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The drug, N,N bis (ethylene)-P (1-adamantyl) phosphonic diamide inhibits focus formation of Rous Sarcoma Virus in tissue culture. Transformation of chick cells was inhibited when the drug was added to chick cells prior to infection. The drug did not inhibit the transformation of Normal Rat Kidney Cells infected with RSV, when the cells were grown at non-permissive temperatures and shifted to permissive temperatures upon addition of the drug. Nor did the drug revert cells transformed at permissive temperatures. These studies indicated that the inhibition of RSV is in the early stage of viral growth, possible penetration or uncoating.

N^6,O^2' -Dibutyryl cyclic adenosine 3',5'-monophosphate (Bt_2cAMP) was investigated for its effects on various tissue culture cells infected with temperature-sensitive (ts) mutant, LA31 and Bratislava 77 (B77), a wild-type Rous sarcoma virus. Specifically, known parameters of transformation were investigated and a possible site of action has been tenably proposed. The drug Bt_2cAMP was found to have little effect on the transformation related properties of primary chick embryo fibroblasts (CEF) infected with either virus or normal rat kidney fibroblasts (NRK) infected with the wild-type B77-RSV. However, significant inhibition of the transforming properties in NRK infected with the ts mutant LA31 (LA31-NRK) were reported at the permissive temperature 33 degrees centigrade (33 C).

LA31-NRK and B77-NRK are established cell lines that were normal rat kidney cells transformed with temperature-sensitive mutant (LA31) and wild-type Bratislava 77 (B77) of Rous sarcoma virus. It is recognized that many transformation-induced changes differentiate between normal and transformed cells. Morphology and four parameters of transformed cells such as saturation density, anchorage independence, plasminogen activator, and colony stimulating factor were used as indicators to observe the effect of human alpha interferon on the growth of NRK, LA31-NRK and B77-NRK. The results show that interferon could neither reverse the transformed cells to normal fashion nor change their behaviors or cause release of protease.

Human chorionic gonodotropin (HCG) affected in various ways cell cultures infected with strains of Rous sarcoma virus (RSV). The cell cultures studied were chick embryo fibroblasts (CEF), normal rat kidney cells infected with temperature-sensitive mutant (LA31-NRK) and a wild type RSV (B77-NRK). HCG increased the rate of transformation and viral titer of CEF cells infected with RSV, but not B77-NRK. HCG increased significantly transformation rates of LA31-NRK, only if the temperature sensitive transformation process was first delayed by incubation at non-permissive temperatures. It is suggested that some postinfective, pretransformational event(s) may operate before viralmediated transformation rates are increased by HCG.

Ribavirin, a synthetic nucleoside, was found to inhibit the replication of Rous sarcoma viruses (RSV) and subsequent cell transformation in chick embryo fibroblasts (CEF). It also blocked the transformation of normal rat kidney (NRK) cells infected with temperature-sensitive mutants of RSV. The action of Ribavirin was found to be reversible as removal of the drug from the NRK cells reversed the effects on cell transformation. Ribavirin appears to have a static effect on cell growth of both NRK and CEF cells. In addition, guanosine, xanthosine and inosine altered the effect of Ribavirin on cell growth.

Typescript. / Thesis (Ph. D.)--University of Hawaii at Manoa, 1990. / Includes bibliographical references (leaf 80) / Microfiche. / viii, 80 leaves, bound ill. 29 cm

Chick embryo fibroblasts and rat kidney cells infected in vitro with Rous Sarcoma viruses were treated with 3-deazaguanine (3-DG). The findings revealed that 3-DG inhibited virus-induced cellular transformation. Degree of inhibition is dependent on concentration and frequency of media change. 3-DG at the concentrations tested will not reverse transformed cells to the untransformed state and does not have marked effect on replication of viruses. Upon removal of 3-DG, its effect was shown to be reversible. Cell growth was generally retarded in medium containing 3-DG. When xanthosine and inosine were added to the medium, cell growth was unaffected, but it increased in guanosine.