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Wiley Open Access, Molecular Systems Biology, 1(4), p. 230, 2008

DOI: 10.1038/msb.2008.66

Elsevier, International Journal of Infectious Diseases, (12), p. e175, 2008

DOI: 10.1016/j.ijid.2008.05.437

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Hepatitis C virus infection protein network

Journal article published in 2008 by B. de Chassey, V. Navratil, L. Tafforeau, M. S. Hiet, A. Aublin‐Gex, S. Agaugué, G. Meiffren, F. Pradezynski, B. F. Faria, T. Chantier, M. Le Breton, J. Pellet, N. Davoust, P. E. Mangeot ORCID, A. Chaboud and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Replication of Hepatitis C virus (HCV) relies on multiple interactions with host factors but how these interactions determine infection, sensitivity to treatment and patho- genesis remain largely undefined. In a first attempt to provide a comprehensive view of a cellular infection by HCV, we present here a proteome-wide mapping of interactions between HCV and human cellular proteins. This interaction map was first generated by stringent high-throughput yeast two-hybrid (Y2H) screening, using both full-length HCV pro- teins and domains as baits. This map was then completed by an extensive mining of the literature. A total of 314 pairwise interactions between HCV and human proteins was identified by Y2H, and 170 by literature mining. The entire dataset was integrated into a reconstructed human interac- tome composed of 9,520 proteins and 44,223 interactions. The topological analysis of this network indicated that cel- lular proteins interacting with HCV are enriched in highly central and interconnected proteins, suggesting that HCV preferentially targets proteins with essential functions. A global analysis of these proteins based on functional anno- tation showed a highly significant enrichment for cellular pathways related to pathogenesis. A network comprising proteins associated to frequent clinical disorders of chron- ically infected patients was constructed by connecting the insulin, Jak/STAT and TGF-beta pathways with cellular pro- teins targeted by HCV. CORE protein appeared as a major perturbator of this network. The focal adhesion was also identified as a new function affected by the virus, mainly by NS3 and NS5A proteins. ; info:eu-repo/semantics/published