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Updated 11/07/02 Polio, Hepatitis B and AIDS:
The
following paper was accepted for publication in the Journal of Medical
Hypotheses. The final edited manuscript was published May 2001,
Vol. 56, No. 5, pp. 553-694. Slight differences exist between this
paper and the final publication. Abstract The hypothesis that simian virus 40 (SV40) infected polio vaccines may be linked to the evolution of acquired immunodeficiency disorder (AIDS), and certain cancers, has been advanced. Most recently, investigators discussed the likelihood of "gene-reshuffling" following SV40 infection as a precursor to acquired immune dysfunction. Findings of recent SV40 infections in four children born after 1982 suggest infections were transmitted vertically along gene lines. Earlier observations proved activation of a retrovirus gene by a hepatitis B virus (HBV) protein. This paper proposes a new integrative theory on the origin of AIDS. It advances the possibility of genetic recombinations with oncogene activation by HBV involving SV40, chimpanzee immunodeficiency virus (SIVcpz), and other simian viruses containing reverse transcriptase, that likely infected polio vaccinated blood donors to the initial hepatitis B (HB) vaccine trails conducted on gay men in New York City and other minority groups including Blacks in Uganda in the early to mid-1970s. Introduction and Background Scientific reports have advanced a theory of a polio vaccine linked evolution of AIDS and certain cancers.(1-4) A possible link between SV40, that contaminated early Salk and Sabin polio vaccines, and AIDS, was initially explored by Kyle in The Lancet in 1992.(4) Investigators Urnovitz(1), Butel(2-3) and others(4), discussed the likelihood of "gene-reshuffling" following SV40 infection as a precursor to acquired immune dysfunction and the development of certain cancers. Likewise, Butel revealed evidence of recent SV40 infections in four children born after 1982.(3) Her team advanced the likelihood that the infections were transmitted vertically, along gene lines, from parents who had received tainted polio vaccines. Earlier, she observed the activation of a HTLV-1 retrovirus gene by a HB virus protein.(5) With
an acknowledged threat of SV40 recombination in association with
immune suppression, and possible oncogene development or activation
in polio vaccine and possibly HB vaccine recipients and their offspring,
this paper advances an integrative theory on the origin of AIDS.
It asserts the possibility of genetic recombinations between SV40,
chimpanzee immunodeficiency virus (SIVcpz), and/or other simian
viruses containing reverse transcriptase such as the foamy retroviruses
(SFR), that likely infected blood donors who had first received
contaminated polio vaccines in the 1950s and early 1960s, before
volunteering for the HB vaccine trails conducted on gay men in New
York City (NYC), Blacks in central Africa, and other minority groups
in 1974 through 1975. Ten years later, in 1984, the Centers for Disease Control and Prevention (CDC) first responded to concerns that experimental HB vaccines, administered during the 1970s to homosexual men in the United States, were somehow linked to the AIDS epidemic.(6) Anonymous authors representing the CDC, along with others from Merck, Sharp & Dohme (MSD), and the State University of New York (SUNY), reported no trace of the human immunodeficiency virus (HIV-1) in samples of vaccine supplied by MSD. Further, their epidemiologic analyses, conducted on gay HB vaccine trial subjects in Denver and San Francisco, showed no relationship between AIDS cases and HB vaccine exposure. For unexplained reasons, homosexual males from New York City were not included in their study. Genetic Analyses Elucidating HIV-1's Origin Recently, reports by a Spanish team suggested an early genetic evolution of HIV-1.(7) Relatedly, in 1998, Zhu et al. described an African HIV-1 sequence from 1959 and its implications regarding the origin of the AIDS pandemic.(8) Later, Gao et al.(9) provided additional evidence of HIV's link to African chimpanzees by "amplifying" two DNA sequences, from two of six HIV genes, into "four overlapping subgenomic fragments that together comprised a complete pro viral genome," which they termed SIVcpzUS. In an editorial accompanying this report by Weiss and Wragham,(10) it was noted that the chimpanzee Gao et al. studied, "Marilyn," came to the United States Air Force primate center in New Mexico like most other African primate infants--free of sexually transmitted viruses. They implied that Marilyn's infection could have originated in a laboratory. Zhu
et al. further advanced an iatrogenic theory of HIV's origin when
they confessed, "the factors that propelled the initial spread of
HIV-1 in central Africa remain unknown: the role of large-scale
vaccination campaigns . . . should be carefully examined . . ."
