Entry of parainfluenza virus into cells as a target for interrupting childhood respiratory disease
Entry of parainfluenza virus into cells as a target for interrupting childhood respiratory disease
复制标题
DOI：
10.1172/jci25669
复制
发表时间：
2005-07-01
影响因子：
15.9
通讯作者：
Moscona, A
中科院分区：
文献类型：
--
作者：
Moscona, A
人类副流感病毒导致严重的儿童呼吸道疾病，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，然后通过病毒表面糖蛋白的协调作用，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。在这个过程中，受体结合分子必须触发病毒融合蛋白，以介导病毒的融合和进入细胞。这篇综述探讨了副流感病毒3型的结合和进入细胞，重点是受体结合分子如何触发融合过程。在结合、触发和融合的过程中，有几个步骤现在在分子水平上被理解，每个步骤都代表了阻断感染的潜在靶点。
Human parainfluenza viruses cause severa; serious respiratory diseases in children for which there is no effective preventation or therapy. Parainfluenza viruses initiate infection by binding to cell surface receptors and then, via coordinated action of the 2viral 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.