The Truth About AIDS. Biological Warfare at is finest

So you believed the bull*** that blacks had monkey sex and created
AIDS? Don't feel too bad that you were a bit mindless and believed
what the government told you through the media! Understand the truth
and set yourself free.

AIDS was created in a test tube and released into the population. That
is a fact. Believe it or not!

THE ORIGIN OF AIDS

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.

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