Selective inhibition of protein synthesis in virus-infected mammalian cells

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Abstract
A number of translation inhibitors were tested for their effects on control and encephalomyocarditis virus-infected mouse 3T6 cells. The virus-infected cells were specifically inhibited by gougerotin, edeine and blasticidin S, whereas these drugs failed to penetrate into uninfected cells. Inhibition of infected cells by gougerotin became apparent when the synthesis of viral proteins commenced, suggesting that the latter process is accompanied by a permeability change in the cells that allows upake of the drug. This permeability change was not observed in cells treated with cycloheximide soon after viral infection, although treatment with actinomycin D did not prevent inhibition by gougerotin. A specific viral protein may be involved in the permeability change of the plasma membrane. Gougerotin was unable to inhibit protein synthesis in the presence of Zn ions, thus preventing gougerotin from entering into the infected cell. Membrane leakiness was not restricted to the encephalomyocarditis virus-3T6 system; it was also observed in mengovirus-infected 3T6 cells, Semliki Forest virus-infected BHK [baby hamster kidney] cells and SV40-infected CV1 [African green monkey kidney] cells at the time in which the synthesis of late proteins is maximal.