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A NEW THEORY ON THE ORIGIN OF AIDS

(The following manuscript is a revised version of the scientific paper Dr. Leonard G. Horowitz and coauthors presented at the XI International Conference on AIDS in Vancouver, BC Canada on July 10, 1996. For more information contact 508-546-6586, and see "Emerging Viruses: AIDS & Ebola--Nature, Accident, or Intentional?" [Tetrahedron, LLC Press, 1996; $29.95] by Dr. Horowitz)                                  

Abstract

This article reviews scientific and U.S. Government documents that show AIDS-like viruses were developed by National Cancer Institute researchers along with military biological weapons contractors between 1962 and 1974 during the "Special Virus Cancer Program." The possibility of this research giving rise to contaminated experimental hepatitis B (HB) vaccines, and thus, the simultaneous emergence of acquired immunodeficiency syndrome (AIDS) in New York City and Central Africa in 1978 is advanced.

Introduction

Contrary to widespread speculations that human AIDS viruses arose from African green monkey viruses that naturally jumped species, in 1971, National Cancer Institute (NCI) researchers noted that "only one virus [of 27 then known retroviruses] which contains reverse transcriptase, does not seem to be oncogenic", the simian foamy virus (SFV).(1)

Indeed, during the early days of cancer virus and viral vaccine research, simian viruses were common experimental contaminants. Could they have somehow mutated giving rise to the human immunodeficiency viruses (HIV-1 and 2) and AIDS?

Background

The theory that viruses played a major role in carcinogenesis was most actively investigated by researchers at the NCI during the 1960s to mid-1970s. On the eve of Nixon's "war on cancer," NCI investigators explained how retrovirus related cancers such as lymphoma, leukaemia, and sarcoma might develop following virus infections. Twelve years later, in 1984, Dr. Robert Gallo and other esteemed NCI researchers advanced an essentially identical theory to explain AIDS.(1-10)

During the late 1960s and early 1970s, cell tumor biology researchers determined that synthetic RNA and feline leukaemia virus (FELV) "template" added to "human type C" viruses--those associated with cancers of the lymph nodes increased the rate of DNA production (and subsequent provirus and virus reproduction) as much as thirty times.(1) Such hybrid viruses, these researchers reported, may cause many cancers besides leukaemias and lymphomas, including sarcomas. Other NCI and Litton Bionetics teams reported modifying the fortieth discovered simian virus (SV40) by infusing it with nucleic acids from other species including FELV RNA, avian (i.e., chicken) myeloblastosis virus (AMV) RNA, associated with leukemia and sarcoma development, and mouse sarcoma RNA to: 1) make them carcinogenic, 2) prompt extreme immunosuppression in primates,(2,4,11) and 3) study RNA-dependent DNA polymerase (i.e., reverse transcriptase) and its relationship to human carcinogenesis,(6,11-14) For example, early work in viral engineering in relation to human carcinogenesis examined the activity of reverse transcriptase in normal versus acute immature leukaemic lymph cells (i.e., lymphoblasts). To do so, researchers evaluated the single stranded "70S RNA retrovirus" found in chickens which caused white bood cell (WBC) dysfunction, sarcomas, progressive wasting, and death--all prominent features of AIDS.(13)         

Human WBCs were injected with this AMV RNA to determine if the cells were prompted to produce proteins and new viruses called for by the virogene.(14) Another team evaluated the human cancer-causing effects of the single-stranded 70S RNA reverse transcriptase enzyme. They used FELV and Mason-Pfizer monkey viruses to deliver these carcinogens to normal human lymphocytes.(15)

During parts of these experiments, NCI and Bionetics investigators even mixed RNA and DNA from chickens and cats with human WBC fractions including human lymphocyte DNA polymerases to induce cancer type and AIDS-virus-like reactions (see fig. 1).(15)         

Other Gallo publications detailed the steps involved in creating immune-system-destroying cancer-causing viruses by adapting monkey, rat, and bird leukemia and tumor viruses for experimental use in a human (NC-37) cell line.16 One team discussed the synthesis of new RNA tumor viruses induced by 5-iodo-2'-deoxyuridine (IdU), a constituent of RNA in rodent cell cultures, and noted that chemical treatment might be used to halt the reverse transcriptase-linked viral reproduction cycle.(17)

