EARLY HUMAN EXPERIMENTATION WITH CANCER-CAUSING MONKEY VIRUS
The following article describes contagious cancer discovered in African
monkeys, as early as 1957. For would-be biological warfare
the Pentagon and intelligence world, this would be like a wet dream,
a potential means for assassinations or even mass murder.
Incredibly enough, irresponsible researchers describe how such a virus
was promptly taken and injected into human "volunteers".
HUMAN SUSCEPTIBILITY TO A SIMIAN TUMOR VIRUS
James T. Grace Jr. and
Edwin A. Mirand
Roswell Park Memorial Institute, New York Dept. of Health, Buffalo, N.Y.
Article first published online: 15 DEC 2006
In 1957 Bearcroft and Jamieson noted an outbreak of subcutaneous tumors
in a rhesus monkey colony in Yaba, Nigeria. The initial tumor was detected
on the face of a rhesus monkey which was housed in an open air pen. Subsequently,
similar tumors appeared in 20 rhesus monkeys in the same colony.
No tumors developed in African monkeys housed in the same area although
one dog-faced baboon did develop a lesion. The tumors were composed of
large pleomorphic cells, some of which contained cytoplasmic inclusion bodies,
thus strengthening the suspicion that those lesions might be of viral etiology.
Subsequently, Andres and co-workers demonstrated cell-free transmission
of the tumors and identified the etiologic agent as a virus which morphologically
resembled members of the pox virus group. Niven et al in a study of the
histopathology of the tumors concludes that the cell of origin was probably
a fibroblast or fibrocyte. However, a detailed pathogenetic study by Sproul
et al indicated that the cell was the tissue histiocyte and that the
lesion might be properly termed a histiocytoma. This point will be expanded
in a later section of this paper.
Susceptibility to this virus appears to be limited to primates. Extensive
studies involving inoculation of newborn and adult rabbits, guinea pigs, hamsters,
rats, mice and doges by a variety of routes failed to produce proliferative
lesions or evidence of virus replication. The virus produced no lesions in the
embryonated egg following inoculation of the chrioallantoic membrane or
yolk sac. Subsequent inoculation of the egg passage material into monkeys
revealed no evidence of virus. Similarly extensive attempts to propagate the
virus into tissue culture were unsuccessful. Table 1 shows the types of cell
cultures employed and the results. In none of the cell culture systems employed
was there evidence of cytopathogenicity or replication of the virus.
Table2 shows the susceptibility of various monkeys to the virus. Generally
the rhesus and cynomolgus are the most susceptible. Six human volunteers
with far advanced cancer were inoculated with virus obtained from monkey
tumors. These tumor filtrates were cell-free, and as determined by animal
embryonated egg and tissue culture studies, were free of extraneous simian
viruses. The humans developed lesions quite similar to those of the monkeys
The level rose progressively for three weeks and then remained at that level
for four months at which time he developed a nodule at the site of the
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