Although the possible role contaminated vaccines might have played
was not addressed by these authors, they provided additional insights
into the inherent risk of in vitro and in vivo viral recombination(s)
when their data is compared with earlier scientific reports concerning
the HB vaccine. In 1993, Myers and colleagues published their "big bang" theory on the origin of AIDS and HIV-1 based on sophisticated genetic analyses conducted at the U.S. Government's Los Alamos Laboratory. They concluded that subtypes B, D, and F, along with close African/Indian virus relatives A, E and C, simultaneously emerged on three distant contents, in behaviorally divergent populations no less, during the early to mid-1970s, despite recognizing simian virus gene sequences of earlier evolution.(11) Epidemiological Common Sense Based on the above background and genetic findings, an iatrogenic mode of transmission, as opposed to an isolated natural cross-species jump, appears to more likely explain how HIV-1 might have simultaneously emerged on three far removed continents among behaviorally divergent populations during the early to mid 1970s. Several non-iatrogenic origin and cross species transmission rumors have been advanced regarding HIV-1 and its closest relative SIVcpz. The genetically more distant relative HIV-2, and the even more divergent African green monkey virus (SIVagm), are all believed, like HIV-1, to have spontaneously leaped from the African jungle. Related explanations included unprotected sex with nonhuman primates, monkey bites, dining on bloody primate meat, needlestick injuries in primate containment facilities or African hospitals, intercontinental infected passenger travel, and even viral mutations associated with global warming and jungle deforestation.(12) All these theories seem tenuous, if not ludicrous, when considered in light of the evidence compiled herein. Given the above, including the findings of Urnovitz(1), Butel(2-3) and others(4), it is most reasonable to consider the polio vaccine as a likely factor in the origin of AIDS. As reported by Essex, African green monkey derived oral polio vaccines (OPV) were a constant reservoir for SIV.(13) During OPV manufacturing procedures, viral mutations and vaccine contaminations routinely occurred without much ado. In America, for instance, the Food and Drug Administration (FDA), even to the time of this writing, have not been able to assure the quality and safety of vaccines, including those for polio and HB.(14) Regarding the Salk and Sabin polio vaccines, according to Martin (a previous FDA vaccine and cancer virus official) and Kyle's report,(4) doses of OPV routinely contained as many as 100 simian virus particles, including SV40, SIVs, and SFRs overlooked by FDA overseers to uphold pharmaceutical industry and regulatory standards. However, as per Myers's findings, HIV contaminated polio vaccines alone would not account for the 1970s "big bang." Given the generally recognized seven to ten year incubation period for HIV/AIDS expression, an early polio vaccine transmitted pandemic would have likely prompted initial indentifications of non-gay AIDS cases before 1970, and certainly no later than 1975. Instead, the first gay-related-immunodeficiency disease (GRID) cases were heralded in New York City in 1981.(15) Moreover, had the Salk or early Sabin vaccines transmitted HIV between 1955 and 1965 as some have advanced,(1-4) then Myers's conclusion would have likely reflected this, as would a North American AIDS outbreak not initially confined to homosexual males. Thus, it seems prudent to consider the findings of Butel(5) concerning HB as a potential retrovirus (e.g. HIV or HIV progenitor) activating agent, and cofactor, delivered with the 1970-75 HB vaccines involving New York's gay men, Willowbrook State School (WSS) mentally retarded children, and Ugandan Blacks who had approximately ten years earlier received monkey virus contaminated polio vaccines. Integrating Polio and HB Vaccine Theories of AIDS Given the administration of simian virus contaminated, monkey kidney tissue derived, polio vaccines in North America and Subsahara Africa from the mid 1950s through at least the early 1960s; then later, in the same or overlapping populations, the pilot testing of HB vaccines in these same regions from 1973 to 1975, the major group subtypes, B/D/F, as well as strains A/E, might have evolved in experimental chimpanzees, and/or human test subjects, during the viral vaccine production and testing processes. Subsequent HB vaccine production methods for later trials incorporated additional contamination risks with the mixing of chimpanzee incubated HB virus with human blood. According to a 1975 report by Robert Purcell from the Laboratory of Infectious Diseases of the National Institute for Allergies and Infectious Diseases (NIAID), this blood was subsequently pooled to produce four subtypes of experimental HB vaccine (referred to as adw, ayw, adr, and ayr).