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)
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.
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?
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.
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
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
"In June,  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,
"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
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.
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
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
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
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