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Originally published In Press as doi:10.1074/jbc.M209628200 on February 19, 2003

J. Biol. Chem., Vol. 278, Issue 18, 16151-16158, May 2, 2003
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ISG20, a New Interferon-induced RNase Specific for Single-stranded RNA, Defines an Alternative Antiviral Pathway against RNA Genomic Viruses*

Lucile EspertDagger , Genevieve DegolsDagger , Celine GongoraDagger , Danielle Blondel§, Bryan R. Williams, Robert H. Silverman, and Nadir MechtiDagger ||

From the Dagger  UMR CNRS 5094, EFS, 240 avenue Emile Jeanbrau, 34094 Montpellier Cedex 5, France, § Laboratoire de Virologie Moléculaire et Structurale, UMR CNRS 2472, 91198 Gif-sur-Yvette, France, and  Department of Cancer Biology, The Lerner Institute, Cleveland, Ohio 44195

Interferons (IFNs) encode a family of secreted proteins that provide the front-line defense against viral infections. Their diverse biological actions are thought to be mediated by the products of specific but usually overlapping sets of cellular genes induced in the target cells. We have recently isolated a new human IFN-induced gene that we have termed ISG20, which codes for a 3' to 5' exonuclease with specificity for single-stranded RNA and, to a lesser extent, for DNA. In this report, we demonstrate that ISG20 is involved in the antiviral functions of IFN. In the absence of IFN treatment, ISG20-overexpressing HeLa cells showed resistance to infections by vesicular stomatitis virus (VSV), influenza virus, and encephalomyocarditis virus (three RNA genomic viruses) but not to the DNA genomic adenovirus. ISG20 specifically interfered with VSV mRNA synthesis and protein production while leaving the expression of cellular control genes unaffected. No antiviral effect was observed in cells overexpressing a mutated ISG20 protein defective in exonuclease activity, demonstrating that the antiviral effects were due to the exonuclease activity of ISG20. In addition, the inactive mutant ISG20 protein, which is able to inhibit ISG20 exonuclease activity in vitro, significantly reduced the ability of IFN to block VSV development. Taken together, these data suggested that the antiviral activity of IFN against VSV is partly mediated by ISG20. We thus show that, besides RNase L, ISG20 has an antiviral activity, supporting the idea that it might represent a novel antiviral pathway in the mechanism of IFN action.

* This work was supported by grants from the Association pour la Recherche contre le Cancer, the Institut National de la Santé et de la Recherche Médicale, the Centre National de la Recherche Scientifique, the Ligue Contre le Cancer Comités de l'Herault et du Gard, and the Fondation pour la Recherche Médicale.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed. Tel.: 33-4-67-52-03-79; Fax: 33-4-67-52-18-29; E-mail: nadir.mechti@ibph.pharma.univ-montp1.fr.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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