Two distinct antiviral activities can be detected in L cells treated with low levels of interferon and infected with a one-step interferon-sensitive mutant of mengovirus (-1). The first antiviral activity (AVA-1) primarily delayed virus RNA and protein synthesis and thereby lengthened the virus replication cycle. It did not prevent cell death. The second antiviral activity (AVA-2) allowed the virus-induced inhibition of host macromolecular synthesis but inhibited all other virus functions. By 9 to 12 h post-infection host synthesis resumed and most cells survived. The data suggest that some step in the virus replication cycle activates AVA-2 leading to the destruction of the virus genome 6 to 12 h after infection. In unprotected cells the yields of parental virus ( ) and -1 were similar. No qualitative or quantitative differences in virus products were observed by several techniques. The -1 virus seems to have lost a wild-type function which normally blocks the action of AVA-2.


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