title: Dominance of temperature-sensitive phenotypes. II. Vesicular stomatitis virus mutants from a persistent infection interfere with shut-off of host protein synthesis by wild-type virus.
abstract: The dominance of a mutant (VSV-PI) isolated from a long-term persistent infection over wild-type vesicular stomatitis virus (wt-VSV) is reported. This dominance has some important differences from and similarities to the dominance of conventional ts mutants studied previously (J. S. Youngner, D. W. Frielle, and P. Whitaker-Dowling, 1986, Virology 155, 225-235). Unlike the ts mutants representing complementation groups I and IV, coinfection with VSV-PI does not reduce the yield of infectious wt-VSV at either the permissive (37 degrees) or nonpermissive (39.5 degrees) temperatures. However, in double infections with wt-VSV and VSV-PI at 37 degrees, viral RNA synthesis patterns were converted to those of the RNA synthesis phenotype of VSV-PI: reduced mRNA transcription and enhanced replication of genomic RNA. In addition, VSV-PI which shuts off host protein synthesis very inefficiently was able to interfere in double infections with the ability of wt-VSV to rapidly shut off host protein synthesis. This finding suggests that the mutant virus is not just missing the factor(s) responsible for the inhibition of host protein synthesis but has a dominant activity which works in trans to interfere with the shut-off function of wt-VSV. Ultraviolet irradiation of VSV-PI was used to determine the target size of the interference function. The calculated value for the uv target size is equal to that of the viral genome. This suggests that either viral replication or the expression of the last gene on the viral genome (encoding the L protein) is required for interference by VSV-PI with the shut-off of host cell protein synthesis by wt-VSV.
mesh_terms: D000818:Animals; D005799:Genes, Dominant; D007739:L Cells; D051379:Mice; D009154:Mutation; D010641:Phenotype; D014176:Protein Biosynthesis; D013696:Temperature; D014721:Vesicular stomatitis Indiana virus / Q000235:genetics* / Q000502:physiology; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
chemical_list: D014764:Viral Proteins