drug should only be used in a last-case scenario for critically-ill AIDS patients, due to the drug’s extreme toxicity. Dr. Anthony Fauci, head of the National Institutes of Health (NIH), was now pushing to expand prescription.’

‘Burroughs Wellcome stock went through the roof when the announcement was made. At a price of $8,000 per patient per year (not including blood work and transfusions), AZT is the most expensive drug ever marketed. Burroughs Wellcome’s gross profits for next year are estimated at $230 million. Stock market analysts predict that Burroughs Wellcome may be selling as much as $2 billion worth of AZT, under the brand name Retrovir, each year by the mid-1990s – matching Burroughs Wellcome’s total sales for all its products last year.’

‘As it happened, AZT was rampantly prescribed as soon as it was released, way beyond its purported parameters. The worst-case scenario had come true: Doctors interviewed by the New York Times later in 1987 revealed that they were already giving AZT to healthy people who had tested positive for antibodies to HIV.’

‘AZT was singled out among hundreds of compounds when Dr. Sam Broder, the head of the National Cancer Institutes (NCI), found that it “inhibited HIV viral replication in vitro.”

‘The last surviving patient from the original AZT trial, according to Burroughs Wellcome, died recently. When he died, he had been on AZT for three and one-half years. He was the longest surviving AZT recipient. The longest surviving AIDS patient overall, not on AZT, has lived for eight and one-half years.’

‘The news that AZT will soon be prescribed to asymptomatic people has left many leading AIDS doctors dumbfounded and furious. Every doctor and scientist I asked felt that it was highly unprofessional and reckless to announce a study with no data to look at, making recommendations with such drastic public health implications. “This simply does not happen,” says Bialy. “The government is reporting scientific facts before they’ve been reviewed? It’s unheard of.”

“It’s beyond belief,” says Dr. Sonnabend in a voice tinged with desperation. “I don’t know what to do. I have to go in and face an office full of patients asking for AZT. I’m terrified. I don’t know what to do as a responsible physician. The first study was ridiculous. Margaret Fishl, who has done both of these studies, obviously doesn’t know the first thing about clinical trials. I don’t trust her. Or the others. They’re simply not good enough. We’re being held hostage by second-rate scientists. We let them get away with the first disaster; now they’re doing it again.”

In 1989-1990, a series of articles published by Shyh-Ching Lo of the Armed Forces Institute of Pathology was discussed in AIDS TREATMENT NEWS No. 095 – January 26, 1990, written by John S. James:

MYCOPLASMA INCOGNITUS: Newly Discovered Treatable Opportunistic Infection?

Researchers at the U. S. Armed Forces Institute of Pathology (AFIP) in Washington, D. C., and the Warren Grant Magnuson Clinical Center at the National Institutes of Health, have found compelling evidence that a previously unrecognized opportunistic infection — one potentially treatable with antibiotics — may be a major cause of illness in people with AIDS. Many infections of organs including the brain, spleen, liver, or lymph nodes — as well as some systemic infections — might be caused by the newly-discovered organism, called Mycoplasma incognitus. Until now, these infections would be counted among the many which cannot be diagnosed. While the first report of the organism now known as Mycoplasma incognitus was published over three years ago, most of what is now known was learned later and published last year. And only in the last few weeks has the AIDS research community paid serious attention.

Until recently the new organism was mistakenly believed to be a virus, and its discovery seemed to have little immediate relevance to treatment. Then a series of five articles by Shyh-Ching Lo and others in the American Journal of Tropical Medicine and Hygiene, between February and November 1989, showed: (1) The new organism is a mycoplasma — which is potentially treatable. Mycoplasma, a form of life between bacteria and viruses in complexity, was discovered about 100 years ago. Some species are known to cause human diseases.

The published articles only hint that the new organism might be treatable with antibiotics. But scientists at AFIP tested 15 common antibiotics against the Mycoplasma incognitus in the laboratory. A detailed report is being prepared for publication, but because of the public-health importance of the information, AFIP released a list of the drugs and their effective concentrations in a separate document. Doxycycline, tetracycline, clindamycin, lincomycin, and ciprofloxacin were found to be effective against Mycoplasma incognitus. But erythromycin, the antibiotic most commonly used to treat mycoplasma infections, was not effective — and penicillin, streptomycin, gentamicin, and others also had no effect. (2)

Mycoplasma incognitus was found in the thymus, liver, spleen, lymph node, or brain of 22 of 34 persons who had died of AIDS. The patients who were selected for this autopsy study had all had evidence of organ failures. (3) In a separate study with different patients, the mycoplasma was found in seven of ten persons with AIDS. Also, a much earlier study had found Mycoplasma incognitus in blood lymphocytes of 12 of 23 living persons with AIDS — but in none of 22 healthy blood donors used as controls. (4) The mycoplasma was also found in six HIV-negative patients (with no sign of AIDS) from different parts of the world, who had died in one to seven weeks of an undiagnosed infection. No one knows how the organism spreads, but evidently it is not by casual contact, as family members of infected persons have not become infected themselves. (5)

Four monkeys were injected with Mycoplasma incognitus; all died in seven to nine months. The organism was found in the spleens of all the monkeys, and in some other organs as well. It was not found in a fifth monkey tested as a control. (6)

Extensive evidence from electron-microscope examinations, from specially designed PCR tests to look for the DNA of Mycoplasma incognitus, and from immunologic tests, showed that the organism was concentrated in lesions in affected organs. Mycoplasma incognitus is unusual in that it often infects and kills tissue without causing an inflammatory reaction, suggesting that it disables or evades part of the immune system.

The publication of this evidence, much of it in November 1989, led to a meeting between Dr. Anthony Fauci, director of NIAID (the National Institute of Allergy and Infectious Diseases) and other AIDS experts, with Dr. Lo and his colleagues at AFIP. The meeting, on December 14, 1989 in San Antonio, was chaired by Dr. Joel B. Baseman, chairman of the Department of Microbiology at the University of Texas Health Sciences Center in San Antonio, an expert on mycoplasma. An article in THE WASHINGTON POST (January 5) quoted Dr. Baseman as saying that Lo’s mycoplasma “might be a significant agent for many infectious diseases, not just AIDS. There is enough information to say that this agent is real.” The same article quoted Dr. Fauci as saying that Mycoplasma incognitus “may be an important opportunistic infection …If it’s real, it could have an important impact on how doctors look at AIDS patients with unexplained problems.” An in-depth history of the discovery of Mycoplasma incognitus and its early dismissal by parts of the scientific community was published in THE NEW YORK TIMES, January 16, 1990. What Should Be Done Now? Awareness of the new importance of Mycoplasma incognitus has not yet spread far in the medical community. The biggest problem is that there is no readily available test for the organism; at this time, there may be only one research lab which can do the test reliably. Other mycoplasmologists are becoming involved, however, and a much easier blood test is being developed. In addition, clinical trials are now being planned. The AIDS physician and patient community should help make sure that trials proceed quickly. There may also be immediate uses of the new information, for example: (1) Empirical Use of Antibiotics Several months ago, before Mycoplasma incognitus was known, Dr. Nathaniel Pier mentioned that he had found good results trying doxycycline for patients who had an apparent infection which could not be diagnosed. (Doxycycline is the antibiotic most often discussed as a possible treatment for Mycoplasma incognitus; however neither it nor any other antibiotic has yet been tested for treating this infection in humans.) Incidentally, the next physician we asked about empirical use of antibiotics preferred erythromycin, which would not be effective against the mycoplasma. The discovery of Mycoplasma incognitus provides an additional rationale for trying doxycycline (or one of the other antibiotics found effective against this organism in the laboratory) for certain patients, such as those with signs of undiagnosed infection, especially in the central nervous system, spleen, or certain other organs. Patients should know that antibiotics can cause side effects — some of which, such as overgrowth of Candida, might be more severe in persons with HIV [file:///Users/andrewma/Desktop/AIDS%20Campaign/Lo%20mycoplasm%20synopsis.html].

In 1990, the noted historian of science, immunologist, and MacArthur Fellow, Robert Root-Bernstein wrote an article in Perspectives in Biology and Medicine [20]:

“Most investigators believe that acquired immunodeficiency syndrome (AIDS) is caused solely by human immunodeficiency virus (HIV) (1,2). However several puzzling facts cast doubt on this conclusion: about 5 percent of all AIDS patients have been tested for seroconversion (3); seroconversion may not indicate active infection but, rather, a successful immunological response to HIV, at least in some cases ((47); a single T lymphotropic virus cannot explain the simultaneous immunosuppression of T cells, natural killer cells, B cells, and macrophages that characterizes the immune system of AIDS patients (47); several other immunosuppressive viruses and bacteria are as highly correlated with the sydrome as is HIV (8); Koch’s postulates have not been satisfied, nor have chimpanzees infected with HIV displayed any of the typical symptoms of AIDS (67); and seroconversion following HIV exposure is so varied (anything from seroconversion after a single unprotected sexual contact with an HIV carrier to no seroconversion after hundreds of unprotected encounters) that even HIV proponents are admitting that there must exist some “as yet unexplained biologic variation in transmissibility or susceptibility” to HIV infection (9). Indeed, between 30 and 100 hemophilacs may use the same lot of clotting factor concentrates, and yet there are no reported cases of more than one hemophilia developing AIDS from an AIDS-donorcontaminated lot (10, 11).”

