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猿猴病毒40复制和病毒体成熟的结构要求。

Structural requirements for simian virus 40 replication and virion maturation.

作者信息

Schirmbeck R, von der Weth A, Deppert W

机构信息

Abteilung Tumorvirologie, Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Hamburg, Germany.

出版信息

J Virol. 1993 Feb;67(2):894-901. doi: 10.1128/JVI.67.2.894-901.1993.

DOI:10.1128/JVI.67.2.894-901.1993
PMID:8380471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC237443/
Abstract

The nuclear matrix plays an important role in simian virus 40 (SV40) DNA replication in vivo, since functional replication complexes containing large T and replicating SV40 minichromosomes are anchored to this structure (R. Schirmbeck and W. Deppert, J. Virol. 65:2578-2588, 1991). In the present study, we have analyzed the course of events leading from nuclear matrix-associated replicating SV40 minichromosomes to fully replicated minichromosomes and, further, to their encapsidation into mature SV40 virions. Pulse-chase experiments revealed that newly replicated SV40 minichromosomes accumulated at the nuclear matrix and were directly encapsidated into DNase-resistant SV40 virions at this nuclear structure. Alternatively, a small fraction of newly replicated minichromosomes left the nuclear matrix to associate with the cellular chromatin. During the course of infection, progeny virions continuously were released from the nuclear matrix to the cellular chromatin and into the cytoplasm-nucleoplasm. The bulk of SV40 progeny virions, however, remained at the nuclear matrix until virus-induced cell lysis.

摘要

核基质在体内猿猴病毒40(SV40)DNA复制中起重要作用,因为含有大T抗原和正在复制的SV40微型染色体的功能性复制复合物锚定在该结构上(R. Schirmbeck和W. Deppert,《病毒学杂志》65:2578 - 2588,1991)。在本研究中,我们分析了从与核基质相关的正在复制的SV40微型染色体到完全复制的微型染色体,进而到它们被包装进成熟SV40病毒粒子的一系列事件过程。脉冲追踪实验表明,新复制的SV40微型染色体在核基质处积累,并在此核结构处直接被包装进抗DNA酶的SV40病毒粒子中。另外,一小部分新复制的微型染色体离开核基质与细胞染色质结合。在感染过程中,子代病毒粒子不断地从核基质释放到细胞染色质以及细胞质 - 核质中。然而,大部分SV40子代病毒粒子留在核基质处,直到病毒诱导的细胞裂解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/ed1d09b90d5e/jvirol00023-0285-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/fc8b50bfe5eb/jvirol00023-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/95597a7334aa/jvirol00023-0283-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/20940fdd2aab/jvirol00023-0283-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/45227965f60a/jvirol00023-0284-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/ed1d09b90d5e/jvirol00023-0285-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/fc8b50bfe5eb/jvirol00023-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/95597a7334aa/jvirol00023-0283-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/20940fdd2aab/jvirol00023-0283-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/45227965f60a/jvirol00023-0284-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea8/237443/ed1d09b90d5e/jvirol00023-0285-a.jpg

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本文引用的文献

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Wild-type p53 is not a negative regulator of simian virus 40 DNA replication in infected monkey cells.野生型p53不是感染猴细胞中猿猴病毒40 DNA复制的负调控因子。
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