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Department of Bacteriology and Virology, Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT, U.K.
Vaccinia virus WR induces an immediate and rapid inhibition of HeLa S3 cell RNA synthesis as determined by pulse-labelling with [3H]uridine. The inhibition was independent of the purity of the infecting virus preparation and the multiplicity of infection over the range of 4 to 200 pk.f.u./cell. Inhibition was not evident in cells pretreated with cycloheximide or following infection with u.v.- or heat-inactivated virus, suggesting that viral protein synthesis was required. There was no apparent selective inhibition of any particular species of RNA. Following infection, the uptake of [3H]uridine into cellular pools and the subsequent biosynthesis of UTP proceeded at the same rate as in mock-infected control cells. The rate of degradation of pre-labelled RNA was not enhanced in infected cells compared to controls. Analysis of the nuclear DNA-dependent RNA polymerase (EC 2.7.7.6 [EC] ) activities revealed a progressive and eventually total loss of RNA polymerase B activity, no obvious effect on RNA polymerase A and the presence of a viral RNA polymerase, the possible significance of which is discussed.
Keywords: vaccinia virus, RNA synthesis inhibition, RNA polymerases
Present address: Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, U.K.
Received 16 January 1984;
accepted 19 June 1984.
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