“Furthermore, there is a logical problem that is often overlooked by uncritical HIV proponents: AIDS patients die of previously identified diseases, not of HIV infection per se. That is why AIDS is a syndrome, not a distinct disease entity. Thus, the putative role of HIV is solely to cause the immunosuppression that sets the stage for subsequent fatal opportunistic infections. But before we can accept HIV as the sole cause of immuosuppression characteristic of AIDS patients, it is necessary to assure ourselves that alternative explanations of the data do not exist. After all, theories, just like experiments, need controls; for just as experimental artifacts are reproducible, so can a theory explain existing data and yet, as Aristotle’s theory of falling bodies demonstrates, still not be the best explanation. In the present context we must, therefore, before accepting HIV as the sole cause of the immunosuppression typifying AIDS, demonstrate directly that HIV actually does cause immunosuppression in animals or human beings and also assure ourselves that other immunosuppressive agents cannot explain the etiology of AIDS. In other words, we must determine that the HIV theory is necessary and sufficient to explain AIDS and that no other theory is necessary or sufficient. Are there, for example, individuals who are immunosuppressed whose sole infection is HIV? If so, then we can assure ourselves that HIV is sufficient to cause immunosuppression. Do AIDS patients in general have any identified immunosuppressive risks other than HIV? If so, are these sufficient to explain the immunosuppression associated with AIDS in the absence of HIV, or not?”

“Existing data do not, as yet, allow us to establish HIV as the unequivocal cause of immuosuppression in AIDS. No nonhuman animal other than the chimpanzee appears to be infected by HIV, and HIV-infected chimpanzees do not display longterm immunological abnormalities (6,7). Moreover, all AIDS patients do have multiple, well-established causes of immuosuppression prior to, concomitant with, subsequent to, and sometimes in the absence of, HIV infection. These immunosuppressive agenst are of seven basic types: chronic or repeated infectious diseases caused by immunosuppressive microorganisms; recreational and addictive drugs; anesthetics; antibiotics; semen components; blood; and malnutrition. While no AIDS patient is likely to encounter all of these agents, all AIDS pateitns encounter several. Healthy heterosexuals and lesbians rarely encounter more than one. Therefore, the conclusion that HIV is the sole cause of immunosuppression in AIDS, and the sole factor differentiating AIDS patients from non-AIDS patients, cannot be maintained, and alternative hypotheses remain possible?”

“Intravenous drug abusers also share an immunosuppressive risk factor with hemophilicas and blood transfusion recipients: they receive other people’s blood. I am unable to find any data concerning the immunological effects of small doses of untyped blood such as drug abusers might encounter repeatedly by sharing needles: however, it is a well established principle of immunology that repeated injections of very small amounts of almost any antigen eventually result in suppression of the immune response (72). (given that these small, repeated blood injection will include a proportion of leukocytes, it is likely that immunosuppression to various HLA types will eventually occur. This mechanism of immunosuppression has previously been suggested for semen, which also contains small numbers of leukocytes.”

Anti-HLA alloimmunization has already been observed in multiply transfused patients (74,75). Repeated use of anticlotting factors results in abnormal suppressor:helper T-cell ratios even among otherwise healthy hemophiliacs and even in countries like Australia, in which HIV is virtually nonexistent (76, 78). Almost every hemophilic also contracts hepatitis (79) and presumably various other viral agents that are transmissible in blood, such as CMV and EBV (80, 82, 84). Physicians have known for over a decade that blood transfusions depress the immune response effectively enough to facilitate the acceptacnce of organ transplants and to increase significantly the risk of death from cancer (85, 89). This immunosuppression is dose related, and it is therefore significant that the average transfusion-relate4d AIDS patient receives blood from 16 to 21 donor-five or more times that of the average surgery patient (a statistically significant difference) (90, 91). Although the exact mechanism of transfusion induced immunosuppression is unknown, T cells are certainly a primary target, and B cells and macrophages are also involved. Thus, recent studies show that anyone receiving multiple transfusion or blood-derived products such as clotting agents-hemophilacs, those with sickle cell anemia (92), trauma patients (93), and surgery patients (94)-are at high risk for developing the lymphadenopathy, low helper T cell: suppressor T cell ratio, and low-grade fever associated with AIDS related complex (ARC). These symptoms generally preced HIV seroconversion.”

In 1991, another so-called specific marker for “HIV” was reportedly found in normal (non-“HIV-infected”) human placentas [21].

In 1992, it was reported that “HIV-sequences” exist in normal in human, chimpanzee, and rhesus monkey DNAs” [22].

That same year, it was reported that the hepatitis B vaccine causes false positive “HIV” test results [23].

Also in 1992, The Veterans Affairs Cooperative Study Group reported that:

“In symptomatic patients with HIV infection, early treatment with zidouvdine delays progression to AIDS, but did not improve survival, and was associated with MORE side effects. There were 43 deaths, 23 in the early-therapy group, and 20 in the late-therapy group. The medium time from the diagnosis of AIDS to death was 16 months in the early therapy group, and 19 months in the late-therapy group.”

“The racial and ethnic groups appeared to respond differently to the timing of zidpovudine therapy. Fewer minority (African American and Hispanic) patients died in the late therapy group (two deaths) than in the early-therapy group (nine deaths), but the difference was not significant. Among non-Hispanic white patients, early therapy significantly delayed the onset of AIDS but had no effect upon survival. Minority patients were much more likely than white patients to be intravenous drug users (40% vs. 10%). After two years of follow-up, we found no difference in survival between the two treatment groups.”

Therefore, the Hamilton et al study concluded:

AZT kills more healthy patients (early group) than sicker (late treatment) patients, and in addition, AZT disproportionately harmed Blacks and Hispanics, and provided no benefit to the quelling of advancing immune suppression in Caucasians [24].

In 1993, Defer et al. in a paper entitled, “Multicentre quality control of polymerase chain reaction [viral load] for detection of HIV DNA” claimed that: “False-positive and false-negative results were observed in all laboratories (concordance with serology ranged from 40 to 100%). In addition, the number of positive PCR results did not differ significantly between high- and low-risk seronegatives. The use of crude cell lysates in DNA preparation produced the same PCR results as phenol-extracted DNA. Discrepancies between laboratories indicated that factors other than primer pairs contributed strongly to laboratory variability. “[25].

Also in 1993, cervical cancer was included in the revision of the surveillance case definition for AIDS in 1993. The suggestion that cervical cancer is caused by “HIV” brought the number of cancers either caused directly or indirectly by “HIV” to include six different cancers:

1-Kaposi’ s sarcoma in a patient < 60 years of age, + antibodies or genomic fragments indirectly associated* with “HIV” (Although Kaposi’s sarcoma was the original AIDS-defining cancer, it is no longer considered by AIDS experts as being caused by “HIV,” but by Herpesvirus VIII – (Papadopulos-Eleopulos E, Turner VF, Papadimitriou J, Page B, Causer D, Alfonso H, Mhlongo S, Miller T, Maniotis A, Fiala C. A critique of the Montagnier evidence for the HIV/AIDS hypothesis. Med Hypotheses. 63(4):597-601, 2004).

2-Cervical cancer or mouth cancer + antibodies or genomic fragments indirectly associated with the molecular signature of “HIV.” (Cervical dysplasia and cervical cancer were added to the AIDS definition in 1993 causing the number of women classified with AIDS to increase notably. Even though some 65,000 Americans are diagnosed each year with cervical cancers, and only a small fraction of these (about .0015%) are among women that test “HIV” positive, and doctors assumed that “HIV-associated antibodies” + cervical abnormalities = AIDS. Cancer of the mouth was added this year as announced by “The New Scientist”, although no comprehensive studies can be found documenting this on MEDLINE.” (Wed Feb 25, 2004. LONDON Reuters – Although the risk is small and it is more likely to result from heavy drinking and smoking, scientists have suggested that oral sex can cause mouth cancer);

3-Lymphoma of the brain (primary) affecting a patient < 60 years of age + antibodies or genomic fragments indirectly associated with “HIV;”

4-Lymphoma, non-Hodgkins + antibodies or genomic fragments indirectly associated with “HIV;”

5-Lymph system cancer diagnosed three or more months after a diagnosis of any opportunistic infection + antibodies or genomic fragments indirectly associated with “HIV;”

6-Progressive multifocal leukoencephalopathy + antibodies or genomic fragments indirectly associated with “HIV;”

When these cancers occurred without the molecular signatures of “HIV” were treated, they were treated using the standards of care in the manner they were before ARV’s were introduced. However, if the molecular signature of “HIV” was detected in association with these cancers, then patients were given not only the standard of care for treatment of these cancers, they were additionally given ARV’s.

In 1993, Robert Root-Bernstein published the book, “Rethinking AIDS; The tragic cost of premature consensus”[26], in which he outlined an hypothesis he called Multiple
Antigen Mediated Autoimmunity (MAMA) to explain how idiotypic and anti-idiotypic immune mechanism could create an autoimmune syndrome like AIDS, given that the molecular mimicry of the signatures attributed to the presence of “HIV,” and the anti-idiotypic moieties that normally shut down the production of those antigens stimulated by “HIV’s molecular signature interact, which might cause an autoimmune disease that targets the immune system.

In 1993, it was reported that half of infants that test “HIV” positive at birth serorevert (reverse) their “HIV-positive status within 18 months [27].

In 1994, the Concorde study, which was up until then the longest, largest, and most carefully controlled AZT trail reported:

“The results of Concorde do not encourage the early use of zidovudine in symptom-free HIV-infected adults. They also call into question the uncritical use of CD4 cell counts as a surrogate endpoint for assessment of benefit from long-term antiretroviral therapy” [28].

