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高温对诺维科夫大鼠肝癌细胞中门戈病毒核糖核酸合成及病毒产生的影响。

Effects of elevated temperatures on mengovirus ribonucleic acid synthesis and virus production in Novikoff rat hepatoma cells.

作者信息

Shea M A, Plagemann P G

出版信息

J Virol. 1971 Jan;7(1):144-54. doi: 10.1128/JVI.7.1.144-154.1971.

Abstract

The production of mengovirus in Novikoff rat hepatoma cells is progressively reduced with an increase in incubation temperature of the cells from 34 to 40 C, in spite of the fact that about the same amounts of single-stranded and double-stranded viral ribonucleic acid (RNA) are synthesized at 34, 37, and 40 C; the rate of overall protein synthesis is as high at 40 C as at 37 C. At 40 C, progeny viral RNA accumulates in an undegraded form without being incorporated into virus particles. The results suggest that virus maturation is preferentially inhibited at supraoptimal temperatures. At 42 C, on the other hand, no viral RNA is produced and no viral RNA polymerase activity is detectable in cell lysates. Failure of infected cells to form viral RNA polymerase at 42 C is probably due to an impairment of protein synthesis since most of the polyribosomes are rapidly lost during incubation at 42 C and the rate of amino acid incorporation into protein is 70% lower at 42 C than at 37 C. When infected cells are shifted from 37 to 42 C during the period of active viral RNA synthesis, viral RNA polymerase activity is rapidly lost from the cells, and viral RNA synthesis ceases within 45 min. In contrast, the RNA polymerase is as active in vitro at 42 C as at 37 C, and the activity is relatively stable at 42 C.

摘要

诺维科夫大鼠肝癌细胞中脑心肌炎病毒的产量会随着细胞培养温度从34℃升高到40℃而逐渐降低,尽管在34℃、37℃和40℃时合成的单链和双链病毒核糖核酸(RNA)量大致相同;40℃时总的蛋白质合成速率与37℃时一样高。在40℃时,子代病毒RNA以未降解的形式积累,而未被整合到病毒颗粒中。结果表明,在超适宜温度下病毒成熟受到优先抑制。另一方面,在42℃时,不产生病毒RNA,并且在细胞裂解物中检测不到病毒RNA聚合酶活性。感染细胞在42℃时无法形成病毒RNA聚合酶,这可能是由于蛋白质合成受损,因为在42℃培养期间大多数多核糖体迅速丢失,并且42℃时氨基酸掺入蛋白质的速率比37℃时低70%。当感染细胞在活跃的病毒RNA合成期间从37℃转移到42℃时,病毒RNA聚合酶活性会迅速从细胞中丧失,并且病毒RNA合成在45分钟内停止。相比之下,RNA聚合酶在42℃体外的活性与37℃时一样,并且在42℃时活性相对稳定。

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