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Resistance to Rhabdoviridae Infection and Subversion of Antiviral Responses

Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS UMR 9198, Université Paris-Sud, Gif-sur-Yvette 91190, France
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
Viruses 2015, 7(7), 3675-3702;
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)
PDF [771 KB, uploaded 7 July 2015]


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

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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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