Also in 1994, the details of why Dr. David Acer committed suicide were provided. It was discovered that on the basis of mistaken charges that he spread “HIV” to his patients [29], which the CDC later exonerated him of doing (after his suicide), the CDC could “find no evidence the dentist’s HIV-positive patients contracted their infections from him because their virus’ DNA did not match his, and also concluded the dentist’s patients did not contract the virus from one another — in effect, that unclean dental implements did not act as conduits.”

In 1995, it was reported that flu vaccines cause false positive “HIV” test results [30]. It was suggested later that this false positive rate was believed to have been the result of bad “HIV” tests, rather than the possibility that “HIV’s” molecular signature includes epitopes that are the same as those of influenza viruses.

In 1995, it also was confirmed again that about 67% of infants that test “HIV” positive at birth serorevert (reverse) their “HIV-positive status by 18 months [31].

In 1995, the Nobel Laureate, Kary Mullis published a new hypothesis attempting to show how immune collapse need not be due to any particular virus, but by a chain reaction.
If previously latent virus with a distinct epitope would provoke a new immune response, every immune response would be perpetually generating new immunogens. The immune system so infected would be perpetually generating new immunogens. As the frequency of infection increased such an immune chain reaction would be progressively more debilitating for the stability and effectiveness of immune function [32]. This hypothesis was important because it predicts that a vaccine against any specific virus would be ineffective against AIDS.

“If correct, then an experimental animal model of AIDS should be induced in laboratory animals by infecting them at a low multiplicity with a very large number of diverse viruses. One way of doing this would involve collecting the blood from a large number of wild mice from geographically distant locations, mixing it together and injecting it into healthy mice. The number of mice that would be required to produce such a lethal injection or series of injections is not predicted by this hypothesis, although from the numbers suggested by the behavior patterns of the human victims of AIDS the number of individuals whose viruses must be pooled might be quite high. The hypothesis suggests that some level of diverse infection would cause AIDS-like malfunction of the immune system to appear rapidly, and that this could not be reproduced by simply isolating a particular infectious specifies and infecting similar animals with only this species.”

“The hypothesis also suggests that blood from a single human AIDS patient should be capable of transferring the appropriate level of diversity of infection to another organism, given that the recipient organism contains a functional human immune system.”

“The hypothesis suggests further that aliquots of an appropriate dilution of the blood from a single AIDS patient injected into a large number of experimental animals with a human immune system would not be able to produce AIDS-like immune dysfunction in any one of them.”

IN 1995, The conclusions of The Office of Technology Assessment Book (1995 Congress of the United States: Office of Technology assessment. Adverse Reactions to HIV Vaccines: Medical, Ethical, and Legal Issues. Roger C. Herdman, Director) are presented to the 1995 Congress of the United States in 1994 by the AIDS Research Advisory Committee (ARAC) of the National Institute of Allergy and Infectious Dieases (NIAID) that recommended that Phase III clinical trials with enveloped vaccines should not proceed in the United States because of scientific, political, and ethical issues, and the significant level of scientific uncertainty about the wisdom of immediate trials.

Some of the conclusions include:
Vaccines may cause a false-positive HIV screening testing test?resulting in discrimination against vaccine recipients in, for example, military service, health insurance, life insurance, employment, and travel.

Participation in an HIV vaccine trial, itself, may result in stigmatization, as others may assume that all vaccine trial participants are members of groups, such as injection drug users and men who have sex with men, who are at increased risk for HIV infection.

Vaccinees, relying on the protection afforded by an experimental vaccine, may engage in behaviors that increase their risk for HIV infection.

There is the potential for the viruses to be inadequately attenuated, for an adequately attenuated viral vaccine to cause disease in immunocompromised individuals (Read AIDS patients), and for an adequately attenuated virus to revert to virulence. There is also concern that a live attenuated vaccine could induce tumors.

At the end of the Congressional document, the term “original antigenic sin” is advanced to describe:

A) When a vaccinated individual is exposed to a noncross- reactive strain of HIV that induces the production of antibodies specific for the vaccine strain that are unable to neutralize the newly encountered strain (in other words when a vaccine doesn’t work).

B)The fixing of an immune response in a non-adaptive pattern.

C) When vaccinated individuals may be no worse off than unvaccinated individuals because unvaccinated individuals also have a lag in generation of antibody to HIV because their immune response has not been “primed” by vaccination.

Also in 1995, a critical analysis of the HIV-T4-Cell-AIDS hypothesis appeared in Genetica by Papadopulos-Eleopulos et al., that reviewed the problematic issues associated with culturing “HIV” in vitro, and questioned whether the in vitro models can model anything like the AIDS syndrome [33]. In the article, the work of Laurent-Crawford et al. (of the Pasteur group) and the work of others were challenged variations in culturing techniques for “HIV” production in the lab have been ascribed to unbalanced signals and apoptosis or syncytial formation or persistant non-pathogenic viral production depending on whether lymphocytes are “immature or “mature,” or whether, as Gallo et al. had amplified the molecular signature of “HIV” using continuous cancer cell lines.

Also in 1995 Lewis Dalakas published an important paper in Nature Medicine entitled:
Mitochondrial toxicity of antiviral drugs. [Nat Med. 1995 May;1(5):417-22].

“Clinical manifestations of ANA [Antiviral Nucleoside Analogs, such as AZT] toxicity: It is self-evident that ANAs, like all drugs, have side-effects. However, the prevalent and at times serious ANA mitochondrial toxic side-effects are particularly broad ranging with respect to their tissue target and mechanisms of toxicity: ? Haematalogical toxicity [anemia, and other blood disorders] ? Myopathy [muscle disorders] ? Cardiotoxicity [heart disorders] ? Hepatic toxicity [liver disorders] ? Peripheral neuropathy [nerve damage].”

In 1997, it was reported that “no seroconversions” were observed among 175 HIV-discordant couples (where one partner tests positive, one negative), for a total of approximately 282 couple-years of follow up in a 10- year study [34].

Also in 1997, two teams of investigators, one consisting of a French-German collaboration [35], and another whose investigators were involved in the AIDS Vaccine Program, SAIC, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland [36], reported that PHA (phytohemagglutinin) and IL2 (interleukin-2) stimulated healthy cells produce “viral like particles” and the molecular signature of “HIV” only when stimulated with PHA and IL-2. They also claimed that microvesicles were a source of contaminating cellular proteins found in purified HIV-1 preparations, as their titles of their papers suggest:

“Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations” (Gluschankof et al.,1997) [35].

“Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations” (Bess et al., 1997) [36].

This work not only underscored the problem that there are no tissue or cell culture models of “HIV’s pathogenic effect as raised by Papadopulos-Eleopulos et al. in their Genetica article [33], but these facts raised issue regarding the basis of Gallo’s and Montagnier’s isolation, challenged Duesberg’s claims that the nucleic acids have been uniquely cloned, and discredited the hypothesis that the signature of “HIV” is due to a specific virus.

For example, in figure 3 in the Bess et al. paper, cellular debris was not distinguishable from any other object in the EM micrographs. These preparations published by both the Gluschankof et al., and Bess et al. groups, used the best techniques to date for the isolation and characterization of “HIV”s molecular components, including its nucleic acids and molecules such as p24 protein, p19, p24, p39, p45 and p55 viral core proteins as well as gp46, gp63 glycoprotein, but yet nothing that looked like a virus could be discerned in sucrose gradient-derived electron micrographs of “HIV.”

A comparison of retroviral preparations that could potentially yield pure components for vaccines, or test kits, versus those that are primarily composed of cellular debris, can be seen by comparing de Harven’s preparation of MMTV:


to these isolations presented by Gelderblom et al., (1997) and Bess et al., (1997):


In their 1997 paper, the Bess et al. authors also specifically emphasized that:

“Identification and analysis of the virus are complicated by the presence of cellular membrane vesicles which COPURIFY with the virus.”

“We recently reported a proteolytic procedure (Ott et al., 1995b) that effectively removes greater than 95% of proteins associated with these membrane vesicles. This procedure has allowed us to demonstrate that the cytoskeletal proteins, actin, ezrin, moesin, and cofilin are located in the interior of virions.”

Such statements raised questions such as:

If actin, exrin, and cytoskeletal proteins are located INSIDE the virions, how can one tell if p24, for instance, which is a faint band on most cellular gels that come from non-“HIV–infected” cells in most labs, if p24 and the other molecules thought to represent the specific molecules of “HIV” aren’t also proteins of cellular origin? For example, the gel shown in figure 1 of the Bess et al. paper (the non-infected lane) has weaker bands at all of these weight designations that supposedly the infected supernatants were run (Lanes B,C). The p24 band is visible in lane A, which is the uninfected lane.

Other issues Bess et al., raised, included the issues that Papadopulos-Eleopulos had raised in their Genetica article [33]:

“PHA activated human PBLs were also shown to produce microvesicles that incorporated cellular proteins (Fig. 6).”

“In addition to proteins, microvesicles were also shown to contain both RNA and DNA. Approximately 10ug of RNA and 4 ug of DNA were found per mg of protein. The major RNA species in microvesicles were ribosomal 28S and 18S subuitis and some low molecular species, PERHAPS tRNA.”

“Clearly, future experiments utilizing purified viruses must be carefully controlled to account for the effects of cellular antigens present on microvessels,”

“Numerous other cellular proteins have been identified in purified preparations of HIV-1. It is not known if these are physically associated with HIV particles and, if so, whether or not they have a role in the virus replication cycle. Identification of which cellular proteins are associated with the virus is a prerequisite to studying the potential function of cellular proteins in the virus replication cycle.”