In another report NCI researchers isolated a virus-like particle from human acute leukemic WBCs which had a specific density of 1.16-1.17g/ml, which allowed it to be repeatedly recovered without being destroyed by physical handling. Moreover, it was capable of producing the principal rapidly growing cancers seen in AIDS, including leukemias, sarcomas, and carcinomas.(19)

Defense Industry Interest

On April 4 and 5, 1969, at Fort Detrick, Maryland--America's premier biological weapons testing facility, a controversial symposium on the entry and control of foreign nucleic acids into human cells was held.(10) That year the National Academy of Sciences-National Research Council informed Department of Defense (DOD) officials that "synthetic biological agents" that caused treatment resistant immunosupression could be developed "over the next five years" at a cost of $10 million.(9) A year later, NCI researchers described the experimental entry of bacterial RNA into human WBCs before a special symposium sponsored by the North Atlantic Treaty Organization (NATO). Their paper, published in the Proceedings of the National Academy of Sciences, discussed several possible mechanisms prompting the entry of foreign nucleic acids into lymphocytes.(2) Soon thereafter, the NCI acquired the lion's share of Fort Detrick's facilities.(10)

According to a 1970 Congressional Record, Bionetics Research Laboratories, a subsidiary of Litton Industries, Inc., was sixth on the list of U.S. Army biological weapons (BW) contractors.(20) Later Congressional Records showed that Bionetics's affiliate--Litton Systems, Inc., another subsidiary of Litton Industries, Inc.--was among the most frequently contracted companies involved in BW research and development between 1960 and 1970.(21)

The Litton Industries, Inc. 1977-1978 annual reports stated,

"In June, [1976] Litton Bionetics won the fourth renewal of its contract to manage the operations of the National Cancer Institute's Frederick (Md.) Cancer Research Center."(22)  

Later, Litton sold Bionetics Research Labs to Medpath--a subsidiary of Dow Corning--among the largest medical laboratories in the United States, yet continued to administer the lion's share of NCI's Frederick operations funding to the time of this writing.

Furthermore, NCI staff reports revealed that Litton Bionetics had been granted the service contract to supply all NCI researchers, worldwide, with virtually every primate cancer research material requested, including seed viruses and viral hybrids, experimental reagents, and colony born monkeys, including M. mulatta, associated with the major monkey AIDS virus outbreaks in California's Davis Lab, and the 1967 Marburg virus outbreaks in three European vaccine production facilities and the African green C. aethiops.(24-26) Furthermore, from these publications, a list of the viruses and virus recombinants that Bionetics researchers developed, tested, and supplied to other NCI researchers during the 1960s and early 1970s was developed (see fig. 2).

A 1971 Litton Bionetics research report noted that "highest priority was given to the search for human leukemia viruses resembling the type-C viruses causing chicken and mouse leukemias" beginning as early as 1962.(23) Bionetics researchers, who received approximately $2 million annually for this work, reported:

"Several of the Type C viruses are established as the causative agents in leukemias, lymphomas, and sarcomas of chickens, mice, cats and hamsters. Many of these can infect and produce malignancies in other species (e.g., a sarcoma virus of the cat produces tumors in marmoset monkeys). Furthermore, some of these viruses can cause malignant transformation to occur in animal and human cells grown in the laboratory (e.g., cat leukemia and sarcoma viruses alter embryonic human cells). Type C virus particles have been found in association with malignancies of a spectrum of animal species including nonhuman primates, rats, cattle, wooley monkeys, gibbons, and man. . . ."(24)

Though some contemporary investigators have argued that HIV-1 and 2 are not type-C viruses,(27) more recently, researchers noted they go through a stage of type-C morphogenesis during replication and look and behave similar to the type-C viruses. "Although not classified as type-C viruses, lentiviruses follow a similar assembly strategy, by which capsid [shell] formation and budding [of the virus from the infected cell] occur simultaneously."(28)

