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参与乳头瘤病毒进入的宿主细胞因子。

Host-cell factors involved in papillomavirus entry.

机构信息

Department of Medical Microbiology and Hygiene, University Medical Centre of the Johannes Gutenberg University, Obere Zahlbacher Strasse 67, 55131 Mainz, Germany.

出版信息

Med Microbiol Immunol. 2012 Nov;201(4):437-48. doi: 10.1007/s00430-012-0270-1. Epub 2012 Sep 13.

DOI:10.1007/s00430-012-0270-1
PMID:22972234
Abstract

Papillomaviruses infect skin and mucosa where they induce warts and cancers. For entry to occur, they sequentially engage numerous host proteins, allowing them to deliver their genetic information into target cells. This multistep process starts with initial binding via its L1 major capsid protein, followed by structural changes of the capsid on the cell surface, engagement of different receptors, and endocytosis. The post-entry phase includes capsid disassembly, endosomal escape of a complex of the minor capsid protein L2 and the viral genome, its transport into the nucleus, and accumulation at nuclear substructures. This review summarizes the current knowledge of the papillomavirus entry pathway and the role of cellular proteins involved in this course of events.

摘要

乳头瘤病毒感染皮肤和黏膜,在那里引发疣和癌症。为了发生感染,它们依次结合许多宿主蛋白,使它们能够将其遗传信息递送到靶细胞。这个多步骤过程始于通过其 L1 主要衣壳蛋白的初始结合,随后在细胞表面发生衣壳的结构变化,与不同的受体结合,以及内吞作用。进入后阶段包括衣壳解体,小衣壳蛋白 L2 和病毒基因组的复合物从内体中逃逸,其运送到细胞核,并在核亚结构中积累。这篇综述总结了乳头瘤病毒进入途径的最新知识,以及参与这一事件过程的细胞蛋白的作用。

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Entry of human papillomavirus type 16 by actin-dependent, clathrin- and lipid raft-independent endocytosis.
富含四跨膜蛋白的微结构域包含CD151、CD9和TSPAN 8——包括SARS-CoV-2在内的呼吸道病毒进入和退出机制的潜在介质。
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