The following article describes contagious cancer discovered in African

monkeys, as early as 1957.  For would-be biological warfare advocates in
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".






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

DOI: 10.1111/j.1749-6632.1963.tb13439.x


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

 needle puncture