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Simian Virus 40-Host Cell Interaction During Lytic Infection

机译:血糖病毒40-宿主细胞相互作用在裂解感染期间

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Both exponentially growing and serum-arrested subcloned CV-1 cell cultures were infected with simian virus 40 (SV40). By 24 h after infection 96% of the nuclei of these permissive cells contained SV40 T-antigen. Analysis of the average DNA content per cell at various times after infection indicated that by 24 h most of the cells contained amounts of DNA similar to those normally found in G2 cells. Analysis of cell cycle distributions indicated that a G2 DNA complement was maintained by over 90% of the cells in the infected populations 24 to 48 h postinfection. Cells continued to synthesize SV40 DNA during the first 50 h after infection, and cytopathic effect was first observed 60 h after inoculation. After infection the number of mitotic cells that could be recovered by selective detachment decreased precipitously and was drastically reduced by 24 h. A study of the kinetics of decline in the number of mitotic cells suggests that this decline is related to an event during the cell cycle at or near the G1-S-phase border upon which commencement of SV40 DNA replication apparently depends. It was concluded that after SV40 infection, stationary cells are induced to cycle, and cycling cells complete one round of cellular DNA synthesis but do not divide. Although the infected cells continue to synthesize viral DNA, they do not appear able to reinitiate cellular DNA replication units. These results imply that the abundance of T-antigen (produced independently of cell cycle phase) in the presence of the enzymes required for continued DNA synthesis is not sufficient for reinitiation of cellular DNA synthesis.
机译:指数增长和血清被滞留的亚克隆的CV-1细胞培养物感染了Simian病毒40(SV40)。在感染后24小时,含有SV40 T-抗原的这些允许细胞的96%核。感染后各次每次细胞平均DNA含量分析,表明含有24小时的细胞含有与通常在G 2℃的细胞中相似的DNA的量。细胞周期分布的分析表明,G 2 DNA补充剂通过90%的90%在感染群体中的90%的细胞中维持。在感染后,细胞继续在前50小时期间合成SV40 DNA,并且在接种后首先观察到细胞病变效果60小时。感染后,通过选择性脱离可以恢复的有丝分裂细胞的数量急剧下降,并急剧减少24小时。对有丝分裂细胞数量下降的动力学的研究表明,这种下降与在G 1 -s-阶段边界处或附近的细胞周期期间的事件有关,在其上开始SV40 DNA复制显然取决于。得出结论是,在SV40感染后,静止细胞循环,循环细胞完成一轮细胞DNA合成,但不分裂。虽然感染的细胞继续合成病毒DNA,但它们不会出现能够重新调节细胞DNA复制单元。这些结果意味着在持续DNA合成所需的酶存在下的T-抗原(独立于细胞周期阶段产生)的丰度不足以用于改善细胞DNA合成。

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  • 来源
    《Journal of Virology》 |1979年第1期|共8页
  • 作者

    Edward L. Gershey;

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  • 收录信息 美国《科学引文索引》(SCI);
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