(16,17) These experimental HB vaccine subtypes were tested primarily in NYC and portions of Africa-regions largely overlapping the predominance of major HIV-1 strains B, D, and F. According to a 1979 NIAID task force report,(16) the four live HB viral subtypes were subsequently transmitted to "high risk" humans. As explained in contemporary medical bioethics texts, the "high risk" label, applied to groups predisposed to blood borne pathogen infections, served to also justify gross violations of bioethics and informed consent particularly during the HB vaccine experiments conducted by Krugman and colleagues at the New York University Medical Center (NYUMC) and affiliated NYC Blood Center labs.(18) Dr. Krugman was credited with "isolating" the first HB (MS-2) strain of virus from a mentally retarded child. This pathogen was originally called the "Australian antigen (AuAg)" due to its earlier identification in Australia. Subsequently, Krugman et al., cultured the virus in mentally retarded children before extracting AuAg for subsequent HB vaccine trials. In related studies, a report by Litton Bionetics staff to the National Cancer Institute (NCI) showed that by 1968, AuAg had been extracted from human "plasma/serum" and injected into eleven simians. Seven were reported "dead or transferred" by 1971.(19) Litton Bionetics was reported to be the leading supplier of African simians for the NCI and America's biomedical community.(19) They were also the U.S. military's sixth leading biological weapons contractor according to the 1969 Congressional Record.(20) The question of laboratory contamination is raised here by NCI documents showing hepatitis, herpes, and retrovirus recombinants (including acute lymphocytic leukemia virus hybridized with influenza or parainfluenza viruses to propagate airborne leukemia) were being cultured and tested before 1971 at Bionetics and collaborating laboratories in northwest Uganda and near Bethesda.(19) Bionetics also administered the "Special Virus Cancer Program" for the NCI and National Institutes of Health (NIH) including HB collaborative studies between New York investigators representing the Merck pharmaceutical company and the International Agency for Research on Cancer operating in France and Uganda.(19) Experimental subjects for these HB vaccine trials included homosexual males in NYC, Willowbrook State School (WSS) mentally retarded children on Staten Island, and African Blacks. All subjects were not informed that the four subtype HB vaccines being tested were partially processed in live potentially contaminated chimpanzees, shipped from Africa by Bionetics, then housed in NYC where biohazard and containment problems, including the horizontal transmission of infectious diseases, was routine.(17,18) Further scrutinizing the development and testing of these four HB vaccine subtypes, the blood from these experimentally infected human subjects was later pooled and used to develop "perhaps 200,000 human doses" according to Merck's vaccine chief, Maurice Hilleman.(18) Again, these doses containing HB viruses serially passed from Australian humans, to WSS children, into African chimpanzees before being reinoculated into New Yorkers and central Africans by way of vaccines by 1975.(21) This was perfect timing for the initial outbreak of GRID/AIDS cases in these regions by the late 1970s. Relatedly, in a recovered interview, Dr. Hilleman reported unwittingly importing AIDS virus into North America in contaminated monkeys destined for vaccine research and development at Merck.(22) Likewise, Dr. Hilleman's coauthor and senior Merck vaccine developer, Benjamin Sweet, expressed regret that their early SV40 contaminated polio vaccines may have contributed to contemporary cancer epidemics. "[N]ow, with the theoretical links to HIV and cancer," he reported in 1998 on the internet, "it just blows my mind."(23) HIV-2 and the Possible Iatrogenic Origin of HIV-1 Ample scientific evidence exists to advance the generic thesis of vaccine laboratory contamination associated with retroviral transmissions risking epidemic outcomes. A classic example intimately related to this polio/HB vaccine/AIDS hypothesis is the identification of HIV-2 by Max Essex and colleagues at the Harvard AIDS Institute. These investigators published discovering HIV-2 among healthy Senegalese female prostitutes.(24) In Senegal, prostitution is legal and the sex workers are required to report for clinical examinations and HB vaccinations periodically for relicensure. Eventually investigators determined that the simian immunodeficiency virus from the macaque monkey (SIVmac) and Essex's HIV-2 were genetically identical.(25,26) Moreover, wild macaques were found not to harbor this virus whatsoever. SIVmac was only found in laboratory contaminated primates.(27) Thus, Shultz concluded that culturing monkey viruses in human tissues, as is often done in viral vaccine production labs, risks activating previously benign "retroviral genomes carried in the germline for millions of years" into pathogens capable of inducing immune dysfunction. He, therefore, advised reexamining "any remaining [polio] vaccine lots by the polymerase chain reaction" so as to identify HIV or related lentiviruses.(27) Given the above evidence, the same should be urged for the earliest HB vaccine lots. Following
Dr. Essex's 1996 presentation at the National AIDS Update Conference
in San Francisco, I had the opportunity to question him as to, "How,
other than through contaminated vaccines, could a monkey virus that
doesn't exist in the wild, end up infecting Senegalese female prostitutes?"
