Cell division does not affect Sendai virus genome replication in persistently infected BHK cells.
The extent of Sendai virus genome replication in persistently infected BHK cells actively growing or at confluence was followed by estimation of the [3H]uridine incorporated into intracellular nucleocapsid RNA. First, we showed that, in the presence of actinomycin D, actively growing persistently infected cells were taking up threefold more [3H]uridine than resting cells. This higher uptake exhibited by growing cells was observed neither in persistently infected cells in the absence of actinomycin D, nor in acutely infected cells in the presence of actinomycin D. Assuming that the cellular pool of unlabelled uridine stays constant, we used a correction factor for this difference in [3H]uridine uptake and estimated [3H]uridine incorporation in nucleocapsid RNA, normalizing the data either to the amount of cell or of viral template. Results showed that the viral genome replication, expressed either way, was not significantly influenced by cell growth conditions.
D000818:Animals; D002455:Cell Division; D002460:Cell Line; D002472:Cell Transformation, Viral; D006224:Cricetinae; D004261:DNA Replication / Q000187:drug effects; D003609:Dactinomycin / Q000494:pharmacology; D005814:Genes, Viral; D007668:Kidney; D007700:Kinetics; D010222:Parainfluenza Virus 1, Human / Q000235:genetics*; D012367:RNA, Viral / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects; D014779:Virus Replication
D012367:RNA, Viral; D003609:Dactinomycin