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紧密连接蛋白与病毒感染的致病机制。

Claudins and pathogenesis of viral infection.

作者信息

Tawar Rajiv G, Colpitts Che C, Lupberger Joachim, El-Saghire Hussein, Zeisel Mirjam B, Baumert Thomas F

机构信息

Inserm, U1110, Institut des Maladies Virales et Hépatiques, Strasbourg, France; University of Strasbourg, Strasbourg, France.

Inserm, U1110, Institut des Maladies Virales et Hépatiques, Strasbourg, France; University of Strasbourg, Strasbourg, France; Institut Hospitalo-Universitaire, Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.

出版信息

Semin Cell Dev Biol. 2015 Jun;42:39-46. doi: 10.1016/j.semcdb.2015.04.011. Epub 2015 May 7.

Abstract

Since their discovery, tremendous progress has been made in our understanding of the roles of claudins in tight junction physiology. In addition, interactions between claudins and other cellular proteins have highlighted their novel roles in cell physiology. Moreover, the importance of claudins is becoming apparent in the pathophysiology of several diseases, including viral infections. Notable is the discovery of CLDN1 as an essential host factor for hepatitis C virus (HCV) entry, which led to detailed characterization of CLDN1 and its association with tetraspanin CD81 for the initiation of HCV infection. CLDN1 has also been shown to facilitate dengue virus entry. Furthermore, owing to the roles of claudins in forming anatomical barriers, several viruses have been shown to alter claudin expression at the tight junction. This review summarizes the role of claudins in viral infection, with particular emphasis on HCV.

摘要

自被发现以来,我们对紧密连接蛋白在紧密连接生理学中的作用的理解取得了巨大进展。此外,紧密连接蛋白与其他细胞蛋白之间的相互作用凸显了它们在细胞生理学中的新作用。此外,紧密连接蛋白在包括病毒感染在内的几种疾病的病理生理学中的重要性正变得日益明显。值得注意的是,发现紧密连接蛋白1(CLDN1)是丙型肝炎病毒(HCV)进入的必需宿主因子,这导致了对CLDN1及其与四跨膜蛋白CD81的关联进行详细表征,以启动HCV感染。CLDN1也已被证明促进登革病毒进入。此外,由于紧密连接蛋白在形成解剖屏障中的作用,已显示几种病毒会改变紧密连接处紧密连接蛋白的表达。本综述总结了紧密连接蛋白在病毒感染中的作用,尤其着重于HCV。

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