Evading the question he replied, "I can tell you how my monkeys
got infected. . . . Researchers had inoculated the monkeys with
human tissues during experiments [unrelated to HIV] prior to them
coming to my lab."(21) More Support For A HB Vaccine AIDS Link During the early 1970s, researchers at the NYUMC led the world in determining blood group compatibility between humans and simians. Investigators here set the stage for the use of monkey blood in human vaccine trials.(21) NYUMC dermatologists and hematologists were credited with the discovery and analysis of the first gay Kaposi's sarcoma (KS) lesion.(28) Across town, at the Sloan-Kettering Institute for Cancer Research, Dermatology Department, Dr. Eleanor R. Lappano-Colletta was busy studying viral infected tissue taken from young gay men with KS. Between 1973 and 1974 she revealed, her dermatology department directors were routinely communicating with NCI chiefs and Litton affiliates including their 1971 retrovirus "project officer," Dr. Robert Gallo, regarding the subject of her investigation-the unique retroviral particles she was studying in the tissue samples taken from gay KS victims.(29) Dr. Lappano-Colletta's testimony raises the spectre that the 1984 contested discovery of HTLV-III (i.e., HIV-1) by Dr. Gallo, actually followed his learning about the teratogenic effects of a pathogenically related virus in gay men ten years previously, and just prior to the administration of the suspected HB vaccines in the same city and same unique population. Besides Litton Bionetics, the NYUMC was also listed among the Army's top biological weapons contracting labs by 1969.(20) Under Army contract Dr. Krugman routinely used mentally retarded children and gay men to grow/culture and/or test HB viral strains and vaccines following his MS-2 studies.(30) The pilot HB vaccines theoretically linked here to the earliest GRID cases in NYC was overseen as well by an advisory committee chaired by Dr. Krugman,(31) and researched by intimate Krugman collaborator, Abbott Laboratory's L. R. Overby. Together, Krugman and Overby evaluated HB susceptibility and vaccination methods on NYC subjects between 1965 and the mid-1970s.(18,30,32) Subsequently, Abbott Labs began commercially marketing MSD's HB vaccine.(28,32,33) Later, large scale HB vaccine trial marshal Wolf Szmuness, also affiliated with the NYC Blood Center explained the selection criteria for Dr. Krugman's early, and his later, HB vaccine experiments. He wrote: Several populations in the United States with a high risk of HBV infection were considered for such a trial: patients institutionalized for mental retardation, patients undergoing hemodialysis, members of the medical staff of dialysis centers, American Indians, and homosexual men. Of these groups, a population of HBV-susceptible homosexual healthy young men appeared to be the most suitable. Their risk of HBV infection is unusually high, they are readily accessible through numerous gay organizations, and their cooperation in previous studies has been excellent.(31) It is well known that HIV/AIDS rates among native Americans, people of color, blood product recipients, and homosexual males, have far exceeded those of the general population. It might be this overlap between populations most affected by HIV/AIDS and those selected for early and later HB vaccine experiments, more than lifestyle risks, provides as a common denominator for the AIDS pandemic. Given this fact alone, the report by Poiesz et al., including anonymous CDC authors, excluding gay NYC HB vaccine study participants, is highly irregular at best.(21) Considering the epidemiology suggestive of a HB vaccine triggered outbreak of GRID in America, the data below is noteworthy: Following HB vaccine pilot studies as discussed above, additional trials were conducted during the mid-1970s in NYC. In 1976, the WSS was forced to close allegedly due to abuses sustained by the children at the hands of school administrators. Based on the information documented above, it is likely that many of the approximately 5,000 children sent back to their communities in 1976 were among the world's first AIDS victims.