Perhaps not coincidentally, during the metamorphosis of HIV, researchers found "a reproducible peak of viral protein in the fraction corresponding to a density of approximately 1.15 to 1.16g/ml . . . in gradients of gag HIV," that is, the gene that codes for the inner shell, capsid-like structure, of the AIDS virus.28 It may be recalled that Gallo et al. reported this number also, but in 1973, after repeatedly recovering the same density "virus-like particle" from human leukemic cells that was capable of producing the principal rapidly growing cancers seen in AIDS.19 Moreover, Kyle noted the United States Food and Drug Administration (FDA) Bureau of Biologics found a similar characteristic in the "adventitious virus" found in some live polio vaccine approved by and released in 1977.(29)   

It is known that RNA viruses in general, and type-C and D lentiviruses in particular, "undergo extensive genetic variation as a result of error-prone replication and recombination such that they are considered to exist as 'quasispecies,'" that is, a population of relatives with similar genes.30 One researcher noted "the exceptional ability of HIV-1 to mutate results in rapid development of quasispecies which evade host defenses and become resistant to various antiviral" agents.(31)

Bionetics/NCI researchers went on to report that, "Reactions between Type C viruses causing leukemias and sarcomas (solid tumors)," were a major area of interest for cancer prevention studies including the detection of cancer viruses, and viral vaccine experiments. The investigators wrote:

"When inoculated into appropriate cell cultures, type C sarcoma viruses of chickens, mice and cats produce foci [cancerous growths] of altered cells. This fundamental discovery provides a readily visible indicator reaction for the detection of sarcoma viruses. On the other hand, leukemia viruses grown in tissue culture do not cause foci or other detectable changes. The finding that leukemia viruses can either inhibit or enhance focus formation by sarcoma viruses of the same species has led to the development of methods for the detection and quantitation of leukemia viruses indirectly.

Certain of the chicken, cat and mouse sarcoma viruses are "defective" in that they do not produce foci in cell cultures or tumors in animals in the absence of a co-infecting, 'helper' leukemia virus. [Note the researchers called carcinogenic viruses "defective" if they were unable to produce cancers without the help of other factors including chemicals, radiation, and here leukemia viruses.] Further, in the presence of a defective sarcoma virus the helper action of leukemia viruses can be used as a specific indicator for their detection and quantitation. It is now believed that defective sarcoma virus leukemia virus interactions may be more widespread in nature than originally thought and that similar systems may be found in man. A mouse leukemia virus which has been adapted to grow in human cells is now available to search for defective human sarcoma viruses, if they exist."(24)

In continuing this effort, they developed an "alternative approach" for the detection of possible human leukemia viruses that employed recombinant cat and mouse leukemia and sarcoma viruses engineered to cross species.

"A defective mouse sarcoma virus and its leukemia virus helper can be made to form tight functional aggregates, which behave as one virus. Using a mixture of mouse sarcoma virus and cat leukemia virus, a hybrid aggregate which could be grown continuously in cat cells was produced. [As Gallo et al. also reported.(14,15)] Because the aggregate is defective, it requires the simultaneous presence of a cat leukemia virus for producing altered foci in cat cells. Thus, a focus forming sarcoma virus of the mouse, artificially changed to one possessing infectivity for cat cells, can now be used in cultures for the detection of cat leukemia viruses.  

This hybrid virus, as well as the cat leukemia virus, will also grow in human embryonic cells in tissue culture. If sufficient amounts of the Type C particles found in association with human leukemia can be obtained, the possibility exists that the cat-adapted mouse sarcoma virus can be hybridized with the human agent to produce an indicator system for the detection of human leukemia viruses. [Figure 3 presents a graphic description of this work.](24)         

The NCI staff went on to explain their work elucidating: 1) the "biochemical pathways of tumor virus infection and replication," 2) reverse transcriptase activity "in cells of patients with acute lymphoblastic leukemia . . . sarcomas, Burkitt's lymphoma and breast cancer," 3) experiments with Type B viruses thought to be associated with breast cancer, 4) Herpes-type viruses "associated with some forms of chronic leukemia, lymphoma, and postnasal carcinoma," and 5) Epstein-Barr viruses extracted from Burkitt's lymphomas and postnasal carcinomas. Vaccines, the NCI researchers explained, were expected to be developed from these efforts to help prevent and treat human cancers as coordinated "through the International Agency for Research on Cancer (IARC) in the West Nile District of Uganda."(24)

