Format

Send to

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

Claudins and pathogenesis of viral infection.

Author information

1
Inserm, U1110, Institut des Maladies Virales et Hépatiques, Strasbourg, France; University of Strasbourg, Strasbourg, France.
2
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. Electronic address: Thomas.Baumert@unistra.fr.

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.

KEYWORDS:

Claudins; Co-receptor complex; Immunotherapy; Tight junctions; Viruses

PMID:
25960372
DOI:
10.1016/j.semcdb.2015.04.011
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center