November 30, 1996

Ms. Terry Allen
Editor
CovertAction Quarterly
1500 Massachusetts Avenue NW, #732
Washington, DC 20005

Dear Terry,

Thank you for inviting me to reply to the article “Tracking the Real Genocide” by David Gilbert.

The following is my response:

Dear Editor:

I applaud David Gilbert’s effort to set the record straight regarding “AIDS: Conspiracy or Unnatural Disaster?” in your Fall 1996 issue. His claim that the “real genocide” may be tracked to “a two-tiered public health system rooted in racism, sexism, and profiteering” is supported by substantial evidence. However, his review on the subject of the manmade theory of AIDS for population control was incomplete at best. His central thesis–to examine “the validity of one set of theories . . . that HIV was deliberately spliced together in a lab as a weapon of genocide” missed its mark.

Mr. Gilbert too quickly accepted the flawed opinion of his “friend” Janet Stavnezer, a “professor of molecular genetics and microbiology specializing in immunology,” who stated that the “splice theory is scientifically impossible. . . none of the viruses posited in the various splice theories has nearly enough genetic similarity (homology) with HIV to be one of its parents.” This was similar to the opinion expressed by Dr. Robert Gallo, on July 10, 1996 when I offered a new theory on the origin of AIDS, and questioned Gallo on the matter during the XI International Conference on AIDS in Vancouver. His and Stavnezer’s opinion is no longer shared by a growing number of equally credentialed scientists for several reasons.

For the record, Dr. Gallo once firmly believed HIV was closely related to the leukemia viruses HTLV-1 and HTLV-II. Hence the name HTLV-III. As a matter of fact there was a publication in Science (see: Homology of AIDS-associated virus with genomes of human T-cell leukemia viruses, Arya SK, et al. Science 1984;225:927-930) showing molecular similarity. Human leukemia viruses were commonly studied by Robert Gallo and Litton Bionetics–among the Army’s top biological weapons contractors–during the highly funded and largely secret “Special Virus Cancer Program” (SVCP) operating from 1962 to 1976.

I agree that since there are no known viruses in the evolutionary scheme that look very similar to HIVs, HIV must be considered unique by design. But HIV is not totally unique. In very general terms it is similar to both type C and type D cancer viruses along with the inclusion of regulatory genes typical of lentiviruses.

Could HIV have evolved from laboratory experiments in which chance or intentional encounters occurred between different viruses of foreign species? The answer, as Dr. Gallo admitted during a recent interview, is very plausibly “yes,” despite the fact we may be unaware of the largest contributing virus(es).

If you use SV40 for example–a common monkey virus found contaminating oral polio vaccines and now linked to cancer (see Money magazine, December, 1996)–research shows how this and another very dissimilar virus–the human adenovirus–were found to combine, creating a potentially deadly mutant–the ad-SV40 hybrid. In 1973, Andrew Lewis, at the NIAID (see: Biohazards in Biological Research, Cold Spring Harbor Laboratory, 1973, pp. 96-113.) showed that following unexpected and unexplained recombination of these grossly different viruses, hybrids emerged that contained as little as 6% of the original SV40 gene sequence. Lewis concluded, “Until satisfactory studies evaluate the long-term effects of SV40 infection in humans and clarify the relationship between SV40 and SV40-related agents to chronic degenerative central nervous system disease in humans, it appears to this reviewer that the laboratory manipulation of SV40 involves some risks.”

Gallo and Bionetics researchers worked with SV40 as well as other monkey viruses and viral hybrids in the process of studying the unique leukemia, lymphoma, sarcoma, immune suppression cancer complex that never existed in humans before the first AIDS cases in 1978.

Likewise, reflecting on Gallo’s work with human white blood cells and type-C cancer viruses, George Todaro concluded:

“These hybrid cells are being extensively explored by geneticists all over the world who do not realize that they contain high titers of potentially oncogenic [cancer causing] viruses. . . .What is not clear is the nature of the relationship between the acquisition of oncogenic potential by a cell and the expression of that cell’s endogenous type C viral information. Type C viruses carry oncogenic information and can produce tumors (leukemias, lymphomas and sarcomas) by exogenous infection; whether horizontal spread (cell to cell and/or animal to animal) of exogenous type C virus is responsible for a significant portion of naturally occurring cancers in vertebrates is uncertain; that they can have oncogenic potential and can produce tumors in a variety of species is firmly established. It follows, then, that these viruses and the cells that produce them must be treated as potentially hazardous agents.”