A Possible Iatrogenic Cause of AIDS

In May 1942, George W. Merck was commissioned by President Franklin D. Roosevelt to direct the War Research Service overseeing America's biological weapons industry.(32) Since then, the Merck company, in collaboration with the U.S. Public Health Service, provided ongoing expertise to the U.S. Army and its contractors "to bolster ongoing projects in fields in which it has an independent interest."20

A service contract awarded Merck and Company, Inc., under the "Special Virus Cancer Program (SVCP)," called for "oncogenic virus research and vaccine development." The chief objective of this work was reported as being "of fundamental importance to the goals of SVCP." Their proposed course of study included “work towards development of a feline leukemia-sarcoma virus vaccine and a herpesvirus type 2 vaccine [to] be continued as rapidly as possible."(33)

This grant description revealed that simian viruses (SV40)--currently suspected as being an AIDS virus progenitor29—and their "tumor cell ghosts" were prepared and used as principle carcinogenic triggers against which "non-protective SV40 tumor cell vaccines" were tested.33 This work was done at the same time Merck's chief vaccine developer, tumor cell virologist Maurice Hilleman collaborated with Hepatitis B (HB) vaccine pioneer Dr. Saul Krugman of New York University Medical Center, another documented Army biological weapons contractor,(20) and Robert Purcell of the National Institute for Allergies and Infectious Diseases (NIAID) to develop and test the first "4 lots of vaccine that would amount to perhaps 200,000 human doses" by 1974.(34-36)

Bionetics military supplied rhesus monkeys and chimpanzees were used to develop these vaccines during this "initial limited clinical test for establishing safety and measuring antibody response [in human subjects]." This work was based on pilot investigations conducted between 1967 and 1971 with "heat-inactivated hepatitis B vaccine" in animals and high risk human subjects in New York and Central Africa.(34)

At this time Dr. A. M. Prince, charged with overseeing the Laboratory of Virology at the New York Blood Center, wherein the non-human primates were housed, reported a major biohazard and containment problem. Prince admitted, "I would say more than 70%" of the animals became environmentally infected with hepatitis B (and likely other viruses) during their captivity.(34)

In 1974, Purcell reported failed attempts to grow the HB seed viruses, needed for these vaccines, in cell cultures. Willowbrook State School (Staten Island, NY) mentally retarded children, rhesus monkeys, and chimpanzees, he announced, were successfully used instead to culture the viruses subsequently inoculated into high risk human subjects (e.g., Willowbrook children, Central African villagers, and apparently New York's gay men as well) to develop the various vaccine subtypes.(35) "Cross-challenge experiments, and evaluation of various aspects of passive and active immunization against hepatitis B infection," Purcell explained, then proceeded in collaboration with the FDA.

Thus, simian viruses, and/or Bionetics engineered viral hybrids, infecting chimpanzees during this work might have infected humans and given rise to HIV-1 or its immediate progenitor(s). As Shultz explained, "a lentivirus isolated from chimpanzees (SIVcpz)" is "the closest primate relative of HIV-1."(27) Given, Bionetics's involvement in primate cancer virus and animal supply to these New York/Bethesda/Uganda investigators, SIVcpz might have evolved because the chimps had likely been among the first creatures to be exposed to man-made retroviruses by way of direct inoculation or experimental monkey cohabitation.   

It is also possible, even if Merck's human experimental HB vaccine hadn’t included contaminated chimpanzee serum, only serum taken from New York's children and/or gay men, live viruses injected around 1970 could have combined with the simian viruses (e.g., SV40, SIVagm, or SFV) the donors may have carried following vaccination with Merck's polio vaccines administered during the previous decade.(29)         

These facts provide additional background for evaluating Hilleman's 1986 published comments of having imported AIDS into North America by way of African green monkeys destined for use in Merck's viral and vaccine research. In an effort to reduce laboratory and vaccine contamination, Hilleman reported, "I brought African greens in. I didn't know we were importing AIDS virus at the time."(37)

