Abstract

The addition of the protein inhibitor cycloheximide, at concentrations which suppress virus replication, to HeLa cell monolayers infected with reovirus type 2 results in the appearance of accelerated cytopathic effects (CPE). At high multiplicity of infection, CPE appeared after a lag period of 2 to 3 hr and increased progressively, until by 12 hr the entire monolayer had rounded and sloughed off. During this same period, both the uninfected cycloheximide-treated and untreated virus-infected controls exhibited no CPE. The phenomenon is affected by the kind of cell species employed and can be reversed if the antibiotic is removed within 1 hr after exposure. The evidence obtained through studies in which specific metabolic inhibitors and direct biochemical analyses were used suggests that the accelerated CPE observed in cycloheximide-treated reovirus-infected cells is the consequence of the combined inhibition of the synthesis of both cellular protein and ribonucleic acid. The accelerated CPE is also induced in the antibiotic-treated cells by reovirus serotypes 1 and 3.

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