Antiviral activity of polyinosinic-polycytidylic acid in the absence of cell-controlled RNA synthesis.

When Detroit cells are infected with poliovirus in the presence of 5/~g./ml. of actinomycin, cell-controlled RNA synthesis is blocked and 2-[14C]uridine is incorporated only into poliovirus-specific RNA. The addition of polyinosinic-polycytidylic acid (5/%/ml.) under such conditions results in the inhibition of synthesis of 35s intracellular, infectious poliovirus RNA. A high molecular weight fraction of poliovirus-specific RNA migrating on polyacrylamide gels, as would be expected of the double-stranded, replicative form of poliovirus RNA, is synthesized to the same extent as in the absence of interferon inducer. This RNA was digested with RNase and DNase and was resistant to the enzymes, confirming that the compound was replicative form poliovirus RNA. A low molecular weight, virus-induced RNA of 4s and unknown function is also synthesized independently of polyinosinic-polycytidylic acid. The significance of the differential inhibition in the synthesis of the compounds presumed to be poliovirus RNA and replicative form poliovirus RNA, and the fact that the capacity of polyinosinic-polycytidylic acid to inhibit the synthesis of infectious RNA is insensitive to actinomycin, is discussed.