Summary and Conclusions

This article reviews scientific literature and U. S. government documents that provide additional insight into the iatrogenic theory of AIDS. All it may have taken was one monkey used to develop the initial pilot HB vaccine lots, administered virtually simultaneously in New York City and Central Africa by 1974, carrying iatrogenically evolved or genetically engineered simian sarcoma-leukemia virus hybrids, to have started the AIDS epidemic.(38) This knowledge is important for at least three reasons: 1) the guilt and stigma attached to the victims of AIDS, homophobia, and racism, may ease in light of these findings; 2) new therapies might evolve from this knowledge; and 3) a thorough independent investigation and analysis of the aforementioned facts may help to prevent future outbreaks and epidemics.(39)

This work additionally supports others who have called for careful PCR analyses of suspected vaccine lots allegedly in safe keeping at the FDA.(38) Furthermore, as this report unearths evidence linking Willowbrook State School children, and apparently other high risk groups in New York City and Central Africa, to possibly contaminated experimental HB vaccines developed in chimpanzees, look-back studies of AIDS cases among those who received these early vaccines is clearly warranted.


References
1. 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.
2. 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," the year in which $10 million in funds were appropriated by the Department of Defense for the development of AIDS-like viruses.
3. Gallo RC, Perry S and Breitman RT. The enzymatic mechanisms for deoxythymidine synthesis in human leukocytes. Journal of Biological Chemistry 1967;242;21:5059-5068.
4. Gallo RC and Perry S. Enzymatic abnormality in human leukaemia.Nature 1968;218:465-466.
5. Gallo RC and Breitman TR. The enzymatic mechanisms for deoxythymidine synthesis in human leukocytes: Inhibition of deoxythymidine phosphorylase by purines. Journal of Biological Chemistry 1968;243;19:4943-4951.
6. Gallo RC, Yang SS and Ting RC. RNA dependent DNA Polymerase of human acute leukaemic cells. Nature 1970;228:927-929.
7. Gallo RC and Longmore JL. Asparaginyl-tRNA and resistance of murine leukaemias to L-asparaginase. Nature 1970;227:1134-1136.
8. Horowitz LG. Deadly Innocence: The Kimberly Bergalis Case: Solving the Greatest Murder Mystery in the History of American Medicine.
Tetrahedron, LLC., 1994, p. 14.
9. 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, Dept. of the Army. U.S., July 1, 1969, Government Printing Office, Washington, D.C., pg. 79 and page 129 of supplemental record obtained through the Freedom of Information Act.
10. Washington Correspondent. Relief of Fort Detrick. Nature 1970;228:803; regarding controversial conference see: Boffey PM. Detrick birthday: Dipute flares over biological warfare center. Science April 19, 1968;171;285-288.
11. Gallaher RE, Ting RC and Gallo RC. A common change aspartyl-tRNA in polyoma and SV transformed cells. Biochimica Et Biophysica Acta 1972;272:568-582.
12. Fujioka S and Gallo RC. Aminoacyl transfer RNA profiles in human myeloma cells. Blood 1971;38;2:246-252.
13. Smith RG and Gallo RC. DNA-dependent DNA polymerases I and II from normal human-blood lymphocytes. Proceedings of the National Academy ofSciences 1972;69;10:2879-2884.
14. Bobrow SN, Smith RG, Reitz MS and Gallo RC. Stimulated normal human lymphocytes contain a ribonuclease-sensitive DNA polymerase distinct from viral RNA-directed DNA polymerase. Proceedings National Academy of Sciences 1972;69;11:3228-3232.
15. Robert MS, Smith RG, Gallo RC, Sarin PS and Abrell JW. Viral and cellular DNA polymerase: Comparison of activities with synthetic and
natural RNA templates. Science 1972;176:798-800.
16. Gallo RC, Abrell JW, Robert MS, Yang SS and Smith RG. Reversetranscriptase from Mason-Pfizer monkey tumor virus, avian myeloblastosis
virus, and Rauscher leukemia virus and its response to rifamycin derivatives. Journal of the National Cancer Institute 1972;48;4:1185-1189.
17. Wu AM, Ting RC, Paran M and Gallo RC. Cordycepin inhibits induction of murine leukovirus production by 5-iodo-2’-deoxyuridine. Proceedings of the National Academy of Sciences 1972;69;12:3820-3824.
