-Caveat Lector-

CHAPTER SIXTEEN: Epilogue

We have examined some of the more important leukemia/sarcoma research over
the last 50+ years and have attempted to trace the evolution of that
research as it moved from virus to virus and species to species. As we have
examined the evolutionary progress of this research we have seen a fairly
clear picture of the paradigm guiding studies of leukemia/sarcoma. At the
risk of gross simplification of that paradigm but in the interest of some
summarization, our study of the related history has shown:


1. Interest in a chicken sarcoma (Rous's sarcoma) going back to at least
1911.
2. Investigations of enzymatic/metabolic cellular process during the 1930s.
3. Interest in T-cell agents, e.g., lymphocytic choriomeningitis (LCM), as
well as mouse mammary tumor-related agents and experimentally-induced
allergic encephalomyelitis in the mid-to-late 1930s.  These studies were in
the context of discerning agents capable of neurological attack.
4. Extensive interest in Rous's sarcoma, latent progressively-infecting
viruses, e.g. progressive mouse pneumonia, as well as allergic
encephalomyelitis in the early 1940s during World War II.
5. Further study of aspects of erythroblastosis and myeloblastosis effects
of Rous's sarcoma as well as growing interest in mouse mammary tumor-related
agents in the later 1940s and early 1950s.
6. Creation/passage of mouse T-cell-related-leukemias using mammary
tumor-prone mice during the early 1950s (e.g., Gross's AKR work with
C3H-strain mammary tumor-prone mice). Other studies involved infection of
bovine and human cells with the slow-infecting sheep Maedi-Visna virus.
7. Investigations and recovery of various simian viruses, simian foamy
viruses, ECHO viruses (e.g., ECHO-10), polio virus, and measles and
understanding their interaction with cells during the mid-1950s. Many viral
agents of the myxovirus/paramyxovirus family were studied.
8. Discovery by Burkitt of jaw tumors in African children and the associated
Burkitt's B-cell-tropic/immunoglobin IgM-related lymphoma in 1958.
9. Infection of mouse and rat cells with "Prague-strain" Rous avian sarcoma
virus in the early 1960s.
10. Discovery of viral agents capable of disturbing important metabolic
enzyme processes (e.g., lactic dehydrogenase-elevating virus) and their
association with cancers in the early 1960s.
11. Discovery/creation/passage of new mouse/rat leukemia/sarcoma viruses
throughout the decade of the 1960s, e.g., the Rauscher, Moloney, Kirsten,
and Harvey retroviruses.
12. Attempts to hybridize both types of viruses and types of species' cells
using such agents as Simian Virus 40 (SV40), reoviruses (e.g., reovirus type
3), human adenoviruses (e.g., adenovirus types 2, 12, and 18), bovine
reovirus and parainfluenza type 3 throughout the decade of the 1960s.
13. Infection of human and simian cells with the "Prague-strain" of Rous
avian sarcoma in 1964.
14. Use of genes from the Moloney sarcoma virus to alter virtually any mouse
leukemia virus into its related sarcoma virus in the later 1960s; thus
hypothetically allowing for creation of an infinite number of sarcomas from
leukemias originating from viral, chemical, or radiation-related causes.
15. Passage of various Moloney sarcoma-related agents to various species'
cells, e.g. to cats, in the later 1960s and hybridization of Moloney-related
cat sarcomas with dog-related melanomas to create a transmissible
fibrosaroma virus. Also seen is the infection of human embryonic cells with
the Rauscher mouse leukemia agent.
16. Appearance of unusual numbers of Kaposi's sarcoma occurring in residents
of Tanzania, a country in east Africa in 1967.
17. Appearance of a fibrosarcoma in a pet Woolly monkey and the transmission
of that disease to a gibbon ape (also kept as a pet) causing a
T-cell-related leukemia in infected gibbons in the late 1960s. Both bovine
(cow) cells and porcine (pig) cells are infected by the ovine (sheep)
Maedi-Visna virus in 1968.
18. Appearance of patients with acute lymphocytic leukemias related to the
gibbon ape/woolly monkey retrovirus as well as Kirsten virus-related
myelogenous leukemia in the early 1970s.
19. Appearance of "new" T-cell-tropic human leukemias (later called "Human
T-cell Lymphotropic Viruses" or HTLV) in the mid-to-later 1970s. Some of
these viruses show genetic elements similar to the Rauscher mouse leukemia
virus. In 1977, human acute/chronic leukemic cells are found to be capable
of being productively infected by the "Bovine Visna Virus" (not yet called
the Bovine Immunodeficiency Virus). HIV-1 retrovirus physically resembles
the Visna virus and both are considered "lentiviruses," i.e., slow-acting
infectious agents.
20. First recognition of HIV-1 infection and "AIDS" in North Americans in
the early 1980s. Genetic elements of HIV-1 also include nucleotide sequences
similar to the Rauscher mouse leukemia virus as well as the Maedi-Visna
virus and Bovine leukemia virus.
The above very simplistic yet accurate summary of the related history
preceding the official advent of AIDS is the result of our overall
investigation of some 1600 references across the 50+ years. Obviously we
have not examined all of the history (that would require examining perhaps,
as a conservative estimate, over a million studies) nor, by the way, is all
of the history available for investigation (much scientific work is
unpublished). We can see, though, with a good degree of accuracy what did
happen across the period in a fashion similar to how "Cliff Notes" summarize
Shakespear. In essence, we have isolated the "scientific paradigm" guiding
the development of historic research and, by doing so, are now in a position
to ask "why" this research was pursued.
In trying to answer the question of "why," there are obviously several
possible answers. To dichotomize, possible answers include:

1. Basic step-by-step research designed to determine the actions of
leukemias/sarcomas in an effort to cure same.
2. Research designed to create retroviral biological weapons capable of some
race-specificity (based on exploitation of metabolic/genetic differences
among races).
Assuming the above two answers accurately represent the dichotomy there must
be some very specific body of knowledge capable of integrating these two
options, i.e., if the points represent the possible two cuts of the "sword
of Damoclese," what then, in fact, is the sword? Moreover, what "sword" will
integrate into an intelligent gestalt the various animal species, viruses,
and research we have examined?
The "sword" is the immune system, and, more specifically, the activities of
the immune system at the surface of individual cells. According to Amos et
al. (1972) the most important aspect of the immune system operating at the
surface of individual cells are "histocompatibility antigens" [Amos, D. B.;
Bodmer, W. F.; Ceppellini, R., et al. (1972) "Biological significance of
histocompaltibility antigens." Federation Proceedings, 31:3:1087-1104]. Amos
continues,


"Histocompatibility antigens are genetically controlled cell surface
structures which may differ between individuals. They are in principle
defined by the fact that grafts exchanged between individuals which differ
with respect to these antigens are rejected by the immune mechanisms of the
recipient. Some of these antigens can be recognized by serological methods,
which is the present basis for tissue typing. So far tissue typing has been
developed mainly through antigens which express themselves on the formed
elements of the blood. A number of lines of evidence point to the great
biological significance of these cell surface structures. Possible
biological functions for these gene products, such as the control of the
immune response and susceptibility to oncogenic viruses have been suggested
recently..." [Amos, D. B.; Bodmer, W. F.; Ceppellini, R., et al. (1972)
"Biological significance of histocompatibility antigens." Federation
Proceedings, 31:3:1087-1104].

