Targets for VSV Inhibition of RNA Synthesis

Among the potential targets for VSV inhibition of cellular RNA synthesis are transport of nucleoside triphosphates across the cell membrane, enzymatic conversion to nucleotides, initiation/chain elongation/termination of nuclear chromatin transcription, polyaden-ylation, processing, transport to the cytoplasm of completed RNA transcripts, and stability. Quite obviously, RNA synthesis inhibition could be at the level of ribosomal, messenger, and/or transfer RNA catalyzed by polymerases I, II, and III, respectively. 

Wu and Lucas-Lenard (1980) confirmed the findings published by Week and Wagner (1979a) they used ts mutants Gll(I), 052(11), G3KIII), G33(III), G41(IV), WIO(IV), 045(V), and wt VSV to infect L cells and determine their effects at the permissive (30°C) and nonpermissive temperature (40°C) on uridine transport. The results suggest that the decreased incorporation of [ H]uridine into acid-insol- 

RNA Processing, Transport, and StabUity of RNA in Cells Infected with Vesicular Stomatitis Virus 

The only report of possible degradation of cellular RNA by VSV was made by Kolakofsky and Altman (1978) who disrupted purified VSV with detergent and found endoribonucleolytic activity associated with the virus nucleocapsid when assayed by using tRNA as a substrate. Further characterization of this endoribonuclease activity 

Wu and Lucas-Lenard (1980) examined RNA precursors in L-929 cells infected with wild-type and ts mutants of VSV. In agreement with previous reports, they found a decrease in the synthesis of cellular RNA. A close examination of the overall distribution of cellular rRNAs by Wu and Lucas-Lenard (1980) revealed a decreased amount of synthesis but no change in the relative amount of each species of rRNA. 

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