(21) Larger scale HB vaccine trials in NYC began after the closing of WSS. In 1978, 1,083 gay men were inoculated with the Merck developed and Abbott marketed vaccine. In March, 1980, approximately eighteen months after the NYC inoculations ended, gay men in five other American cities began to receive the vaccine. These cities included Los Angeles, San Francisco, Denver, St. Louis, and Chicago from where 1,402 homosexuals were initially recruited from VD clinics. Later, thousands more joined additional HB vaccine trials. Between 1978 and 1984 the percentage of HIV-positive gay men in NYC rose dramatically. In other HB vaccine study populations the rise in HIV-1 sero-prevalence and AIDS was also disconcerting. In San Francisco, for instance, among those who had been subjects in the trials (n=6,875) the HIV/AIDS rate rose from 4 to 68 percent between 1978 and 1984.(18) This increase was precipitous contrasting the rate of HIV infection among homosexual men reported elsewhere in 1989. Across the U.S. HIV/AIDS rates varied from 0 percent in many communities to 70 percent in NYC, with significantly less in San Francisco. In 1982, concerns were expressed at the Pasteur Institute regarding the possible link between AIDS and the Merck-manufactured HB vaccine. Luc Montagnier was then assured by CDC HB chief Don Francis, Max Essex's protege, that "no link between AIDS and the [HB] vaccine inoculations" had been found. Yet, a year later, Dr. Francis sent Dr. Montagnier thirteen blood samples from GRID patients all of whom received experimental HB vaccines.(21, 33) Dr. Francis had expressed concern regarding the apparent association between feline leukemia virus like illness striking gay men in NYC, Los Angeles, and San Francisco and the distribution of HB cases. "Combine these two diseases-feline leukemia and hepatitis-and you have the immune deficiency," he surmised.(34) This was much like what a NATO scientific audience discussed in 1971 when Gallo et al., explained combining synthetic RNA and feline leukaemia virus (FELV) "template" with "human type C" viruses-those associated with cancers of the lymph nodes-to increase the rate of DNA production (and subsequent provirus and virus reproduction) "as much as thirty times."(35) Such hybrid viruses, these researchers reported, caused many cancers besides leukemias and lymphomas, including sarcomas. Other Gallo, NCI, and Litton Bionetics teams reported modifying, at that time, SV40 by infusing it with nucleic acids from other species including FELV, avian myeloblastosis virus (AMV), both associated with leukemia and sarcoma development, and mouse sarcoma RNA to make them severely immunosuppression for primates(36) Additionally, in 1985, Harold Jaffe, deputy director for AIDS science at the CDC, with co-worker Andrew Moss, "presented data from the San Francisco HB study that found the virus was present in blood of 4.5 percent of the study's subjects in 1978, 20 percent in 1980, and 67 percent by late 1984."(37) In contrast, "only about 40 percent of a randomly selected sample of gay men [also in San Francisco at that time] were infected. Based on this evidence, again considering the 7-10 year incubation period for HIV/AIDS, the "big bang" most likely occurred as Myers proposed during the early to mid-1970s with the HB vaccine cohort preceding the general gay, and later heterosexual, populations for epidemic onset.(11) To further examine this predominance of HIV/AIDS cases among NYC and San Francisco HB vaccine recipients, Francis examined the blood collected from 6,800 gay men enrolled in the larger (post-pilot) HB vaccine trials. From samples drawn between 1978 and 1980, he recorded a 25 percent rise in HIV positivity. He too concluded that the new pathogen had appeared among gay men by 1976 or 1977 and spread quickly from there.(38) Corroborating data is cited by CDC official Paul O' Malley who concluded his investigation into a suspected GRID/HB vaccine link as follows: "[A]n inordinate number of GRID victims," he stated were in the HB vaccine trial. "Of the first twenty-four GRID cases in San Francisco, in fact, eleven were in the hepatitis B cohort."(34) Based on CDC reports, as scrutinized by investigative journalist and gay physician Alan Cantwell, the first 26 AIDS cases were all homosexual men-20 were from NYC, and 6 were from Los Angeles.(17, 39) Conducting an independent study paralleling this author's,(21) and drawing similar conclusions, Dr. Cantwell reported a gross absence of scientific prowess on the part of CDC officials investigating an apparent HB vaccine AIDS link.