Requirement for host transcription in the replication of Sindbis virus

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Abstract
Host cell involvement in Sindbis virus (SB) replication was examined in cells which had been treated with either actinomycin D (AMD) or .alpha.-amanitin (.alpha.-A). Treatment with these inhibitors of host transcription before infection reduced the ability of cells to support SB growth by 1-2 orders of magnitude, while having little or no effect on the replication of vesicular stomatitis virus. SB replication was sensitive to .alpha.-A in wild-type Chinese hamster ovary (CHO) cells but was resistant to .alpha.-A in CHOama-1 cells, a line which contains an .alpha.-A-resistant RNA polymerase II. A mutant of SB, SBamr, was isolated by mutagenesis followed by selection in cells which had been treated with AMD. SBamr grew normally not only in cells treated with AMD but also in .alpha.-A-treated cells. Evidently, the synthesis of cellular mRNA (and presumably protein) is required for replication of SB, prior treatment with either drugs affects the same aspect of SB replication and mutations in the SB genome allow the virus to overcome the effect of inhibitors of host transcription.