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在细胞DNA合成和宿主多肽合成关闭方面存在缺陷的温度敏感型单纯疱疹病毒1型突变体。

Temperature-sensitive herpes simplex virus type 1 mutants defective in the shutoff of cellular DNA synthesis and host polypeptide synthesis.

作者信息

Daksis J I, Cocking J M, Skinner M A, Chan V L

出版信息

Virus Res. 1987 Jan;6(4):297-315. doi: 10.1016/0168-1702(87)90063-3.

Abstract

Two temperature-sensitive herpes simplex virus type 1 mutants, ts 1-8 and ts 199, belonging to different complementation groups, were isolated. Both mutants were defective in the shutoff of host DNA synthesis at 39.5 degrees C (nonpermissive temperature). ts 1-8 exhibited intermediate levels of viral DNA synthesis at 39.5 degrees C, while ts 199 was completely deficient in viral DNA synthesis at 39.5 degrees C. Comparative polyacrylamide gel electrophoresis of the ts 1-8, ts 199 and wild-type viral-coded polypeptides and cellular proteins produced in vivo at 34 degrees C and 39.5 degrees C during various periods post infection was performed. The results indicated that ts 1-8 and ts 199 were temperature-sensitive for the secondary suppression of host polypeptide synthesis. Production of the beta (early) and gamma (late) viral polypeptides was slightly delayed in the mutant-infected cells at early times post infection at both 34 degrees C and 39.5 degrees C. This delayed protein production was not evident at later times post-infection. The ts 1-8 and ts 199 mutants were distinct from the HSV-1 viron-associated host shutoff (vhs) mutants of Read and Frenkel (J. Virol. 46 (1983) 498).

摘要

分离出了两种属于不同互补组的温度敏感型单纯疱疹病毒1型突变体,即ts 1-8和ts 199。在39.5℃(非允许温度)时,这两种突变体在宿主DNA合成的关闭方面均存在缺陷。ts 1-8在39.5℃时病毒DNA合成呈现中等水平,而ts 199在39.5℃时完全缺乏病毒DNA合成。对ts 1-8、ts 199和野生型病毒编码的多肽以及感染后不同时期在34℃和39.5℃体内产生的细胞蛋白进行了聚丙烯酰胺凝胶电泳比较。结果表明,ts 1-8和ts 199在宿主多肽合成的二次抑制方面对温度敏感。在34℃和39.5℃感染后早期,突变体感染的细胞中β(早期)和γ(晚期)病毒多肽的产生略有延迟。这种蛋白质产生延迟在感染后期并不明显。ts 1-8和ts 199突变体与Read和Frenkel的单纯疱疹病毒1型病毒体相关宿主关闭(vhs)突变体不同(《病毒学杂志》46(1983)498)。

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