Also in 1997, The DAIDS official “HIV” culturing manual that details the use of a series of standard protocols for culturing “HIV,” from the Reporting Results Section (section VII), the rationale was presented to identify non-“HIV-infected cells if:

“Two consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml (read: from a healthy donor source), of which the second value is at least four times greater than the first value or out of range” (O.D.>2) or

“Two consecutive HIV p24 antigen VQA CORRECTED values (read: from a healthy donor source) that are out of range” (Optical density.> 2); or

“Three consecutive HIV p24 antigen VQA CORRECTED values of > 30 pg/ml (read: from a healthy donor source), where neither consecutive value is > four times the previous sample, but the third value is at least four times greater than the first.”

Therefore, according to DIADS, cells were considered to be “HIV-negative” by “HIV” cell culturing labs if the 3 consecutive HIV p24 antigen VQA corrected values read (first test) 25 pg/ml, and (second test) 15 pg/ml, (third test) 5 pg/ml. Stated another way, cells would be considered non-infected if they read 25 on the first reading, and 15 on the second and 5 on the third. They would be considered positive if the values read, 30pg/ml, 31, pg/ml, and 31pg/ml.

Also with respect to the arbitrary cut-off values for p24 protein, it is also important to point out that p24 is found in the thymus gland of “HIV-negative” children [37].

“Abstract: An immunopathologic study of normal and severely atrophic thymuses (STA) was undertaken in order to evaluate the expression of human retrovirus (envelope and core) molecules in thymic epithelial cells (TEC) in HIV negative children. Both normal and STE thymuses disclosed p19, p24, p39, p45 and p55 viral core proteins as well as gp46, gp63 glycoprotein of envelope origin. No evidence of gp160, gp120 and gp41 molecules were observed in TEC which suggested endogenous lack of receptor molecules for HIV. The results are discussed in the context of possible thymus oriented autoimmune reaction in HIV and non-HIV bearing patients and in consequence, severe injury of TEC forming microenvironment.”

In 1998, and although during the AIDS era, the enzyme reverse transcriptase
(RT) was part of the molecular signature used to detect
“HIV,” as a substitute for viral isolation and purification, The Center For Biologics Evaluation and Research Advisory Committee on Vaccines and Related Biological Products claimed in November, 1998, in a chapter regarding the Update On Reverse Transcriptase Activity In Chicken Cell Derived Vaccines, by Dr. Arifa Khan (pages 13-15), that:

“Initially Boni et al. (1996) published that low level reverse transcriptase activity was detected in ALL chicken cell derived vaccines using a highly sensitive PCR-based reverse transcriptase assay called PERT, which can detect one to ten virions which was reported to the WHO, and then additional studies were done by several laboratories in Europe, as well as the U.S., including the NIBSC, the CDC, as well as labs in the FDA to confirm this initial finding. However, after further work, it was discovered that this reverse transcriptase activity could be eliminated by treatment of extracts with DNAase, and that using Alu-based EAV sequence integration studies, that no integration of anything derived from the chicken cell supernatants was detected in Human PBMC cells.”

In 1999, it was published in The Journal, AIDS, that children born to ZDV-treated mothers “are more likely to have a rapid course of HIV-1 infection compared with children born to untreated mothers, as disease progression and immunological deterioration are significantly more rapid and the risk of death is actually increased during the first 3 years of life” [38].

In 1999, it was also known that goat and cow sera test “HIV-positive” [39], yet goats and cows do not develop AIDS.

In 2000, it was reported that pregnant women test positive for “HIV” at high frequency [40], and the appearance of the so-called specific and unique antigens of an “HIV’s” molecular signature thus shares common molecular epitopes (molecular configurations) with those detected during pregnancy of certain women.


FROM: PEDIATRICS Vol. 105 No. 6 June 2000, p. e80

Methods: The medical records of 17 pediatric HIV-infected patients, in whom GT was used to improve HAART adherence, were retrospectively^ reviewed for clinical and laboratory parameters. Each record was reviewed for the period of 1 year before and after GT insertion. The main outcome parameters were virologic (plasma HIV RNA polymerase^ chain reaction quantification) and immunologic (CD4 cell counts)?

Results: GT was well-tolerated with minor complications, such as local site tenderness, reported by 4 patients (23%). Before GT insertion,^ only 6 patients (35%) were documented as being adherent, compared^ with all patients after GT insertion.

Conclusions: GT is well-tolerated in pediatric HIV-infected patients and should be considered for selected patients to overcome difficulties with medication administration and to improve adherence. For maximal virologic response, combination therapy should be changed at the time of GT insertion.

At 1-year post-GT insertion nearly 59% of patients had >= 2 log VL decrease (responder group). Both responders and nonresponders were similar in baseline VL, protease inhibitor exposure, and use of double protease inhibitor therapy. Yet responders were^ more likely to have changed therapy at or soon after GT placement, whereas nonresponders had no therapy changes after GT placement. These data suggest that to
minimize the impact of viral resistance secondary to nonadherence, HAART should be changed immediately^ after GT placement. Thereafter, the improved adherence will minimize^ development of resistance to the new combination. We found that^ the CD4 lymphocyte percentage changes in responders and nonresponders were not different (7% and 10% increase, respectively). One possible explanation for this may be related to the
relatively short period of follow-up post-GT insertion, which may have been insufficient to observe an immunologic response. Alternatively, a disconnect between viral response and CD4 cell response has been previously^ reported.19-21 Several mechanisms for this
phenomenon have been suggested including the possibility that protease-resistant mutants may have an altered pathogenicity related to lack of viral fitness.

Also in 2000, regarding one microbicide trial funded by The Gates foundation, it was claimed that spermicide doesn’t actually reduce any risk of transmission of “HIV’s” molecular signature, but actually increased the rate of the appearance of its signatures. This finding ran contrary to what is known about how safe sex practices, including condoms and spermicide (Maggie Fox. Spermicide worsens HIV risk, study finds. Reuters 12 July 2000):

“South Africa — Researchers hoping to find a way for women to protect
themselves from AIDS have said they were dismayed to find that a product they thought may prevent infection actually increased the risk.

The product, a spermicide called nonoxynol-9, did not protect prostitutes in Benin, Ivory Coast, Thailand and South Africa from infection with HIV, a
team of U.N.-sponsored researchers said.

“We were dismayed to find out that the group using the N-9 gel had a higher rate of HIV infection than the group using a placebo,” Dr Joseph Perriens, who heads the UNAIDS microbicide effort, told an AIDS conference Wednesday.

They tested nearly 1,000 women and found 59 of those who used the spermicide became infected with HIV, compared to 41 of those who used a dummy gel.

“We were extremely disappointed,” Lut van Damme, a researcher at the
Institute of Tropical Medicine in Antwerp who led the study, told a news

She said researchers may be forced to suspend other trials involving the
product, marketed under the trade name Advantage S by U.S.-based Columbia Laboratories Inc.

“The long-term safety of nonoxynol-9 as a family planning method may have to be re-evaluated,” she said.

Activists and researchers have been clamoring for the development of a
microbicide — a gel or cream sometimes described as an “invisible condom” — that women and men could use to protect themselves not only from HIV, but from other sexually transmitted diseases such as syphilis and gonorrhea.

“I think this may be the end of nonoxynol-9 as a potential microbicide,”
Van Damme said, although she said the trials did show that women — in this case prostitutes at high risk of HIV infection — would use a microbicide if one was available.

CDC Expresses Concern

The Centers for Disease Control and Prevention (CDC) said it was concerned by the findings because some groups advise people to use nonoxynol-9 to protect themselves from HIV if they cannot use a condom.

“I think it’s pretty clear we have to tell men who have sex with men not to
use it,” Dr. Lynn Paxton, a microbicides expert at the CDC, said in an

“I think they are most at risk and I know they are using it.” She said it
was less clear whether women who use nonoxynol-9 as a contraceptive — women who are not at risk of getting HIV — should avoid it.

“One possible reason for the findings was that the women who used the
spermicide had more lesions than the women who did not,” Van Damme said.

“If you use nonoxynol-9 (to protect from HIV), you are probably wasting your money. You may possibly be wasting your life,” Perriens said. But, he
added: “There is nothing in this trial to suggest you should stop using it
as a spermicide.”

UNAIDS said it was pressing for the development of other products.

“We know that there are more products to come,” Perriens said. “This
shouldn’t be the end of the field… One of the things holding up
development, increasingly, is a lack of private sector interest in this area.”

The Bill and Melinda Gates Foundation said it would try to help with a $25 million grant for microbicide research.”

“A total of 16 microbicides — a gel or cream used to block infection — are currently being evaluated. Of those, five are in major advanced studies. Drug trials into oral prevention drugs are also underway.”

At the conference, Melinda Gates further encouraged researchers and politicians alike to move past the stigma of HIV/AIDS:

“Stigma is so cruel,” she said. “It’s also irrational. Stigma makes it easier for political leaders to stand in the way of saving lives.”

The couple last week announced that their foundation would contribute $500 million over five years to fight HIV-AIDS, and met with Bill Clinton, the former U.S. president, to present their priorities for ending the epidemic.

In 2002, it was reported in The Journal of Virology, that saquinovir and other protease inhibitors are severely toxic to T-cells in the absence of “HIV” infection [41].

In 2004, it was reported in the New England Journal of Medicine that vitamin supplements can ward off progression to AIDS in the absence of HAART (Highly Active Anti-Retroviral Therapy) [42].

