The effect of cell density on influenza virus replication in CV-1 cells.
The number of hemadsorbing cells in CV-1 cell monolayers infected with influenza A virus was higher in semi-confluent cultures than in dense contact-inhibited monolayers. The level of virus-specific protein synthesis as well as the accumulation of virus progeny were also inversely correlated with cell density. At a high multiplicity of infection the majority of these cells in dense monolayers did not express HA on the cell surface, did not synthesize virus-specific proteins and survived at least 96 hours after infection. However, these cells developed a partial shut-off of cell protein synthesis and could not be efficiently superinfected. Analysis of the data of virus protein synthesis, progeny virus accumulation, and the assessment of hemadsorption suggest that CV-1 cells in dense monolayers can be infected at a sufficiently high multiplicity of infection, but only a fraction of the infected cells is capable of amplification of virus protein synthesis and progeny virus accumulation. No cell-density effects of comparable extent could be observed in MDCK cells.
D000818:Animals; D002452:Cell Count; D002460:Cell Line; D002642:Chick Embryo; D004285:Dogs; D006168:Guinea Pigs; D009980:Influenza A virus / Q000502:physiology*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
D014764:Viral Proteins