(39) Conflicting interests, he concluded, best explained the blatant biases and flawed methods used by official investigators during studies used to reassure the scientific/medical communities, and the general public, regarding the safety of HB vaccines.(21,28, 39-41) Conclusions A possible route of HIV evolution, and/or transmission, is this: 1) From the mid-1950s through at least the 1960s, simian virus infected polio vaccine recipients were exposed to SV40, SFR, and SIVagm,(1-5) including gay men and mentally retarded children in New York, along with Blacks in central Africa;(17) 2) Researchers in NYC "isolated," and then inoculated into human vaccine study "volunteers" the MS-2 strain of HB virus. Between 1965 and 1970, these injections and pilot HB vaccine studies may have activated an endogenous or exogenous HIV-related retroviral gene in one or more WSS children and/or gay males;(1,2,5,18) 3) These human derived HB viruses, and potentially activated retroviral sequences, were then transferred to chimpanzees, then back again to humans in NYC and central Africa during the development and testing of four genetically altered subtypes of the 1974-1975 experimental HB vaccine; 4) Contamination risks were increased by the subsequent pooling of blood donated by the test subjects who had been injected with the chimpanzee cultured HB strains, along with biohazard and containment problems reported by principle investigators; and finally, 5) The four pooled blood derived HB vaccines were then administered to thousands of test subjects including gay males in NYC, WSS children once again, and central African Blacks.(15) This hypothesis might best explain the conclusion reached by Gerald Myers, chief of the special HIV Sequence Database AIDS Project at the Los Alamos National Laboratory, that "the preponderance of evidence still argues for an explosive event in the mid-1970s."(11) With the sudden, virtually simultaneous, appearance of several HIV major group subtypes primarily striking Africa and NYC by 1978, given the seven to ten year incubation period of HIV/AIDS, the HB vaccine trials, begun as early as 1965 in New York and Uganda, and in NYC gay populations soon after, likely played a catalytic role in the origin of the AIDS pandemic. Additional research using PCR analysis of suspected polio and HB vaccine lots, particularly those given to gay men and WSS children in New York before 1976, is urgently indicated to identify possible retroviral contaminants related to HIV/AIDS. Epidemiological efforts should also be made to contact the families of the WSS children, as well as the gay men in NYC who participated in the pre 1976 HB vaccine pilot studies, to document histories relevant to further considering this hypothesis. Obviously, due to the lethal nature and severe cost of the AIDS pandemic, should this premise be firmly established, it would beg a global reevaluation of vaccination science, politics, and policies. Based on the preliminary findings reported here, and in the author's earlier investigative report,(14) at least two Third World nations have already moved in this direction.(42) Not
readily embraced by individuals, organizations, institutions, and/or
government agencies biased by special interests, the dire implications
of neglecting this hypothesis, and its further investigation, are
unfathomable. It may be that the health and welfare of civilization,
as we know it, depends on silencing the arrogant voices that have
directed disinterest, and even antagonism, towards the study of
AIDS's origin. Reflecting on the publication of this material, their
actions strain the ethical fabric of science, our moral obligations
as global citizens, and as a result, may be contributing to a worsening,
irreversible, and unprecedented attack against humanity.
This paper is dedicated to the fine efforts and genuine honesty of the late Jonathan Mann who, with his wife, a HB vaccine investigator, met an untimely fate on Flight 111. Far more than a medical problem, Dr. Mann believed, AIDS is a socio-political imposition.