Also in 2004, the failure of AIDSVAX, the 120 million dollar effort to vaccinate against “HIV” was announced in the journal Science [43]. Shortly thereafter, it is announced that VAXGEN, Donald Francis’s company that performed the failed “HIV” trial, will receive more than 800 million from the military budget to make a new anthrax vaccine.

In 2004, the Red Cross also reported that even after repeated testing using different test kits, “low-risk” populations, such as blood donors (or military recruits) will typically yield 12 (PCR) positive or 2 (ELISA) positive results out of 37,000,000 samples, leaving potentially 10 out of 12 false positives, depending on which test kit you believe portrays “HIV’s molecular signature most accurately [44]. It is significant that 8 of the 12 PCR tests initially detected with ELISAs seroconverted within several months, thereby obtaining a consistent molecular signature in 8/12 cases, out of 37 million negatives.

That same year (2004) it was announced that the government’s chief of AIDS research, Dr. Edmond Tremont, rewrote a safety report on a U.S.-funded drug study of nevirapine to change its conclusions and delete negative information, and later, ordered the research resumed over the objections of his staff, so that George W. Bush’s pharmaceutical friend’s $500 million dollar plan to distribute nevirapine to African women would proceed, even though the drug’s approval was withdrawn in the U.S. because of excessive toxicity, its association with liver failure, and deaths [45]. In 2005, the Institute of Medicine covered up and trivialized Tremont’s criminal behavior, according to Johnathan Fishbein, who blew the whistle, and was subsequently fired from his position as safety officer for the Nevaripine trials that Tremont, his boss, rewrote [46].

On February 10th, 2005, three articles appeared in the New England Journal of Medicine advocating that it would be timely and cost effective to test every man, woman, and child for “HIV” at least once in their lifetime.

“In all but the lowest-risk populations, routine, voluntary screening for HIV once every three to five years is justified on both clinical and cost-effectiveness grounds. One-time screening in the general population may also be cost-effective” [47, 48, 49].
The authors of these articles did not define with precision who should be selectively biased “in all but the lowest risk populations,” but it is assumed they now recommend testing for children, and monogamous adults now in addition to “high risk” people of color, drug addicts, pregnant women, and men who have sex with men.

Yet again, following the 1995 article by Simonson et al., as recently as March 2006, an article was published in the New England Journal of Medicine warning that:

“A case-control study 2 of 101 blood donors (Simonson et al., 1995) who had been vaccinated against influenza and 191 matched controls showed that recent inoculation with any brand of influenza vaccine was significantly associated with a false positive screening assay for HIV antibodies. Guidelines of both Johns Hopkins and the New York State Department of Health list influenza vaccination as a known cause of indeterminate results on Western blotting for HIV antibodies (Reasons for false-positive, false-negative, and indeterminate results in assays for the detection of antibodies against HIV)” [50]. However, as mentioned before, it was subsequently believed that the false positives were not due to the flu vaccine but instead were due to problems with “HIV” testing.

Due to the seriousness of an “HIV” diagnosis (a reportable disease that lead to the losing of jobs, the abortion of babies, and the end of relationships, etc.), the FDA begins to publish recalls of defective “HIV” tests or statistics software, and testing and reference labs are provided with the lot numbers of defective testing merchandise. Patients who received these tests are quickly notified about the recall of the test they were subjected to. A few recent cases where recalls were made may here be illustrative:

Recall of HIV p24 Antigen Test Kit
Recall of Globus Media REcall HIV test
Recall of ORTHO Antibody to HBsAg ELISA Test FDA recall Ortho HBsAG System
Recall of Antibody to Human Immunodeficiency Virus Type 1 p24 Antigen Test Kits
Recall lancets for HIV kit
FDA Recall of NucliSens HIV test kit
FDA Recall of HCV EIA 2.0 Test Kit
Market Withdrawal of HIV-1 – HCV Assay, FDA recall Procleix
FDA Recall HIV-1 – HIV-2 Plus O EIA Testing Software
Recall of HIV Types 1 &2 (Synthetic Peptide)
FDA Recall of Amplicor HIV test kit

In 2006 at the Toronto International AIDS conference, Barre-Sinoussi said:

“It is not clear if therapeutic vaccines might be useful, since 15 trials to date have not demonstrated definitive evidence of improved outcomes.”

From U.S. Congressional records produced from meetings with vaccine makers in 1995, there were a total of at least 30 different trials for “HIV” vaccines (many of them Phase I or Phase II trials, without a single claim for induction of antibodies against “HIV,” cellular immunity, stimulating of cytotoxic T-cells, or mucosal immunity). [51].

In 2007, it was announced that viral load is only able to predict the rate of progression to disease in 4% to 6% of any HIV-positives studied, challenging much of the basis for current AIDS science and treatment policy for any individual who tests “HIV” positive [52, 53].

In 2006, a documentary appeared [54] in which CNN’s Chief International Correspondent Christiane Amanpour was filmed walking through villages in Kenya, remarking about the fact that the impoverished orphaned children don’t have enough watered down gruel to drink down the drug nevirapine, and the failed drug, AZT. In the documentary, Ms. Amanpour also provided the viewer with an interview with Stephen Lewis about his perspectives as the UN Secretary-General’s Special Envoy for HIV/AIDS in Africa, a post he held since June 2001 as a Commissioner for the World Health Organization’s Commission on the Social Determinants of Health, as Senior Advisor to the Mailman School of Public Health at Columbia University in New York, Director of the Stephen Lewis Foundation, and recipient of many awards and 22 honorary degrees including a Companion of the Order of Canada, Maclean’s Magazine 2003 “Canadian of the Year,” and in Time Magazine’s April 2005 100 most influential people in the world.

In a speech Lewis gave at the closing session of the XVI International AIDS conference in Toronto this summer, he presented a list of issues regarding AIDS in the world and especially in Africa. In his speech, Lewis spent one of the sessions vilifying The South African Minister of Health for advocating foods that are important for nutrition and health.

The sixth most important issue, according to Lewis, was:

“Number 6: It is now accepted as unassailable truth that people in treatment need nutritious food supplements to maintain and tolerate their treatment. And yet, there is a growing clamour from People Living with AIDS that decent nutrition simply isn’t available, leaving them in a desperate predicament. The World Food Programme released a study at this conference calculating the cost of food supplementation at 66 cents a day for an entire family; what madness is it that denies the World Food Programme the necessary money?”

“The growing clamour” from people living with AIDS, as Mr. Lewis described, is another way of saying “we are hungry- we are starving for food and water.” It is made clear in the documentary that the people filmed couldn’t possibly be receiving the amount of protein, in either vegetable or animal form, to sustain immunity. When considering assays in human patients which diagnose “AIDS” by quantifying the number of lymphocytes/ml, patients are not considered to have an AIDS-defining illness if thy have suffered from chronic starvation, as these individuals are known to possess a helper T-cell ratio in the AIDS-defining range or even lower (< 250 cells/ml), and can present with as much as a 90% reduction in their normal T-cell number which is reversible upon nutritional supplementation and a normal diet [55, 56]. Both in Amanpour’s documentary, and in Lewis’s lofty speech before the International AIDS conference where he lists food as number 6 in importance (following of course more important things like circumcision and microbicides to smear on African people’s genitals), the intractable paradox was presented whereby it is difficult to conceive how all the African children could have received highly toxic immune suppressive drugs such as nevirapine and AZT, when they didn’t have enough food and water to wash down the pills.

Methods: We analyzed data from 22217 treatment-naïve HIV-1-infected adults who had started HAART and were followed in one of 12 cohort studies. The probablility of reaching 500 or less HIV-1 RNA copies per mL by 6 months, and the change in CD4 cell counts, were analyzed for patients starting HAART in 1995-96, 1997, 1998, 1999, 2000, 2001, and 2002-03. The primary endpoints were the hazard ratios for AIDS and for death from all causes in the first year of HAART, which were estimated using Cox regression.

Interpretation: Virological response after starting HAART improved over calander years, but such improvement has not translated into a decrease in mortality.
[The Antiretroviral Therapy (ART) cohort Collaboration-www.thelancet.com Vol 368, 451-58, August 5, 2006].

Also in 2006, Dr. John Moore of Weil Medical College, one of the featured speakers in the 2006 International Toronto AIDS Conference described his work, which involved inseminating rhesus macaques up to 5 times after smearing a spermicide cream in their vaginas to prevent “SIV,” In his talk, he claimed that his “Hail Mary” experiments hold great promise and could solve the “AIDS apocalypse in Africa and elsewhere. He argued that multiple inseminations are necessary in order to model the frequent sexual activity that goes on in these 3rd World Nations. To rigorously prove his “SIV-fighting” spermicide worked, his Hail Mary experiments involved inseminating macaques 4-5 times after smearing his microbicides on their genitals. However, although “SIV” has always been a better model of “HIV” than “HIV,” critics suggested that Dr. Moore try Human “HIV,” perhaps with dogs, cows, goats, sheep, or non-infected monkeys, chimps, and humans that have naturally occurring “HIV” sequences, as stated above. Although none of these animals acquire AIDS from “HIV,” neither did his monkeys since he is inseminating them with “SIV.”

On December 14, 2006, a New York Times editorial article appeared, entitled, “Rare Good News About AIDS”:

“The announcement yesterday about the results in two African studies of male circumcision may be the most important development in AIDS research since the debut of antiretroviral drugs more than a decade ago. The National Institutes of Health halted studies in Uganda and Kenya when it became overwhelmingly clear that circumcision significantly reduces men’s chances of catching H.I.V.”

