Below are excerpts from a Progress Report of the Special Virus Cancer
Program
sometime before 1977. Sorry that I've misplaced the exact report number but
I'll find it when I go back to the library. If the experimenters then
weren't able to alter viruses or make a virus to cause something similar to
AIDS, It appears it wasn't for lack of trying.
"initiating chronic infections at the genetic level."
"Emphasis will be shifted to attempts to activate latent viral genomes in
cells originally exposed to chemically-modified or genetically restricted
virus"
"some observations have suggested that ordinarily non-oncogenic viruses may
have oncogenic potential."
And finally the chilling, "to effect immune paralysis."
RUTGERS UNIVERSITY (NIH-71-2077)
Title: Studies on Genetic Acquisition of Oncogenic Potential by RNA
Animal Viruses
Contractor's Project Director: Dr. Robert Simpson
Project Officers (NCI): Dr. Micheal A. Chirigos
Dr. Robert Manaker
Objectives: To determine whether a non-oncogenic RNA animal virus can gain
tumor-producing or cell-transforming capability as a consequence of host
induced genetic modification of the viral RNA, by intracellular persistance
of incomplete but functionally active viral genetic material, or by induced
mutation.
Major Findings: Inactivation of candidate viruses such as vesicular
stomatits
virus (VSV) by polyene antibiotics has been exploited as a method for
initiating chronic infections at the genetic level. The most active
antibiotic found was a water soluble methyl ester of amhoteracin B which
does
not degrade virions or produce detectable changes in the viral RNA.
Collaborative work done with Dr. D. H. L. Bishop indicates that certain
polyenes can replace nonionic detergents in in vitro RNA polymerase reaction
mixtures with VSV suggesting that these antibiotics act to alter properties
of the viral lipoprotein membrane of intact virions.
Newborn guinea pig heart cells originally infected with VSV inactivated by
the compound ethylene iminoquinone (Bayer A 139) have been maintained in
vitro for 3 months with no evidence for production of infectious virus.
Persistent infections have been established in HEp-2 carcinoma cells with
host-range mutants of VSV that replicate nonpermissively in these cells.
Electron microscopic examination of normal guinea pig cell lines developed
in
this project has failed to reveal presence of C-type particles or other
virus
like particles.
Attempts to induce immunological tolerance to VSV in neonatal guinea pigs
were unsuccessful.
Significance to Biomedical Research and the Program of the Institute:
The genetic acquisition of oncogenic potential by RNA viruses is an
intriguing possibility and one of great importance, since it is possible
that
a human cancer virus could be a member of an RNA virus group that normally
causes non-oncogenic disease in man. Although supporting evidence for this
phenomenon in RNA viruses is scarce, some observations have suggested that
ordinarily non-oncogenic viruses may have oncogenic potential. Thus a
thorough investigation of the capacity of non-oncogenic viruses to acquire
genetic oncogenic potential is warranted.
Proposed Course: Emphasis will be shifted to attempts to activate latent
viral genomes in cells originally exposed to chemically-modified or
genetically restricted virus (VSV). Conditional lethal mutants of VSV will
be examined for their pathogenesis in guinea pigs and capacity to effect
immune paralysis. In vitro studies will be continued to ascertain the
spectrum of viral genome expressions in cells harboring non-infectious,
virus
specific, informational molecules.
Date Contract Initiated: February 15, 1971
Current Annual Level: $135,758