18. Gillespie D, Gillespie S, Gallo RC, East J and Dmochowski L. Genetic origin of RD114 and other RNA tumor viruses assayed by molecular hybridization. Nature New Biology 1973;224:52-54.
19. Gallo RC, Miller NR, Saxinger WC and Gillespie D. Primate RNA Tumor Virus-Like DNA Synthesized Endogenously by RNA-Dependent DNA Polymerase in Virus-like Particles from Fresh Human Acute Leukemic Blood Cells. Proceedings National Academy of Sciences 1973;70;11:3219-3224.
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, Dept. of the Army. U.S. Government Printing Office, Washington, D.C., 1969, p. 689; see also Congressional Record, August 8, 1969, p. 23073, and for U.S. Public Health Service involvement and funding see page 23079.
21. Committee on Human Resources, United States Senate. Hearings before the Subcommittee on Health and Scientific Research, Biological Testing Involving Human Subjects by the Department of Defense, 1977: Examination of Serious Deficiencies in the Defense Departments Efforts to Protect the Human Subjects of Drug Research. Washington, D.C.: U.S. Government Printing Office, May 8 and May 23, 1977, pp. 80-100.
22. Litton Industries, Inc. Annual Report[s] to the Securities and Exchange Commission for Fiscal Year Ended July 31, 1977 [and 1978]. Commission file number 1-3998. Securities and Exchange Commission, Office of Reports, October 31, 1977 [and October 30, 1978].
23. 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.
24. Ibid., 15-19; 20-26.
25. Ibid., 187-188; and in 1972 Progress Report #9, pp. 273-289.
26. Fine DL and Arthur LO. Prevalence of natural immunity to Type-D and
Type-C Retroviruses in primates. In: Viruses in Naturally Occurring
Cancers: Book B. Myron Essex, George Todaro and Harald zur Hausen, eds.,
Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1980, Vol. 7,
pp. 793-813; see also Gallo RC, Wong-Staal F, Marhkam PD, Ruscetti R,
Kalyanaraman VS, Ceccherini-Nelli L, Favera RD, Josephs S, Miller NR
and Reitz, Jr MS. Recent studies with infectious primate retroviruses:
Hybridization to primate DNA and some biological effects on fresh
human blood leukocytes by simian sarcoma virus and Gibbon ape leukemia
virus. Ibid.. 793-813.
27. Shultz TF. Origin of AIDS (letter to the editor). The Lancet 1992;339:867.
28. Sakalian M, Parker SD, Weldon RA and Hunter E. Synthesis and assembly of retrovirus gag precursors into immature capsids in vitro.
Journal of Virology 1996;70;6:3706-3715.
29. Kyle WS. Simian retroviruses, poliovaccine, and origin of AIDS. The Lancet 1992;339:600-601; Personal communication from Walter Kyle, May 19, 1996.
30. Drew L, Lichtenstein, Issel CJ and Montelaro RC. Genomic quasispecies associated with the initiation of infection and disease in ponies
experimentally infected with equine infectious anemia virus. Journal of Virology 1996;70;6:3346-3354.
31. Shaheen F, Duan L, Zhu M, Bagasra O and Pomerantz RJ. Targeting human immunodeficiency virus type 1 reverse transcriptase by intracellular expression of single-chain variable fragments to inhibit early stages of the viral life cycle Journal of Virology 1996;70;6:3392-3400.
32. Covert NM. Cutting Edge: A history of Fort Detrick, Maryland 1943-1993. Fort Detrick: United States Army Garrison, 1993, pp. 17-19.
33. NCI staff. Op cit. p. 111; and in 1972 Progress Report #9, pp. 139-141.
34. 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; the General Discussion can be found on pp. 375-379.
35. 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.
36. 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).
37. Shorter E. The Health Century: A companion to the PBS televisioneries. New York: Doubleday, 1987, pp. 67-69; 195-204. Maurice Hilleman
was interviewed by Edward Shorter on February 6, 1987. A copy of the audiotaped interview is held in the archives of the National Library
of Medicine, History Division, Washington, D.C.
38. Horowitz LG. Emerging Viruses: AIDS & Ebola, Nature, Accident or Intentional? Tetrahedron, LLC, 1996 p. 481.
39. Stricker RB and Elswood BF. Origin of AIDS (letter to the editor). The Lancet 1992;339:867.

Copyright c 1996, Leonard G. Horowitz. All rights reserved.


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