Abstract

Biologically distinguishable endogenous type-C RNA viruses of BALB c mouse cells are differentially affected by two classes of chemical inducers, halogenated pyrimidines and inhibitors of protein synthesis. In the present studies, the effects of these chemicals were compared on cells of genetic crosses involving BALB c , C58, and NIH Swiss mouse strains. Cycloheximide was found to activate xenotropic vius from those genetic crosses from which xenotropic virus was inducible by IdU. In contrast, NIH Swiss-tropic endogenous viruses of BALB c and C58 cells were much more resistant to activation by inhibitors of protein synthesis. Steroids possessing glucocorticoid activity enhanced virus release by cells exposed to either class of inducers. Unlike the inducers, which inhibited type-C virus release by exogenously infected cells, steroids augmented chronic virus production. These findings indicate that the mechanisms of action of inhibitors of protein synthesis and halogenated pyrimidines involve the virus-activation process, while steroids enhance rather than initiate virus synthesis.

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