Primary African green monkey kidney cells (GMK) treated with poly(rI).poly(rC) in the presence of DEAE-dextran (‘treated cells’) developed antiviral resistance and concomitantly released interferon into the medium. Treated and untreated cells were infected with herpes simplex virus type 1 (HSV1) in the presence of cytosine arabinoside (araC), and total RNA was isolated and hybridized with purified radio-labelled HSV1 DNA. The intracellular concentration of virus-specific transcripts was not significantly altered in treated cells, but a smaller proportion of the genome of HSV1 hybridized with the extracted RNA. Transcription was similarly restricted when protein synthesis was inhibited by cycloheximide.

To analyse virus translation, proteins were radiolabelled between 6 and 10 h after infection and were immunoprecipitated with a pool of human sera and run on SDS-polyacrylamide gels. No virus-specific proteins could be detected in treated cells. In contrast about 25 HSV1-induced proteins were found in infected cells and about 22 proteins in cells infected in the presence of araC. In particular, two virus proteins with apparent mol. wt. of 128000 and 42500 were immunoprecipitated. Since these two were also detected in cells under conditions where elongation of polypeptide chains was non-specifically retarded, it is unlikely that a similar mechanism was responsible for the impaired growth of HSV1 in our treated cells. We conclude that this impairment probably resulted from regulation at the level of virus translation, probably mediated through interferon.


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