Key result
Cycloheximide and iododeoxyuridine efficiently induce type C virus from BALB/c mouse cells in exponential growth but not in stationary phase, acting via different mechanisms.
Inhibitors of protein synthesis and halogenated pyrimidines act by different mechanisms to induce type C virus release in mouse cells.
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May inform retroviral induction models in proliferating murine cells; leaves open translation to human cardiovascular research.
The information for type C RNA viruses is genetically transmitted within the cellular DNA of the normal mouse cell. These viruses can be induced after exposure of cells to two classes of chemicals, inhibitors of protein synthesis and halogenated pyrimidines. The metabolic requirements for activation of one endogenous virus of BALB/c mouse cells by representatives of each class of drugs were studies. Cycloheximide and iododeoxyuridine each induce virus efficiently from cultures in exponential growth but are inactive on cells in stationary phase. However, cells are maximally sensitive to the actions of each drug at different times within the cell cycle. Further, virus induction in response to each is differentially inhibited under conditions of simultaneous cell exposure to inhibitors of DNA or RNA synthesis. The results provide support for the concept that inhibitors of protein synthesis and halogenated pyrimidines act by different mechanisms to induce type C virus release.
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Greenberger et al. (1975) studied Xenotropic type C virus induction. Cycloheximide and iododeoxyuridine was evaluated on Virus induction. Cycloheximide and iododeoxyuridine efficiently induce type C virus from BALB/c mouse cells in exponential growth but not in stationary phase, acting via different mechanisms.
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