I grant that some degree of homology is needed for recombination, and the more homology the more recombination. However, neither the whole genome needs to be homologous nor is there a requirement that the homologous regions be contiguous. Small stretches of even a few base pairs are all that is needed for recombination of type-C cancer viruses–the focus of substantial SVCP, NCI and Bionetics research. By the way, HIV has been shown to evolve through type-C like morphogenesis. (Salakian, P et al. J Virology 70:3706-3715)

Furthermore, as these animal viruses were mixed with human tissues, another Gallo mentor, Ray Gilden stated: “[A] new virus with no growth restrictions may be accidentally introduced in a new species, perhaps by vaccine, and these become epigenetic as opposed to a rarely seen endogenous virus. Possibilities of recombinants are thus raised . . . , which could have an extended or newly acquired oncogenic potential.” Gilden’s warning obviously foreshadowed the AIDS pandemic. (See: Viruses, Evolution, and Cancer: Basic Considerations–International Conference of Comparative Virology, 2nd, Mont Gabriel, Can., 1973. New York: Academic Press, 1974, pp. 235-256.)

Thus, molecular virology entails a lot more than homologous recombination. One could practically construct new viruses residue by residue using the general pattern of established viruses viz, the LTR, gag, pol, env and all the interesting genes sprinkled in. Though building and then testing the stability and function of new constructs is a painstaking and time consuming process, documented evidence shows this is precisely what was done during the 1960s and early 1970s by biological weapons contractors (see: Geissler E. Biological and Toxin Weapons Today. London: Oxford University Press, 1986 with contributions by David Baltimore and Raymond Zilinskas).

Additionally significant is that HIV does not fit the mold for naturally evolved viruses. There is a lone~40 percent homologous virus–HIV-2–which may or may not have been a progenitor of HIV-1, and it may not have originated in monkeys. HIV-2 is definitely not naturally found in (i.e., endogenous) any of the species from which it has been isolated. The fact that we now find them in several monkeys and a group of individuals in one region of Africa is highly suspicious. The “high risk” Senegalese female prostitutes clearly participated in public health research programs, and therefore likely received what I conclude (see Emerging Viruses: AIDS & Ebola–Nature, Accident or Intentional?, Tetrahedron, LLC, 1996), was the most likely initiator of the world’s AIDS pandemic–the Phase I and Phase II pilot experimental hepatitis B vaccine simultaneously tested on 200,000 human subjects in New York and Central Africa in 1974. The New York recipients included Willowbrook State School mentally retarded children, gay men, and in Africa, villagers were given the honor in the heart of the African AIDS belt.

Gilbert does not address the theory of sloppy science (e.g., contaminated vaccines for HIV-1 and HIV-2), and this certainly explains a mass of circumstantial and scientific evidence, but even so, it would be unscientific and inexcusable to disregard the genocidal theory of AIDS. Enough circumstantial evidence exists to argue this hypothesis despite the notion’s inherent political impoliteness.

Most ironic is that Gilbert advocates mass immunization programs, so that underserved African Americans can gain the “same protection for their children,” when contaminated vaccinations have now been linked to various types of cancer, chronic fatigue immune dysfunction syndrome (CFIDS), autoimmune diseases including Guillaen Barre’s syndrome and rheumatoid arthritis, polio, meningitis, encephalopathy, hyperactivity and attention deficit disorders in children, and currently offer the most plausible method of halving the American population as recommended by some Council on Foreign Relations members (see: Negative Population Growth, Inc., “Why we need a small U.S. population and how we can achieve it.” Foreign Affairs Magazine. Council on Foreign Relations, March/April, 1996).

Other flaws in Gilbert’s article include: 1) alleged geographical inconsistencies between vaccination campaigns and “the locations of early centers of AIDS,” 2) alleged discoveries of HIV and/or AIDS cases before 1976–all have been refuted or unconfirmed (except the 1968 case which appears not to have been HIV but a progenitor), 3) implying Dr. Robert Strecker is in the same camp as Dr. William Campbell Douglass or Lyndon LaRouche. He does not deserve, because of his significant contribution, to be written off as a “scientific . . . reactionary,” or as another author simply slandered, “an anti-vivisectionist.”

In conclusion, I appreciated the spirit and intent of Gilbert’s article, but let’s leave this important scientific debate to scientists.

Sincerely yours,

Leonard G. Horowitz, D.M.D., M.A., M.P.H,
Author of Emerging Viruses: AIDS & Ebola–Nature Accident or Intentional?