We propose a new theory regarding the
origin of human immunodeficiency virus (HIV-1). The simian immunodeficiency virus from the
chimpanzee (SIVcpz) is generally considered the closest nonhuman primate virus related to
HIV-1. We believe this virus, or a closely related simian virus, most likely contaminated
the experimental hepatitis B vaccines that were administered to gay men in New York City
and to blacks in Central Africa during the 1970s. The introduction of a monkey virus
into the human species via contaminated vaccine programs could have given rise to a new
and unprecedented human immunodeficiency disease, now commonly known as AIDS.
Robert Gallo, the foremost authority on AIDS, has theorized that HIV-1 evolved from a virus in African green monkeys that jumped species to infect the black African population. Based on our extensive review of the scientific literature, we conclude that HIV-1 most likely evolved and jumped species due to iatrogenic (i.e. man-made) causes.
In the late 1970s the simultaneous
emergence of the earliest cases of AIDS in Central Africa and in New York City closely
followed a period of major scientific advances in molecular recombinant biology and
retrovirology. By the early 1970s, researchers had already isolated RNA-dependent DNA
polymerase. Synthetic RNA and cat leukemia retrovirus templates were added to human type-C
viruses associated with lymphatic cancer. Experimental infection with these genetically
engineered hybrid viruses were reported to cause leukemia, lymphoma and sarcoma.
By the mid 1970s the role of
T-lymphocytes in immunosuppression was clarified. Specific enzymes and other biochemical
processes needed to induce immune system collapse were also identified. In 1971, Fujioka
and Gallo designed experiments in which tumor specific cell tRNA was added directly to
normal human white blood cells. To achieve this, simian monkey virus 40
(SV-40) and mouse parotid tumor (polyoma) virus were routinely employed to deliver foreign
cancer-causing tRNA into these normal human white blood cells. In other
experiments the DNA in SV-40 was commonly replaced with RNA from various animals,
including RNA associated with cat leukemia and chicken sarcoma. Gallo and other
researchers commonly modified monkey viruses enabling these viruses to induce AIDS-like
immunosuppression, cancer, and wasting and death in primates and lower animals.
It is widely believed that HIV-2
(which purportedly preceded the evolution of HIV-1) and HIV-1 both share a common viral
ancestor, the so-called simian immunodeficiency virus from the African green monkey
(SIVagm). In addition, SIVmac, a macaque monkey virus laboratory contaminant, has also
been found to be identical to HIV-2. Because HIV-2 has never been found in macaques in the
wild, humans who
are now infected with HIV-2 were most
likely infected via contaminated vaccines.
Narayan et al. have produced an
experimental AIDS-like illness in monkeys by using a hybrid of HIV-1 which contains a core
of the monkey virus and an outer coat of the human AIDS virus. Primate cancer virus
researchers used a similar process (albeit in reverse) to develop AIDS-like viruses that
could infect human cells. Recent research suggests that some HIV-positive individuals may
maintain the envelope of the AIDS virus in their cells as a normal gene. A
gene like this could have recombined with one or more vaccine-induced simian virus
particles to produce an iatrogenic monkey/human hybrid virus like HIV-2. Or it could have
evolved further into HIV-1.
The experimental hepatitis B vaccines
and polio vaccines have been implicated by some investigators as possible sources of HIV
virus contamination and intercontinental transmission. Although one report exonerated the
experimental hepatitis B vaccine used in gay men in 1980 in Denver and San Francisco, no
analysis was performed on possibly contaminated hepatitis B vaccines that were
administered in New York City and in Africa, as early as 1972.
Between 1972 and 1974, hepatitis B
vaccine producers, under contract with the U.S. Army and the National Cancer Institute
(where Gallo worked), used chimpanzees to grow hepatitis B virus that could not be grown
in human or monkey cell cultures. This MS-2 strain of the hepatitis B virus was
subsequently used to develop four subtypes of experimental hepatitis B vaccine that were
used in different parts of the world. Some vaccine researchers have expressed concern that
more than 70% of their experimental animals had been cross-contaminated with
hepatitis B and other viruses.
Up to the present time the U.S. government and pharmaceutical industry disregard simian virus contaminants below 100 particles per dose. Thus, contamination of live polio and other vaccines by SV-40, simian foamy retroviruses and SIVagm can occur. Due to their highly unstable nature, simian foamy virus contaminants can give rise to viral recombinants and can cross the species barrier. We hypothesize that the use of live viral vaccines in New York and Africa during the 1970s could have generated AIDS-virus progenitors, such as HIV-2 and SIVcpz.
In addition, the possibility that
HIV-1 evolved iatrogenically in human subjects (specifically Willowbrook State School
mentally retarded children and/or gay volunteers for the hepatitis B vaccine experiments)
as a result of polio vaccination in the late 1950s or early 1960s cannot be ruled out. One
experimental hepatitis B vaccine manufactured in the mid-1970s was made from the blood
serum of gay men. Some of these young men likely received polio vaccines as children,
which could have been contaminated with SV-40, SIVagm, simian foamy virus, or other HIV-1
progenitor viruses. Since certain hepatitis B vaccine experiments took place
simultaneously in Africa and New York City in the late 1970s, this could explain the
initial AIDS outbreak on both continents in the early 1980s.
To prevent possible conflict of
interests, PCR (polymerase chain reaction) genetic analysis of these suspected vaccines
should be undertaken by independent laboratories. The original vaccines are allegedly in
safe keeping at the FDA. However, our inquiries to the FDAs Bureau of Biologics have
failed to elicit a response because details of these vaccines and their manufacture remain
classified for reasons of national security. Independent epidemiological
studies to ascertain the actual number of deaths from AIDS in groups exposed to these
early experimental hepatitis B vaccines should also be undertaken.
As part of the hepatitis B vaccine
experiments undertaken in the 1970s, the Bureau, along with the CDC, the NIAID, Merck
pharmaceutical company, and other industry contractors, developed certain pools of
hepatitis B virus of known infectivity from the blood of gay men that also contained
subtypes of HBsAg, (i.e. hepatitis B surface antigen). This product was also
administered to chimpanzees in hepatitis B experiments.
Most people believe AIDS originated as
a quirk of nature in which a monkey virus jumped species to infect the African
population. In our view, the widely-accepted green monkey theory is weak in comparison
with our research which supports a man-made, vaccine-induced origin of AIDS.
HIV and its progenitors more likely
evolved from simian (i.e. monkey) viruses altered by the deliberate or inadvertent
insertion of cancer-causing viral particles from other animal species. We hypothesize
these man-made mutants crossed over to infect the human population via contaminated
vaccine experiments and vaccine programs. Such experiments and outcomes were commonplace
in cancer virus research laboratories during the 1970s, at a time when collaborative
vaccine developmental programs were ongoing, and before the initial outbreak of AIDS.
The transmission of hybrid viruses
from contaminated animals and laboratories involved in vaccine production might also best
explain the simultaneous outbreak of the first cases of AIDS in Africa and in New York in
the late 1970s, as well as the peculiar epidemiology of AIDS which initially affected
white homosexual men in the U.S. and black heterosexual Africans. Additional confirmatory
studies are required to provide the scientific and health professional communities, as
well as the general public, with all the facts.