BHK cells expressing Sindbis virus-induced homologous interference allow the translation of nonstructural genes of superinfecting virus.
The process by which Sindbis virus excludes superinfecting homologous virus was investigated with the use of temperature-sensitive mutants. Mutants in two RNA-negative complementation groups were found to be defective in their ability to establish interference at the nonpermissive temperature. These mutants were unable to establish interference in a mixed infection (complementation), suggesting that both were defective in a common gene product. Homologous interference was found to block the replication of superinfecting virus after attachment, penetration, and translation of the nonstructural genes encoded in the virus RNA. The production of nonstructural gene products of superinfecting wild-type virus was found to enhance the replication of certain RNA- temperature-sensitive interfering viruses at the permissive and the nonpermissive temperature. The ability of certain RNA- mutants to establish homologous interference and to demonstrate enhanced growth after superinfection with wild-type virus was interpreted to produce a model implicating both virus and host components in the establishment of homologous interference and in the replication of Sindbis virus RNA.
D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D005814:Genes, Viral; D005816:Genetic Complementation Test; D007668:Kidney; D009154:Mutation; D014176:Protein Biosynthesis; D012367:RNA, Viral / Q000096:biosynthesis; D012845:Sindbis Virus / Q000235:genetics*; D013696:Temperature; D014762:Viral Interference
D012367:RNA, Viral