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副流感病毒进入细胞作为阻断儿童呼吸道疾病的靶点。

Entry of parainfluenza virus into cells as a target for interrupting childhood respiratory disease.

作者信息

Moscona Anne

机构信息

Department of Pediatrics, Weill Medical College of Cornell University, New York, NY 10021, USA.

出版信息

J Clin Invest. 2005 Jul;115(7):1688-98. doi: 10.1172/JCI25669.

DOI:10.1172/JCI25669
PMID:16007245
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1159152/
Abstract

Human parainfluenza viruses cause several serious respiratory diseases in children for which there is no effective prevention or therapy. Parainfluenza viruses initiate infection by binding to cell surface receptors and then, via coordinated action of the 2 viral surface glycoproteins, fuse directly with the cell membrane to release the viral replication machinery into the host cell's cytoplasm. During this process, the receptor-binding molecule must trigger the viral fusion protein to mediate fusion and entry of the virus into a cell. This review explores the binding and entry into cells of parainfluenza virus type 3, focusing on how the receptor-binding molecule triggers the fusion process. There are several steps during the process of binding, triggering, and fusion that are now understood at the molecular level, and each of these steps represents potential targets for interrupting infection.

摘要

人副流感病毒会引发儿童的多种严重呼吸道疾病,目前尚无有效的预防或治疗方法。副流感病毒通过与细胞表面受体结合来启动感染,然后,通过两种病毒表面糖蛋白的协同作用,直接与细胞膜融合,将病毒复制机制释放到宿主细胞的细胞质中。在此过程中,受体结合分子必须触发病毒融合蛋白来介导病毒融合并进入细胞。本综述探讨了3型副流感病毒与细胞的结合及进入过程,重点关注受体结合分子如何触发融合过程。在结合、触发和融合过程中有几个步骤目前已在分子水平上得到了解,这些步骤中的每一个都代表了阻断感染的潜在靶点。

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