Hugentobler A L, Bienz K
Arch Virol. 1980;64(1):25-33. doi: 10.1007/BF01317388.
Hep-2 cells were synchronized by a double thymidine block and infected with poliovirus type I (Mahoney) in hourly intervals after release from the second thymidine block. The S-phase is not prevented by a poliovirus infection but, with cells infected 0-4 hours after release, an increase of its duration is found. With an infection 5 hours and later after release, the duration of the S-phase is not different from that of an uninfected, synchronized control culture. DNA synthesis itself is slower early in S-phase and gets inhibited up to 75 per cent late in S-phase. All cultures show the first signs of a CPE 3.5 hours p.i. and, in spite of CPE, the cells continue to synthesize DNA. In infected cells a slightly higher peak of mitotic cells compared to control cultures is found. The time point of the mitotic peak is dependant of the time of infection and seems no longer controlled by the cell cycle. The mitotic indices are similar for all cultures infected at different times after release. When the cells are infected early after release CPE appears before mitosis and prevents the cells from entering mitosis. Cells which are infected towards the end of the S-phase finish mitosis normally before they exhibit characteristics of CPE. Extent and kinetics of poliovirus RNA synthesis and yield of virus progeny are not altered by the cell cycle.
通过双胸腺嘧啶核苷阻滞使Hep-2细胞同步化,在解除第二次胸腺嘧啶核苷阻滞之后,每隔一小时用I型脊髓灰质炎病毒(Mahoney株)进行感染。脊髓灰质炎病毒感染不会阻止S期,但对于在解除阻滞0至4小时后感染的细胞,会发现其持续时间增加。在解除阻滞5小时及之后进行感染,S期的持续时间与未感染的同步对照培养物无异。DNA合成在S期早期本身较慢,在S期后期会受到抑制,抑制率高达75%。所有培养物在感染后3.5小时均出现细胞病变效应(CPE)的最初迹象,并且尽管出现了CPE,细胞仍继续合成DNA。与对照培养物相比,在感染细胞中发现有丝分裂细胞的峰值略高。有丝分裂峰值的时间点取决于感染时间,似乎不再受细胞周期控制。对于在解除阻滞之后不同时间感染的所有培养物,有丝分裂指数相似。当细胞在解除阻滞之后早期被感染时,CPE在有丝分裂之前出现,并阻止细胞进入有丝分裂。在S期接近结束时被感染的细胞通常在表现出CPE特征之前完成有丝分裂。脊髓灰质炎病毒RNA合成的程度和动力学以及子代病毒的产量不受细胞周期的影响。