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Viruses 2015, 7(7), 3675-3702; doi:10.3390/v7072794

Resistance to Rhabdoviridae Infection and Subversion of Antiviral Responses

1
Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS UMR 9198, Université Paris-Sud, Gif-sur-Yvette 91190, France
2
INSERM UMR-S 1124, Université Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris (FR 3567, CNRS), 75270 Paris Cedex 6, France
*
Author to whom correspondence should be addressed.
Academic Editor: Andrew Mehle
Received: 23 April 2015 / Revised: 29 June 2015 / Accepted: 1 July 2015 / Published: 7 July 2015
(This article belongs to the Special Issue Gene Technology and Resistance to Viruses - Reviews)
View Full-Text   |   Download PDF [771 KB, uploaded 7 July 2015]   |  

Abstract

Interferon (IFN) treatment induces the expression of hundreds of IFN-stimulated genes (ISGs). However, only a selection of their products have been demonstrated to be responsible for the inhibition of rhabdovirus replication in cultured cells; and only a few have been shown to play a role in mediating the antiviral response in vivo using gene knockout mouse models. IFNs inhibit rhabdovirus replication at different stages via the induction of a variety of ISGs. This review will discuss how individual ISG products confer resistance to rhabdoviruses by blocking viral entry, degrading single stranded viral RNA, inhibiting viral translation or preventing release of virions from the cell. Furthermore, this review will highlight how these viruses counteract the host IFN system. View Full-Text
Keywords: interferon; rhabdoviruses; ISG; rabies virus; vesicular stomatitis virus interferon; rhabdoviruses; ISG; rabies virus; vesicular stomatitis virus
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Blondel, D.; Maarifi, G.; Nisole, S.; Chelbi-Alix, M.K. Resistance to Rhabdoviridae Infection and Subversion of Antiviral Responses. Viruses 2015, 7, 3675-3702.

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