A Kenyan AIDS trial was interrupted because a 53 percent reduction in acquisition of “HIV” among circumcised men was observed. Out of 2,784 men studied in the trial, 69 men were “HIV” positive: 22 of these were circumcised, and 47 uncircumcised. Many, if not all 65 of them had received prior (or concurrent) treatment for penile infections, and 28 of the 69 had serologic syphilis at the outset. A year before, it was claimed that a trial of 4,996 HIV-negative men in Rakai, Uganda, showed that HIV acquisition was reduced by 48 percent in circumcised men. In the past, AIDS science by press release, like the Kenyan trial we question in this analysis, has led to horrible consequences for hundreds of thousands during the AIDS era who were experimented on with toxic “life saving” or “life extending” drugs.

Other studies regarding the ability of circumcision to protect against “HIV” acquisition in both males and females have yielded conflicting data regarding the ability of circumcision to block acquisition of “HIV,” and the role that other STD’s or medical conditions play as cofactors in acquiring “HIV.” Uncertainties exist because: data has been acquired at STD clinics or from trial participants with genital ulcer disease (GUD) or other infections, and the relative roles (if any) of biological versus cultural practices that influence “HIV” acquisition have been challenged by the WHO. Uncertainties regarding the damage done by microbicides also exist, which apparently increase the frequency of reported genital lesions and the feared spread of “HIV.” The ability or inability to neutralize “HIV” by washing with mild or concentrated detergents is in question, and the transmission of “HIV” from human to human by providing evidence of seroconversion has yet to be provided in a form that constitutes as careful a study as the 10 year study that followed 175 serodiscordant couples for 10 years that found no conversions. Uncertainties also exist because of the vastly different rates and efficiency of transmission said to be associated with heterosexual, homosexual, and IV drug use in different regions, and, because of the ability of gamma globulin in neutralizing “HIV” among well-nourished and healthy individuals. Uncertainties also exist especially because of the validity (and invalidity) of different test kits to identify “HIV” positive participants, and the role (or non-role) of T-cells in progression to AIDS is also still in question.

The role of circumcision in preventing transmission of “HIV” and acquisition of AIDS in Africa is further complicated by compelling evidence from a series of recent studies that identified nosocomial (hospital and doctor-medicated) “HIV” transmission as the single most critically important factor for the spread of AIDS in Africa, which accounts for many anomalies and conundrums that cannot be explained by a sexual transmission hypothesis. For example, many studies report HIV infections in African adults with no sexual exposure to HIV, and in children with HIV-negative mothers. Transfusion has been identified as a very high risk factor, and unexplained high rates of HIV incidence have been observed in African women only during antenatal and postpartum periods. There are many studies that claim to show that 20%-40% of HIV infections in African adults are associated with injections at clinics. From the 1950s into the 1980s, unsafe injections may have contributed to the silent spread of HIV in Africa in much the same way that other types of vaccination campaigns, including injections for schistosomiasis and other treatments in Egypt, established “hepatitis C” as a major blood-borne pathogen. While evidence for nosocomial transmission of “HIV” continues to accumulate since the long established fact that hepatitis B and flu vaccines cause “HIV” positive tests in some individuals, six Bulgarian health care workers (The Tripoli Six) are currently about to be executed by firing squad in Libya for their alleged role in supposedly transmitting “HIV” to more than 400 Libyan children. The confusing nature of secondary syphilis and yaws in Africa also have contributed to the confusion of diagnosis, in addition to a host of other diseases such as syphilis, or dozens of syndromes that can be mistaken as “AIDS.”

To examine the potential value of circumcision versus the possibility of nosocomial transmission, misdiagnosis, and other possibilities regarding the acquisition of AIDS in Africa, examination of both established and new AIDS policies that will affect millions of people should include the vital statistics generated by Africans themselves if they are available, as well as recommendations by physicians who have direct, empirical knowledge of African AIDS from their hospital or clinical setting. Evidence suggests that it is difficult, if not nearly impossible to attribute specific illnesses to “HIV/AIDS” in Africa because there are so many other confounding reasons/factors that cloud the unequivocal identification of “HIV” or “AIDS” diagnosis, a recent comprehensive study published in The New England Journal of Medicine reported that the number of alleged “HIV/AIDS” cases is negligible compared to morbidity associated with malnutrition, malaria, and TB. This assertion by the New England Journal of Medicine authors, that “HIV” is not a significant threat to Africans, also is supported by a wealth of data obtained directly from Statistics South Africa and other sources, which reported for both 2003 and 2004, that “HIV diseases” were officially ranked #21 in the list of leading causes of death for South Africa, and constituted between 2-3% of all deaths throughout most regions. These statistics, reported by Africans themselves, are supported by historical, sociological, and cultural considerations, by the accounts of prison officials, as well as by both African and foreign doctors who have written about how serving medical care to Africans has changed or not changed over the period of several decades. Both mortality statistics and doctors who have spent decades serving medical care to Africans collectively indicate that both children and adults in many regions of Africa, instead of suffering from “HIV/AIDS,” suffer from malnutrition, respiratory illnesses with high frequency, tuberculosis, protein insufficiency, and malaria. These observations further suggest that the state of affairs regarding “HIV/AIDS” in Africa has nothing to do with sexual activities, but reflects the changing nature of African political economies since the late 1970s, its devastation on African lives, in some regions, because of the traumas of civil war violence, and the damage to African culture and society due to a proliferation of “HIV” testing, and flood of “HIV/AIDS” health care opportunism. Moreover, experts on African AIDS concur that the HIV tests are dangerous because they cause panic and stigmatization, and they lead to the needless use of potentially dangerous and toxic anti-viral drugs, and by doing so, are drawing attention away from the real sources of immune system deficiencies to the extent that common sense and scientific reason dictate their abandonment.

In 2007, virological failure or drug resistance are technical terms among “HIV-AIDS” proponents that have come to mean that an anti-retroviral drug doesn’t work (fails to suppress virus), or that disease progression is more rapid in those that take a particular drug. In the New England Journal of Medicine, it was reported (and despite its known toxicity and withdrawal from the U.S. several years ago):

“Well over 875,000 women and infants have received a single dose of nevirapine. A single dose of nevirapine is the cornerstone of the regimen recommended by the World Health Organization (WHO) to prevent mother-to-child transmission among women without access to antiretroviral treatment and among those not meeting treatment criteria. However, nevirapine resistance is detected (with the use of standard genotyping techniques) in 20 to 69% of women and 33 to 87% of infants after exposure to a single, peripartum dose of nevirapine. Among 60 women starting antiretroviral treatment within 6 months after receiving placebo or a single dose of nevirapine, no women in the placebo group and 41.7% in the nevirapine group had virologic failure (P<0.001). Women who had received a single dose of nevirapine had significantly higher rates of virologic failure on subsequent nevirapine-based antiretroviral treatment than did women who had received placebo. This apparently deleterious effect of a single dose of nevirapine was concentrated in women who initiated antiretroviral treatment within 6 months after receiving a single dose of nevirapine. We did not find that a previous single dose of nevirapine compromised the efficacy of subsequent nevirapine-based antiretroviral treatment in women who started antiretroviral treatment 6 months or more after delivery. Among the 30 HIV-infected infants, a single dose of nevirapine (one each to mother and infant) as compared with placebo was associated with significantly higher rates of virologic failure and smaller CD4+percentage increases in response to subsequent nevirapine-based antiretroviral treatment”[57].

On Monday, July 23, 2007, in Nkange, Botswana, it was reported that (Craig Timberg Washington Post Foreign Service that in Botswana, step to cut AIDS proves a formula for disaster:

“Doctors noticed two troubling things about the limp, sunken-eyed children who flooded pediatric wards across Botswana during the rainy season in early 2006: They were dying from diarrhea, a malady that is rarely fatal here. And few of their mothers were breast-feeding, a practice once all but universal.”

“After the outbreak was over and at least 532 children had died — 20 times the usual toll for diarrhea — a team of U.S. investigators solved the terrible riddle.”

“A decade-long, global push to provide infant formula to mothers with the AIDS virus had backfired in Botswana, leaving children more vulnerable to other, more immediately lethal diseases, the U.S. team found after investigating the outbreak at the request of Botswana’s government.”

On July 23, 2007, and article appeared: “Low-Key Recall of AIDS Drug Hits World’s Poor,” by Elisabeth Rosenthal:

ROME, July 21 – “A total recall of an important AIDS drug widely used in developing countries has disrupted treatment for tens of thousands of the world’s poorest patients, with no clear word from the manufacturer on when shipments will resume.”

“The recall of the drug, Viracept, by Roche Pharmaceuticals of Switzerland, went largely unnoticed in the developed world when it was announced in early June, after the company had discovered that some batches made at its Swiss plant contained a dangerous chemical. But the recall has caused growing concern among global health officials and in AIDS programs in many poor nations. They say the company did an inadequate job of informing patients and officials about the potential risks and helping them find affordable access to newer alternative drugs.”

With respect to understanding the significance of the molecular signature of “HIV” that Dr. Gallo’s group associated with the 48 isolates from AIDS patients, as well as everyone else who has since tried to associate the molecular signature of “HIV” to the disease called AIDS, would it be more prudent to adopt a point of view consistent with the cellular and immunological facts that we do know about immune suppression more generally? In other words, shouldn’t we in the scientific community assume that profound immunosuppression is caused by a myriad of factors and that it is incorrect to group these syndromes under a single disease entity, “HIV/AIDS.” The consequences of this view suggest that different treatment strategies are needed for the spectrum of the previously known “AIDS-indicator diseases,” rather than the toxic and dangerous pharmaceutical or vaccination approaches currently in place.

