Kaverin N V, Klenk H D
D. I. Ivanovsky Institute of Virology, Russian Academy of Medical Sciences, Moscow.
Mol Gen Mikrobiol Virusol. 1995 Apr-Jun(2):26-33.
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.
在感染甲型流感病毒的CV-1细胞单层中，半汇合培养物中的血细胞吸附细胞数量高于紧密接触抑制的单层培养物。病毒特异性蛋白质合成水平以及病毒子代的积累也与细胞密度呈负相关。在高感染复数时，紧密单层中的大多数细胞在细胞表面不表达血凝素（HA），不合成病毒特异性蛋白质，并且在感染后至少存活96小时。然而，这些细胞出现了细胞蛋白质合成的部分关闭，并且不能被有效地再次感染。对病毒蛋白质合成、子代病毒积累的数据分析以及血细胞吸附的评估表明，紧密单层中的CV-1细胞可以在足够高的感染复数下被感染，但只有一小部分被感染的细胞能够扩增病毒蛋白质合成和子代病毒积累。在犬肾传代细胞（MDCK细胞）中未观察到类似程度的细胞密度效应。