Continuing their discussion of the importance of histocompatibility antigens
and, more specifically, the human "HL-A" histocompatibility antigen and its
particular importance in viral/immune system-associated disease, Amos et al.
(1972) state:

"The physiological approach dictates a consideration of viral and/or immune
response factors leading to disease. Thus, investigation of diseases with
suspected viral etiology, such as leukemia, lymphoma, and other reticuloses
(including Burkitt's lymphoma) is indicated, as well as of diseases which
present severe problems in specific localities, such as Kuru, subacute
sclerosing panencephalitis, nasopharxngeal carcinoma, and primary hepatoma.
Also indicated are studies of susceptibility to and morbidity from parasitic
infections in endemic regions, especially with respect to schistosomiasis,
trypanosomiasis, malaria, and the hemorrhagic shock syndrome associated with
dengue fever, where immunological factors may be important in determining
the outcome of infection. In relation to the immune response, a number of
useful experimental approaches can be visualized. One would be a study of
the relationship of HL-A type to the immune response, both humoral and
cellular. . ." [Amos, D. B.; Bodmer, W. F.; Ceppellini, R., et al, (1972)
"Biological significance of histocompatibility antigens." Federation
Proceedings, 31:3:1087-1104].
Co-authors of the above article were, in 1972, from such institutions as
Duke University, Oxford University, the Basel Institute for Immunology
(Basel, Switzerland), National Institutes of Health, University of
California at Los Angeles, the World Health Organization, the Karolinska
Institute (Stockholm, Sweden), the University of Michigan, Albert Einstein
College of Medicine of Yeshiva University, Standford University, the Wistar
Institute, Scripps Institute, the National Cancer Institute, and the
Institute of Experimental Immunology (at the University of Copenhagen,
Denmark).
That our search has been useful, consider the following quote from a U.S.
Army document on biochemical warfare:

"� it is theoretically possible to develop so-called �ethnic chemical
weapons�, which would be designed to exploit naturally occurring differences
in vulnerability among specific populations. Thus, such a weapon would be
capable of incapacitating or killing a selected enemy population to a
significantly greater extent that the population of friendly forces." [US
Army Mobility Equipment Rsearch and Development Center, Decontamination of
Water Containing Chemical Warfare Agent, Fort Belvoir, Virginia, January,
1975]
Considering that efforts to create ethnic group-specific biological weapons
exist is not a flight of fancy and, as the activities of the genetics of the
immune system at the surface of individual cells are more clearly
understood, these biological weapons may eventually be so refined as to be
able to kill specific individuals within ethnic groups.  This is the
direction of the paradigm.  Something to consider as the government is
interested in obtaining DNA samples from all individuals.
Clearly our documented historic investigation reveals an extensive
investigation of leukemia/sarcomas as well as related viruses in a number of
species. Moreover, we have seen documented reports indicating successful
efforts to infect human cells with a variety of those agents and the
appearance of leukemic diseases directly related to those "other species"
agents in human patients. The title of this book, AIDS: An Explosion of the
Biological Timebomb, denotes the focus of our investigation and asks its
question not as "conspiracy-minded" innuendo but on a foundation of facts
taken from highly respected immunology-related journals from articles
published by many of those same persons who are, today, attempting to defeat
the AID retrovirus. Though this current historic investigation could be
expanded to focus on works of specific individuals and specific institutions
I believe that such an expansion would be redundant.  I do, however, wish to
leave you with the idea that the answer to the question of the origin of
AIDS has not yet been sufficiently answered and that the medical community
has failed to account for the presence of genetic elements in HIV-1 of
specific retroviruses subjected to laboratory study and manipulation through
nearly 50 historic years and their appearance in humans.

Efforts by some members of the medical community to address the origin of
AIDS as being a human-created virus have been made, e.g., Dr. Leonard
Horowitz, Dr. Alan Cantwell, and Dr. Robert Strecker. Still, however, these
individuals have not been well received by the scientific community and have
been, unfortunately, largely ignored. As evidence that AIDS' origin is
likely related to the subject of our present investigation, these
individuals will, in time, likely be vindicated.  It is certainly time for
the knowledgeable public investigate the matter in great detail else we are
at-risk for further epidemics.

I conclude, as do hopefully you, asking again, what is the origin of AIDS
and wondering if Gordon Rattray Taylor's Biological Timebomb has exploded.


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