2) Jafar S, Rodriguez-Barradas M, Graham DY and Butel JS. Serological evidence of SV40 infections in HIV-infected and HIV-negative adults. J Med Virol 1998 54;4:276-284. 3) Butel JS, Arrington AS, Wong C, Lednicky JA and Finegold MJ. Molecular evidence of simian virus 40 infections in children. J Infectious Diseases 1999;180:884-887. 4) Kyle WS. Simian retroviruses, poliovaccine, and origin of AIDS. The Lancet 1992;339:600-601. 5) Marriott SJ; Lee TH, Slagle BL and Butel JS. Activation of the HTLV-1 long terminal repeat by the hepatitis B virus X protein. Virology 1996;224;1:206-13. 6) Poiesz B, Tomar R, Lehr B and Moore J. (and anonymous CDC authors). Hepatitis B vaccine: Evidence confirming lack of AIDS transmission. MMWR 1984;33;49:685-687. 7) Casado C, Urtasun I, Martin-Walther MV, Garcia S, Rodriguez C, del Romero J, Lopez-Galindez C. Genetic analysis of HIV-1 samples from Spain. J Acqui Immune Defic Syndr 2000 Jan 1;23(1):68-74. 8) Zhu T, Kober BT, Nahmias AF, Hooper E, Sharp PM, and Ho DD. An African HIV-1 sequence from 1959 and implications for the origin of the epidemic. Nature 1998;391;Feb 5;594-597. 9) Gao F, Bailes E, Robertson DL, et al., Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes (letter). Nature 1999; 397: 436-441. 10) Weiss RA and Wrangham RW. From Pan to pandemic (editorial). Nature 1999; 397:385-386. 11) Myers G. et al. "Phenogenetic moments in the AIDS epidemic," Chapter 12 in S. S. Morse, ed., Emerging Viruses. Oxford, Eng.: Oxford Univ. Press, 1993. 12) Garrett L. The Coming Plague: Newly Emerging Diseases in a World Out of Balance. New York: Penguin Books, 1994, pp. 361-385. 13) Essex M, Kanki P. The origins of the AIDS virus. Scientific American 1988;259:64-71. 14) Horowitz LG and Martin JW. Emerging Viruses: AIDS & Ebola. Tetrahedron, LLC, 1998, pp. XVI-XVII; 488-493. 15 ) CDC staff. Kaposi's sarcoma and pneumocystis pneumonia among homosexual men-New York City and California. MMWR 1981;30:305-308. 16) USDHEW. Virology: Volume 4-Control of Viral Infections. NIAID Task Force Report. Bethesda, MD: Public Health Service, National Institutes of Health (NIH) 79-1834, 1979, p. 20-65-78. 17) Purcell RH. Current understanding of hepatitis B virus infection and its implications for immunoprophylaxis. In: Antiviral Mechanisms: Perspectives in Virology IX. The Gustav Stern Symposium. New York: Academic Press, 1975, pp. 49-76. 18) Krugman S. Viral hepatitis type B: Prospects for active immunization. In: International Symposium on Viral Hepatitis, Milan, Dec. 1974. Develop. biol. Standard. Vol. 30, Munich: S. Karger Basel, 1975, pp. VI; 363-367; relevant general discussion can be found on pp.375-379; See also: Krugman S, Giles JP, Hammond J. Hepatitis virus: effect of health on the infectivity and antigenicity of the MS-1 and MS-2 strains. J Infectious Disease. 1970;122:432-6; Krugman S, Giles JP, Hammond J. Viral hepatitis, type B (MS-2 strain): Studies on active immunization. JAMA 1971;217:41-5; Krugman S, Giles JP. Viral hepatitis, type B (MS-2 strain); further observations on natural history and prevention. New England Journal of Medicine 1973;288:755-60; and Krugman S, Overby LR, Mushahwar IK, Ling C-M, Forsner GG and Deinhardt F. Viral hepatitis, type B: Studies on natural history and prevention reexamined. New England Journal of Medicine 1979;200:101-6. 19) NCI staff. The Special Virus Cancer Program: Progress Report #8 [and #9]. Office of the Associate Scientific Director for Viral Oncology (OASDVO). J. B. Moloney, Ed., Washington, D. C.: U. S. Government Printing Office, 1971 [and 1972]. Note: This is a very hard publication to find. Few library data bases have it listed, including the NCI Library at Fort Detrick. It is available through the Davis Library, The University of North Carolina, Chapel Hill, Government Documents Department Depository, Reference # HE 20.3152:V81. The Litton "support services" contracts that included primate supplies are found on pp. 187-88 and 326-327 of the reports. Litton's list of mutant viruses, including retroviruses, and other experimental infectious agents including AuAg is found on pp. 279-280 and 284 of Project Report #8, of 1971; for additional documentation on hepatitis and herpes experimentation in Uganda before 1971 see: Higginson J and Muir CS. Epidemiologic program of the International Agency for Research on Cancer (IARC). In: The National Cancer Program and International Cancer Research, National Cancer Institute Monograph, 1974; 40:65. 20) Department of Defense Appropriations for 1970: Hearings Before A Subcommittee of the Committee on Appropriations House of Representatives, Ninety-first Congress, First Session, H.B., 15090, Part 5, Research, Development, Test and Evaluation of Biological Weapons, Dept. of the Army. U.S. Government Printing Office, Washington, D.C., 1969, p. 689. 