The L protein of a VSV mutant isolated from a persistent infection is responsible for viral interference and dominance over the wild-type.
The dominance of a mutant isolated from a persistent infection (VSV-Pi) over wild-type vesicular stomatitis virus (wt-VSV) in mixed infections was described previously (J. A. Jordan and J. S. Youngner, 1987, Virology, 158, 407-413). In an attempt to identify the VSV-Pi gene product responsible for transcriptional interference, various combinations of purified VSV-Pi and wt-VSV transcribing core proteins were analyzed in an in vitro transcription assay and compared to homologous wild-type controls. The reconstitution studies revealed that the VSV-Pi RNA dependent-RNA polymerase (L protein) has a dominant activity which works in trans to inhibit wt-VSV transcription.
Jordan
J A
JA
Department of Microbiology, School of Medicine, University of Pittsburgh, Pennsylvania 15261.
Whitaker-Dowling
P
P
Youngner
J S
JS
D000818:Animals; D002460:Cell Line; D004587:Electrophoresis, Agar Gel; D004591:Electrophoresis, Polyacrylamide Gel; D007739:L Cells; D051379:Mice; D009154:Mutation; D012367:RNA, Viral / Q000032:analysis / Q000096:biosynthesis; D012324:RNA-Dependent RNA Polymerase; D013698:Templates, Genetic; D014158:Transcription, Genetic; D014721:Vesicular stomatitis Indiana virus / Q000235:genetics* / Q000502:physiology; D014762:Viral Interference; D014764:Viral Proteins / Q000032:analysis / Q000235:genetics*
D012367:RNA, Viral; D014764:Viral Proteins; C040530:L protein, vesicular stomatitis virus; D012324:RNA-Dependent RNA Polymerase