Will the scientists who continue to support the “HIV=AIDS” paradigm begin to someday ask themselves why “HIV” components aren’t immunogenic or able to prevent AIDS progression in the immunosuppressed after the 30th or perhaps hundredth failed “HIV” vaccine trial, and then allow other scientists to look at other hypotheses, by lifting censorship, and providing funds for hypotheses that do explain the pathogenesis and rational reversal of severe immune suppressive illnesses? When will the AIDS establishment explain why a positive “HIV” test result is something to fear, since it is the same molecular signature that is exhibited by “HIV-positive” individuals that they are trying to evoke with an “HIV” vaccine? A related question may be to ask, if “HIV” vaccines ever do evoke a consistent positive immune response (antibodies as evidence of immunization), then will millions upon millions of “HIV-immunized” people need to carry around letters to announce the fact that they have been vaccinated against “HIV,” so that their sexual partners, insurance agencies, and employers (and ACIP advisory panels staffed with pharmaceutically-backed decision makers), won’t think an “HIV-positive” test result is due to acquiring “HIV” from a source other than a successful vaccination, and so their insurance policies, relationships, or jobs, happiness, and futures won’t be denied to them as they are currently because of the often deadly stigma of testing “HIV-positive?”

Questions about the relationship between “HIV” and “AIDS” haven’t only been advanced by individuals like Nobelist and PCR test-kit inventor Kary Mullis (PCR is used to amplify “HIV’s” unique genome sequence despite Mullis’s warnings that his invention cannot be used to do quantify viral load), DNA foot-print inventor and Nobelist, Walter Gilbert (who said that “the views of people like Duesberg are incredibly important, ” or Alfred Hassig, former head of the European blood banks (who said that AIDS is caused by excessive oxidation and that the death sentence accompanying and AIDS diagnosis should be abolished because doctors aren’t prophets and that AZT causes AIDS), and Dr. Heinz Ludwig Sänger, Emeritus Professor of Molecular Biology and Virology, and former director of the Department of Viroid Research, Max-Planck-Institutes for Biochemy, München, and recipient of the Robert Koch Award in 1978 (who said that “HIV” hasn’t been isolated”), as well and many others who have asked a question about the relationship between the molecular signature of “HIV” and “AIDS.” For instance, in a letter to Süddeutsche Zeitung (Oct. 2000), Dr, Sanger wrote:

“During the past 20 years HIV-AIDS research has shown to a line of critical scientists again and again that the existence of HIV has not been proven without doubt, and that both from a aetiological (causal), and a epidemiological view, it can not be responsible for the immunodeficiency AIDS. In view of the general accepted HIV/AIDS hypothesis this appeared to me so unbelievable that I decided to investigate it myself. After three years of intensive and, above all, critical studies of the relevant original literature, as an experienced virologist and molecular biologist I came to the following surprising conclusion: Up to today there is actually no single scientifically really convincing evidence for the existence of HIV. Not even once such a retrovirus has been isolated and purified by the methods of classical virology.”

In this respect, for many of us who have followed every development in the AIDS debacle since it officially began here in the US in 1984, Wainberg’s statement about incarcerating Peter Duesberg and others who ask questions regarding the biology of AIDS only serves as yet another pathetic example of the Public Health Service and media-censored McCarthyism regarding “HIV” and “AIDS”. In his terse dismissal of Duesberg’s ideas, and his call for jailing National Academy members such as Duesberg who spent a life time defining retroviruses and oncogenes, we clearly can see Dr. Wainberg and his ilk, revisiting the tactics of the Spanish Grand Inquisitors, or patriotic commission run by Senator Joe McCarthy, with Ronald Regan at his side, attempting to cleanse the scientific community of normal scientific discourse. “Have you now, or ever been, someone who dared ask a question regarding the reality and pathogenesis of “HIV,” and its role in causing the previously known diseases or syndromes now collectively called “AIDS?” “And Sir, do you know anyone, especially scientists or physicians, who have asked such a question? Could we please have their names now?”

It is only appropriate that because this history essentially began with Gallo’s and Montagnier’s New England Journal of Medicine article [2], that it should end with a quote from the same article:

“Many lessons can be drawn from this early intense period, and most suggest that science requires greater modesty” [2].


1. In their own words-NIH Research Recall the Early Years of AIDS. http://aidshistory.nih.gov/timeline/index.html#2

2. Gallo RC., Montagnier LM. The discovery of HIV as the cause of AIDS. NEJM Vol. 349:2283-2285, December 2003.

3. Barre-Sinoussi, F,J.C. Chermann J.C., Rey F., Nugeyre MT., Chamaret, S., Gruest J., Dauguet C., Axler-Blin C., Vezinet-Brn F., Rouzioux, C., Rozenbaum R., & Montagnier L. Isolation of a T-lymphotropic retrovirus from a patient at risk for Acquired Immune Deficiency Syndrome. Science 230: 868-871, 1983.

4. Coulter HL. AIDS and Syphilis-The Hidden Link, North Atlantic Books,
Berkeley, CA, pps. 20, 21,1987.

5. Hirsch MS, Wormser GP, Schooley RT, Ho DD, Felsenstein D, Hopkins CC, Joline C, Duncanson F, Sarngadharan MG, Saxinger C et al. Risk of nosocomial infection with human T-cell lymphotropic virus III (HTLV-III).N Engl J Med. Jan 3;312(1):1-4, 1985.

6. Schiff I, Correia B, Ravnikar VA, Schur PH. HTLV-III antibody testing in sperm donors.N Engl J Med. Jun 20;312(25):1638, 1985.

7. Resnick L, Veren K, Salahuddin SZ,Tondreau S, Markham PD.
Stability and inactivation of HTLV-III/LAV under clinical and laboratory
environments. JAMA. Apr 11;255(14):1887-91, 1986.

8. Varmus H. Reverse transcription. Sci Am. 1987 Sep;257(3):56-9, 62-4. Review.

9. Peter H. Duesberg, “Retroviruses as Carcinogens and Pathogens: Expectations and Reality Cancer Research 47, 1199-1220, March 1, 1987.

10. Fauci, A.S. Mechanisms of Corticosteroid Action on lymphocyte Subpopulations I. Redistribution of circulating T and B lymphocytes to the bone marrow. Immunology 28: 669-679. 1975.

11. Fauci, A.S., Dale, D.C., and Balow, J.E. Glucocorticosteroid therapy: Mechanisms of Action and Clinical Considerations. Annals of Internal Medicine 84: 304-15, 1976.

12. Haverkos, 2003, J. Biosci. 1 Vol. 281, No. 4, June, 2003.

13. “The Other Side of AIDS, ” AFI Los Angeles International Film Festival, 2004.

14. Fischl M A, Richman D D, et al and the AZT Collaborative Working Group 1987 The efficacy of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex; N. Engl. J. Med. 317 185-191, 1987.

15. Duesberg et al., J. Biosc, Vol. 28 No. 4, 383-412, June 2003.

16. Lauritsen, The AIDS War, or Poison by Prescription: The AZT Story. Asklepios, 1993.

17. Papadopulos-Eleopulos EP. Is the Oxidation Induced by the Risk Factors the Primary Cause? Medical Hypotheses 25: 151-162, 1988.


19. Varmus H. Reverse transcription in bacteria. Cell 56:721-724, 1989.

20. Robert Root-Bernstein. Do we know the causes of AIDS. Perspectives in Biology and Medicine: Summer, 33:480-500, 1990.

21. Faulk WP, Labarrere CA. HIV proteins in normal human placentae. (American Journal of Reproductive Immunology 25:99-104, 1991.

22. Horwitz MS, Boyce-Jacino MT, Faras AJ. Novel human endogenous sequences related to human immunodeficiency virus type 1. J Virol. Apr; 66 (4):2170-9, 1992.

23. Lee, D, Eby W, Molinaro, G.. HIV false positivity after Hepatitis B vaccination. Lancet 339: 1060, 1992.

24. JD Hamilton et. al. and the Veterans Affairs Cooperative Study Group. A controlled trial of early versus late treatment with zidovudine in symptomatic human immunodifficiency virus infection. New England Journal of Medicine, 326: 437-434, 1992.

25. Defer Defer C, Agut H, Garbarg-Chenon A, Moncany M, Morinet F, Vignon D, Mariotti M, Lefrère JJ. Multicentre quality control of polymerase chain reaction [viral load] for detection of HIV DNA. (AIDS 6: 659-663, 1992).

26. Robert Root-Bernstein, ‘Rethinking AIDS; The tragic cost of premature consensus’ The Free Press/Macmillan USA, 527 pages, 1993. ISBN 0-02-926905-9.

27. Parekh BS, Shaffer N, Coughlin R, et al. Dynamics of maternal IgG antibody decay and HIV-specific antibody synthesis in infants born to seropositive mothers. The NYC Perinatal HIV Transmission Study Group. AIDS Res Hum Retroviruses 9:907-12, 1993.

28. Seligmann et al., Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee. Lancet, Apr 9;343(8902):871-81, 1994.

29. Ted Anthony. STUDY: HIV not contracted from dentist. Associated Press, Thursday, December 1, 1994. ww2.aegis.org/news/ap/1994/AP941233.html].

30. Simonsen L, Buffington J, Shapiro CN, et al. Multiple false reactions in viral antibody screening assays after influenza vaccination. Am J Epidemiol 141:1089-1096,1995.

31. Chantry CJ, Cooper ER, Pelton SI, Zorilla C, Hillyer GV, Diaz C. Seroreversion in human immunodeficiency virus-exposed but uninfected infants. Pediatr Infect Dis J 14:382-7, 1995.

