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A New Theory on the Iatrogenic Origin of AIDS
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by Leonard G Horowitz, DMD; Walter Kyle, JD; and Alan R Cantwell, Jr., MD

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 envelop of the AIDS virus in their cells as a "normal" gene.

A gene like this could have recombined with one of more vaccine-induced simian virus particles to produce an iatrogenic monkey/human hybrid virus like HIV-2. Or 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 viruses contaminants can give rise to viral recombinants and 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 FDA's 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 epidemiologic 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 adminstered 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 inadvertant 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.

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