1887

Abstract

SUMMARY

The proportion of cells absorbing trypan blue ( character) can be used to measure the late c.p.e. of wild-type poliovirus ( . ), which was the same at restrictive (39.2 to 39.6 °C) or permissive (37 °C) temperatures. Of twenty mutants, seven showed normal c.p.e. at 37 °C but were defective in c.p.e. () at 39.5 °C; all seven mutants have previously been shown (Cooper 1971) to give evidence of a primary defect in replicase I activity (to make the complementary or minus strand of virus RNA). The remainder ( ) have all previously been shown to give evidence of a primary defect either in replicase II activity (to make progeny plus strands) or in structural protein. Thus, the late c.p.e. is dependent on a product of the replicase I gene, of which the effector is probably double-stranded RNA. Late c.p.e. is not caused by prevention of host protein, RNA or DNA synthesis and is not necessarily correlated with lysosomal enzyme release. The mutants were also defective in inducing early changes in chromatin () and in prevention of thymidine incorporation (), but the and characters are probably independent expressions of replicase I activity. Virus growth does not depend on repression of DNA synthesis. Poliovirus represses the activities of host DNA-dependent RNA polymerase I and II to an equal extent. There is no evidence that repression of DNA or RNA synthesis results from direct interaction of a virus protein with the DNA.

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1975-04-01
2021-10-28
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