32. Kary B. Mullis. A hypothetical disease of the immune system that may bear some relation to the Acquired Immune Deficiency Syndrome. Genetica 95: 195-1995.

33. Eleni Papadopulos-Eleopulos, Valendar F.Turner, John M. Papadimitriou, David Causer, Bruce Hedland-Thomas, Barry Page. a critical analysis of the HIV-T4-Cell-AIDS hypothesis. Genetica 95: 5-24, 1995.

34. Padian, et al. Heterosexual Transmission of HIV in Northern California: Results from a Ten-Year Study.” American Journal of Epidemiology. August, 1997.

35. Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virology. Mar 31;230(1):125-33, 1997.

36. Bess JW Jr, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virology, Mar 31; 230(1):134-44, 1997.

37. Dura WT; Wozniewicz BM; Expression of antigens homologous to human retrovirus molecules in normal and severely atrophic thymus. Thymus. 22(4):245-54, 1994.

38. de Martino et al., Rapid disease progression in HIV-1 perinatally infected children born to mothers receiving zidovudine monotherapy during pregnancy. AIDS. 13 (8):927-933, May 28, 1999.The Italian Register for HIV Infection in Children. AIDS, 13:927-933, 1999.

39. Willman et al., Heterophile Antibodies to Bovine and Caprine Proteins Causing False-Positive Human Immunodeficiency Virus Type 1 and Other. Enzyme-Linked Immunosorbent Assay Results. Clinical and Diagnostic Laboratory Immunology, p. 615-616, Vol. 6, No. 4, July 1999.

40. Doran TI et al. False-Positive and Indeterminate Human Immunodeficiency Virus Test Results in Pregnant Women. Arch Fam Med. Sep/Oct; 9: 924-9, 2000.

41. Estaquier et al., Effects of Antiretroviral Drugs on Human Immunodeficiency Virus Type 1-Induced CD4+ T-Cell Death Journal of Virology, June, p. 5966-5973, Vol. 76, No. 12, 2002.

42. Wafaie W. Fawzi, et al. A Randomized Trial of Multivitamin Supplements and HIV Disease Progression and Mortality Volume 351:23-32, July 1, Number 1, 2004.

43. Gallo and Others. A sound Rationale needed for Phase III HIV vaccine trials Science, Vol 303 16 January, 2004.

44. Stramer et al. “Detection of HIV-1 and HCV Infections among Antibody-Negative Blood Donors by Nucleic Acid-Amplification Testing. New England Journal of Medicine, Volume 351:760-768, August 19, Number 8, 2004.

45. By John Solomon. “AIDS Research Chief Rewrote Safety Report.” Dec 2004. Associated Press Writer. http://www.ahrp.org/infomail/04/12/15b.php

46. John Solomon. “Institute of Medicine Panel Betrays Mission: Covers-Up Wrongdoing, Hides Conflicts of Interest: Aftermath of the Tremont affair. April 8, 2005.

47. Sanders et al., Cost-Effectiveness of Screening for HIV in the Era of Highly Active Antiretroviral Therapy; NEJM, Volume 352:570-585, February 10, Number 6, 2005.

48. Paltiel et al. Expanded Screening for HIV in the United States – An Analysis of Cost-Effectiveness. Volume 352:586-595, February 10, Number 6, 2005.

49. Samuel A. Bozzette, M.D., Ph.D. Routine Screening for HIV Infection – Timely and Cost-Effective. Volume 352:620-621, February 10, Number 6, 2005.

50. Christian, P. Erickson, Todd McNiff, Jeffrey D. Klausner. Influenza Vaccination and False Positive HIV Results New England Journal of Medicine,Number 13 , Volume 354:1422-1423, March 30, 2006.

51. 1995 Congress of the United States: Office of Technology assessment. Adverse Reactions to HIV Vaccines: Medical, Ethical, and Legal Issues. Roger C. Herdman, Director.

52. Rodriquez B, Sethi AK, Cheruvu VK, et al. Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection. JAMA 296(12):1498-506, 2006.

53. Cohen J. Study says HIV blood levels don’t predict immune decline. Science 313(5795):1868, 2006.

54. Christiane Amanpour. World fails to save Africa’s AIDS orphans Wednesday, July 19, 2006. http://www.cnn.com/2006/WORLD/africa/07/17/amanpour.africa.btsc/index.html

55. Parent et al. In vitro lymphocyte-differentiating effects of thymulin (Zn-FTS) on lymphocyte subpopulation of severely malnourished children. Am. J. Clin. Nutr. 60(2):274-8, 1994

56. Chevalier et al. Immune recovery of malnourished children takes longer than nutritional recovery: implications for treatment and discharge. J. Trop Pediatr 44(5):304-7, 1998.

57. Lockman S. et al., Response to Antiretroviral Therapy after a Single, Peripartum Dose of Nevirapine. The New England Journal of Medicine 356 january 11, 2007.


3 comments so far

  1. Keith Styles on

    My first reaction was one of disbelief that a person with your credentials could support the work of Dr Gallow, his associates and their HIV research.
    Your “Questioning AIDS” Blog is extensive and takes a considerable effort to read and assimilate.
    However, after reading it all, I find that in fact your ARE questioning Dr Gallow’s research, his findings and also seems to suggest the findings and continued declarations that HIV=AIDS are very highly suspect!

    Your conclusions and all the research you reference, seems to suggest science has made almost NO progress in identifying a single cause for HIV and it does not prove the paradigm that HIV=AIDS. It also suggest the WHO and scientific community who so strongly support the theory HIV=AIDS, is severely blinkered in their beliefs.

    Dare I suggest their support is more in line with maintaining their reputations and status within their communities, rather than finding a definitive cause for the Immune Dysfunction so many suffer..

    Please correct my conclusion, if it is in error!

  2. Gene Semon on

    Excellent, a great overview has been provided by Dr Maniotis. It’s clearly a service to the many in need of an accurate history of the tragedy we’ve come to know as AIDS. Should be required reading for all journalists covering this issue.

    And by apologizing to Dr Gallo, I think he’s shown himself to be the bigger man. It should be obvious that certain journalists cannot cover issues scientific without artificially injecting controversy. This is not a very good substitute for technical expertise on the science being covered and appears to be a feeble attempt at demonstrating an escape from the clutches of spin doctors. After all, anyone can check the authors of Montagnier et al’s 1983 –1985 papers to see the CDC – Pasteur Institute collaboration and the article in Nature that showed accidental contaminations as the more likely explanation for the nearly identical “molecular signatures”.

  3. Gene Semon on

    BTW, “the origin of HIV-1 isolate HTLV IIIB”, is the paper published in Nature, Volume 363, June 3-1993, referred to above. The boring technical details belong in the correction to the record and form the basis of the previously stated “accidental-same-molecular-signature” from the Gallo and Montagnier laboratories. I originally posted this at New AIDS Review.

    The confusion over isolating the same “AIDS virus” appears to be due to LAV being contrasted with the different HTLV variants by other research groups. The HTLV Roman-numerating taxonomy was the system that made “III” distinct from “I” and “II” based on an alleged “cell-free transmission”, but also on different nucleic-acid sequences. However, these 3 clones were kept in the same “family” based on partial nucleic acid sequence identities.

    The Nature-93 paper traces the effects of 2 “accidents”, the first being a “contamination of a culture derived from patient BRU by one from patient LAI (that) was responsible for the provenance of HIV-1 Lai/LAV” in Montagnier’s culture. There was a second contamination incident after this culture was sent to Gallo’s laboratory.

    The authors were scientists from Roche laboratories “commissioned” by the “Office of Scientific Integrity at the National Institute of Health (to) analyze archival samples established at the Pasteur Institute and the Laboratory of Tumour Cell Biology [LTCB at the National Cancer Institute] between 1983 and 1985”. They looked at “37 coded archival samples associated with the isolation of HIV-1 Lai/LAV and HIV-1 Lai/IIIB.” The authors: SP Chang, BH Bowman et al state in the Abstract that their “goals were to determine which HIV-1 variants were present in the samples and the sequence diversity among HIV-1 isolates from the earliest stages of the AIDS epidemic”.

    They comment on the controversy that eventually involved the French and US governments. “The striking similarity between the first two … HIV-1 isolates Lai/LAV (formerly LAV, isolated at the Pasteur Institute [1,2]) and Lai/IIIB (formerly HTLV IIIB, reported to be isolated from a pooled culture at the … LTCB) provoked considerable controversy in light of the high level of variability found among subsequent isolates”.

    “We concluded that the (LTCB) pool and probably another LTCB culture …were contaminated between October 1983 and early 1984 by variants of HIV-1 Lai from the” BRU-LAV “culture (sent to LTCB in September 1983). Therefore the origin of HIV-1 Lai/IIIB isolate was patient LAI”.

    Whew! You can’t tell the players without a scorecard. The different “HIV-1” type strains were PCR-assayed using the 268 bp “V1/V2 env region”, which comprises 2 of the original 3 conserved amino acid residue-regions (“similar to other retroviruses – the SU glycoproteins”) identified by Gallo et al, Nature, Jan-1985, page 282.

    Because V1/V2 contains 0-15 bp “hypervariable regions”, Bru clone can be distinguished from LAV clone which can be distinguished from IIIB clone. The assays also enabled the tracing of these sequences from the “LAV” cell-culture of “Montagnier” to the parent “HT aneuploid” culture of the “continuous- isolation” May 1984 Gallo et al Science paper, referred to here as the “LTCB pooled culture”. The order of “strain-sequence bifurcation” is Lai => LAV + IIIB.

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