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热对培养的哺乳动物细胞中病毒蛋白产生和出芽的影响。

Effect of heat on viral protein production and budding in cultured mammalian cells.

作者信息

Herman P P, Yatvin M B

机构信息

Department of Radiation Oncology, Oregon Health Sciences University, Portland 97201.

出版信息

Int J Hyperthermia. 1994 Sep-Oct;10(5):627-41. doi: 10.3109/02656739409022443.

Abstract

The life cycle of enveloped viruses is intimately associated with, and influenced by, host cell membrane organization, which is altered by hyperthermia. Hyperthermia-modified Moloney murine leukaemia virus (M-MuLV) release, protein production and intracellular protein processing in a chronically infected cultured murine cell line, C9CL98 (C9). Both 44 degrees C/45 min and 42.8 degrees C/135 min substantially decreased cell-free viral env protein 8-48 h postheating, but virus release and cellular viral protein content increased following 42.8 degrees C/25 min. Proteolytic processing of viral Pr65 gag precursor to p30 gag protein, normally observed within unheated C9 cells, was blocked for at least 8 h after 44 degrees C/45 min. Virus released from heated C9 cells was as infectious to NIH/3T3 cells as was virus from control cells. Cells surviving exposure to 42.8 degrees C/135 min became thermotolerant to decreased virus release from a second heating if delivered 10-48 h after the initial heating. The mechanism by which virus release is blocked after hyperthermia remains to be elucidated.

摘要

包膜病毒的生命周期与宿主细胞膜组织密切相关并受其影响,而宿主细胞膜组织会因热疗而改变。热疗对慢性感染的培养小鼠细胞系C9CL98(C9)中莫洛尼鼠白血病病毒(M-MuLV)的释放、蛋白质产生及细胞内蛋白质加工均有影响。在加热后8 - 48小时,44℃/45分钟和42.8℃/135分钟均显著降低了无细胞病毒env蛋白水平,但在42.8℃/25分钟后病毒释放及细胞内病毒蛋白含量增加。在未加热的C9细胞中通常可观察到的病毒Pr65 gag前体蛋白向p30 gag蛋白的蛋白水解加工过程,在44℃/45分钟处理后至少8小时被阻断。从加热后的C9细胞释放的病毒对NIH/3T3细胞的感染性与对照细胞释放的病毒相同。暴露于42.8℃/135分钟后存活的细胞,如果在初次加热后10 - 48小时进行第二次加热,会对病毒释放减少产生热耐受性。热疗后病毒释放被阻断的机制仍有待阐明。

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