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脑心肌炎病毒的复制。I. 对宿主细胞大分子合成的影响。

Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell.

作者信息

Plagemann P G, Swim H E

出版信息

J Bacteriol. 1966 Jun;91(6):2317-26. doi: 10.1128/jb.91.6.2317-2326.1966.

Abstract

Plagemann, Peter G. W. (Western Reserve University, Cleveland, Ohio), and H. Earle Swim. Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell. J. Bacteriol. 91:2317-2326. 1966.-The replication of mengovirus was studied in two strains of Novikoff (rat) hepatoma cells propagated in vitro. The replicative cycle in both strains required 6.5 to 7 hr. Infection resulted in a marked depression of ribonucleic acid (RNA) and protein synthesis by strain N1S1-63. Inhibition of RNA synthesis was reflected by a decrease in the deoxyribonucleic acid (DNA)-dependent RNA polymerase activity of isolated nuclei. Mengovirus had no effect on either protein or RNA synthesis or on the DNA-dependent RNA polymerase activity of a second strain, N1S1-67. The time course of viral-induced synthesis of RNA by cells was studied in cells treated with actinomycin D. It was first detectable between 2.5 and 3 hr after infection and continued until 6.5 to 7 hr. The formation of mature virus was estimated biochemically by measuring the amount of RNA synthesized as a result of viral infection which was resistant to degradation by ribonuclease in the presence of deoxycholate. Approximately 70% of the deoxycholate-ribonuclease-resistant RNA was located in mature virus, and the remainder was double-stranded. The formation of mature virus began about 45 min after viral-directed (actinomycin-resistant) synthesis of RNA was detectable in the cell, and only about 18 to 20% of the total RNA synthesized was incorporated into virus. Release of virus from cells began about 1 hr after maturation was first detectable. Release of virus from cells was accompanied by a loss of a large proportion of their cytoplasmic RNA and protein.

摘要

普拉格曼,彼得·G.W.(凯斯西储大学,俄亥俄州克利夫兰),以及H.厄尔·斯威姆。脑心肌炎病毒的复制。I.对宿主细胞大分子合成的影响。《细菌学杂志》91:2317 - 2326。1966年。——在体外培养的两株诺维科夫(大鼠)肝癌细胞中研究了脑心肌炎病毒的复制。两株细胞中的复制周期均需6.5至7小时。感染导致N1S1 - 63株细胞的核糖核酸(RNA)和蛋白质合成显著降低。RNA合成的抑制表现为分离细胞核中依赖脱氧核糖核酸(DNA)的RNA聚合酶活性下降。脑心肌炎病毒对第二株N1S1 - 67细胞的蛋白质或RNA合成以及依赖DNA的RNA聚合酶活性均无影响。在用放线菌素D处理的细胞中研究了病毒诱导细胞合成RNA的时间进程。感染后2.5至3小时首次可检测到,一直持续到6.5至7小时。通过测量在脱氧胆酸盐存在下因病毒感染而合成的、对核糖核酸酶降解具有抗性的RNA量,以生化方法估算成熟病毒的形成。约70%的脱氧胆酸盐 - 核糖核酸酶抗性RNA存在于成熟病毒中,其余为双链。在细胞中可检测到病毒导向(抗放线菌素)的RNA合成后约45分钟开始形成成熟病毒,且合成的总RNA中只有约18%至20%被整合到病毒中。首次可检测到成熟后约1小时开始从细胞中释放病毒。从细胞中释放病毒伴随着大部分细胞质RNA和蛋白质的损失。

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Replication of mengovirus. II. General properties of the viral-induced ribonucleic acid polymerase.
J Bacteriol. 1966 Jun;91(6):2327-32. doi: 10.1128/jb.91.6.2327-2332.1966.

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