21) Horowitz LG and Martin JW. Op. cit., pp. 250-51; for detailed analysis on flawed HB vaccine/gay AIDS study involving the CDC see pp. 240-241, and for Dr. Poiesz's potential conflicts of interest in this regard see p. 249; for data concerning precipitous rise in HIV/AIDS rates among HB vaccine recipients see pp. 242-243; for dialogue with Max Essex, see pp.131-32; for NYUMC blood grouping discussions and references see pp. 443-444; for WSS closing discussion see p. 254. 22) Shorter E. The Hilleman interview, February 6, 1987. A recording for background research in preparation of The Health Century, a companion to the PBS television series. New York: Doubleday, 1987, pp. 67-69; 195-204. Bethesda, Maryland: Audio Archives, National Library of Medicine, 1987. 23) Moriarty TJ. The polio vaccine and simian virus 40: After thirty years, prominent polio vaccine researcher confirms suspicions about monkey-virus contamination. http://www.chronicillnet.org/online/bensweet.html#anchor714274. 24) Kanki PJ, Barin S, M'B oup, et al., New human T-lymphotropic retrovirus (HTLV-IV) related to simian T-lymphotropicvirus Type III (STLV-IIIagm). Science 1986;232:238-43; see also Essex M, Kanki P. The origins of the AIDS virus. Scientific American 1988;259:64-71. 25) Kanki PJ, M'Boup S, Marlink R, et al., Sequence of simian immunodeficiency virus and its relationship to the human immunodeficiency viruses. Nature 1987;328:539-43. 26) Chakrabarti L, Guyader M, Alizon M, et al., Sequence of simian immunodeficiency virus from macaque and its relationship to other human simian retroviruses. Nature 1987;328:543-47. 27) Schulz TF. Origin of AIDS (letter to the editor). The Lancet 1992;339:867. 28) Cantwell Jr. A. Queer Blood. Los Angeles: Aries Rising Press, 1993 p. 104. 29) Personal communication January 25, 1997, with Dr. Eleanor R. Lappano-Colletta, 22A Edmond Court, Jackson, NJ, 08527. For more information call 732-928-9102. 30) Krugman S, Giles JP and Hammond J. Infectious hepatitis: Evidence for two distinctive clinical, epidemiological, and immunological types of infection. JAMA 1967;200;5:366-373(96-103). 31) Szmuness W, Stevens CE, Harley EJ, Zang EA and Oleszko WR et al. Hepatitis B vaccine: Demonstration of efficacy in a controlled clinical trial in a high-risk population in the United States. New England Journal of Medicine 1980;303;15:833-841. 32) Krugman S, Overby LR, Mushahwar IK, Ling C-M, Forsner GG and Deinhardt F. Viral hepatitis, type B: Studies on natural history and prevention reexamined. New England Journal of Medicine 1979;200:101-6. 33) Shilts R. And The Band Played On: Politics, People and the AIDS Epidemic. New York: Penguin Books, 1987, pp. 202-203; 371; 409. 34 ) Ibid., p. 186. 35) Gallo RC, Sarin PS, Allen PT, Newton WA Priori ES, Bowen JM and Dmochowski L. Reverse transcriptase in type C virus particles of human origin. Nature New Biology 1971;232:140-142; see also Gallo RC. Transfer RNA and transfer RNA methylation in growing and "resting" adult and embyonic tissues and in various oncogenic systems. Cancer Research 1971;31:621-29. 36) Herrera F, Adamson RH and Gallo RC. Uptake of transfer ribonucleic acid by normal and leukemic cells. Proc Nat Acad Sci 1970;67;4:1943-1950. This paper was presented before NATO scientists at the "International Symposium on Uptake of Informative Molecules by Living Cells, Mol, Belgium,1970"; see also: Gallo RC and Perry S. Enzymatic abnormality in human leukaemia. Nature 1968;218:465-466; and Gallo RC, Yang SS and Ting RC. RNA dependent DNA Polymerase of human acute leukaemic cells. Nature 1970;228:927-929. 37) Shilts R. Ob cit., p. 553. 38 Shilts R. Ob cit., p. 125; 458. 39) Cantwell, Jr. A. Is AIDS a man-made disease? Internation Journal of Medicine 1998;1;2-4:94-104. See also Cantwell's book AIDS and the Doctors of Death: An Inquiry into the Origin of the AIDS Epidemic, Los Angeles: Aries Rising Press,1992, pp. 83-109. 40) CDC staff. Hepatitis B virus vaccine safety: Report of an inter-agency group. MMWR 1982;31:465-467. 41) CDC staff. The safety of hepatitis B virus vaccine. MMWR 1983;32:134-136. 42) Personal communications: from Major Caleb Gwambo, Director, Department of Defense, Office of the President, P. O. Box 40668, Nairobi, Kenya (2542 884466; 2542583542); and Dr. Alim Muhammad, Health Minister, Nation of Islam, 202-397-4000; 301-894-9345)
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