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微小管在多瘤病毒感染中的作用。

Microtubules in Polyomavirus Infection.

机构信息

Department of Genetics and Microbiology, Faculty of Science, Charles University, BIOCEV, 25250 Postal code Vestec, Czech Republic.

出版信息

Viruses. 2020 Jan 18;12(1):121. doi: 10.3390/v12010121.

DOI:10.3390/v12010121
PMID:31963741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7019765/
Abstract

Microtubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules' network during polyomavirus infection. Polyomaviruses usurp microtubules and their motors to travel via early and late acidic endosomes to the endoplasmic reticulum. As shown for SV40, kinesin-1 and microtubules are engaged in the release of partially disassembled virus from the endoplasmic reticulum to the cytosol, and dynein apparently assists in the further disassembly of virions prior to their translocation to the cell nucleus-the place of their replication. Polyomavirus gene products affect the regulation of microtubule dynamics. Early T antigens destabilize microtubules and cause aberrant mitosis. The role of these activities in tumorigenesis has been documented However, its importance for productive infection remains elusive. On the other hand, in the late phase of infection, the major capsid protein, VP1, of the mouse polyomavirus, counteracts T-antigen-induced destabilization. It physically binds microtubules and stabilizes them. The interaction results in the G2/M block of the cell cycle and prolonged S phase, which is apparently required for successful completion of the viral replication cycle.

摘要

微管是细胞骨架的一部分,对于细胞内运动、细胞分裂以及维持细胞形状和极性至关重要。此外,微管在病毒感染中也起着重要作用。在这篇综述中,我们总结了微管网络在多瘤病毒感染过程中的作用。多瘤病毒劫持微管及其马达,通过早期和晚期酸性内体运输至内质网。正如 SV40 所显示的,驱动蛋白-1 和微管参与了部分组装的病毒从内质网释放到细胞质的过程,而动力蛋白显然有助于在病毒颗粒转运到细胞核(病毒复制的场所)之前进一步解体。多瘤病毒基因产物影响微管动力学的调节。早期 T 抗原使微管不稳定,并导致异常有丝分裂。这些活动在肿瘤发生中的作用已被记录在案,但它们对有效感染的重要性仍不清楚。另一方面,在感染的晚期,小鼠多瘤病毒的主要衣壳蛋白 VP1 可拮抗 T 抗原诱导的微管不稳定。它与微管结合并稳定微管。这种相互作用导致细胞周期的 G2/M 阻断和 S 期延长,这显然是成功完成病毒复制周期所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/1b0741911bfe/viruses-12-00121-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/fd6655230301/viruses-12-00121-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/2e14ccec23b0/viruses-12-00121-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/1b0741911bfe/viruses-12-00121-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/fd6655230301/viruses-12-00121-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/2e14ccec23b0/viruses-12-00121-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f7d/7019765/1b0741911bfe/viruses-12-00121-g003.jpg

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