Abstract

SV5-induced RNA synthesis has been studied in actinomycin-treated primary cultures of rhesus monkey kidney cells. Virus-induced RNA synthesis is first detected about 3 hours after infection, and during the period of maximum virus replication, RNA synthesis precedes virus production by 1 1 2 –2 hours. At its maximum rate, SV5-induced RNA synthesis is <1% of total cellular RNA synthesis. Superinfection with poliovirus of cells already producing SV5 does not inhibit, but rather slightly enhances, the ongoing replication of infective SV5. In contrast, puromycin causes a rapid inhibition of ongoing SV5 replication. The inoculation of poliovirus, 325 PFU/cell, in the presence of guanidine causes inhibition of cellular RNA and protein synthesis; however, such inoculation of cells previously infected with SV5 causes a stimulation of actinomycin-resistant, virus-induced RNA synthesis, and a slight enhancement of infective SV5 production. The results indicate that poliovirus does not shut off SV5 RNA-dependent RNA synthesis although it does shut off cellular DNA-dependent RNA synthesis. Furthermore, poliovirus does not inhibit SV5 protein synthesis under conditions in which it does inhibit cellular protein synthesis, thus providing an example of a functional distinction between SV5 messenger and cellular messenger RNA.

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