Mechanism of interference between influenza A/WSN and B/Kanagawa viruses.
Simultaneous infection of MDCK cells with influenza viruses A/WSN and B/Kanagawa resulted in mutual interference with virus protein synthesis and in significant suppression of A/WSN growth. When infection by one virus preceded the other by 1 or 2 h, growth of the superinfecting virus was selectively inhibited at the level of transcription. Interference by the pre-infecting virus was strongly dependent on the expression of the viral genome but not on haemagglutinin activity. When the replication of both virus types was restricted to primary transcription by cycloheximide, the only translation products following removal of the drug were those of the preinfecting virus. This result was not affected by blocking secondary transcription by actinomycin D. These findings suggest that intertypic interference occurs at the level of primary transcription. This concept was supported further by the observation that a ts mutant of A/WSN (ts-65) with a defect in primary transcription interfered only with superinfection by B/Kanagawa at the permissive temperature.
D000818:Animals; D004285:Dogs; D009980:Influenza A virus / Q000235:genetics*; D009975:Orthomyxoviridae / Q000235:genetics; D012367:RNA, Viral / Q000235:genetics; D014158:Transcription, Genetic; D014466:Ultraviolet Rays; D014762:Viral Interference / Q000528:radiation effects; D014764:Viral Proteins / Q000235:genetics; D014779:Virus Replication
D012367:RNA, Viral; D014764:Viral Proteins