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其他副流感病毒对仙台病毒缺陷干扰基因组的拯救:对基因组复制的影响

Rescue of a Sendai virus DI genome by other parainfluenza viruses: implications for genome replication.

作者信息

Curran J A, Kolakofsky D

机构信息

Department of Microbiology, University of Geneva School of Medicine, Switzerland.

出版信息

Virology. 1991 May;182(1):168-76. doi: 10.1016/0042-6822(91)90660-4.

Abstract

Using a defective interfering Sendai virus stock (DIH4) freed of nondefective helper virus, we found that the closely related parainfluenza viruses 1 and 3 could substitute for the Sendai virus helper in replicating DIH4, creating chimeric nucleocapsids. The morbillivirus measles and the rhabdovirus VSV could not substitute. When DIH4 is incubated intracellularly for 5 days in the absence of help, the ability of PIV3 to rescue DIH4 at this time depended on fresh Sendai virus polymerase. The PIV3 polymerase apparently can only copy the chimeric template, but not that wrapped in the homologous Sendai NP protein. These results suggest that the cis-acting RNA sequences important for genome replication, e.g., the promoter and the encapsidation site, have been conserved among these viruses, but that the interactions between the polymerase and the template protein NP are unique for each virus.

摘要

使用不含非缺陷型辅助病毒的缺陷干扰仙台病毒毒株(DIH4),我们发现密切相关的副流感病毒1型和3型可以替代仙台病毒辅助病毒来复制DIH4,从而产生嵌合核衣壳。麻疹病毒和弹状病毒VSV则无法替代。当在没有辅助病毒的情况下将DIH4在细胞内孵育5天时,此时PIV3拯救DIH4的能力取决于新鲜的仙台病毒聚合酶。PIV3聚合酶显然只能复制嵌合模板,而不能复制包裹在同源仙台NP蛋白中的模板。这些结果表明,对于基因组复制重要的顺式作用RNA序列,例如启动子和包装位点,在这些病毒中是保守的,但聚合酶与模板蛋白NP之间的相互作用对于每种病毒来说是独特的。

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