Hepatitis C virus infection protein network

Benoı̂t de Chassey(Université Claude Bernard Lyon 1), Vincent Navratil(Université Claude Bernard Lyon 1), Lionel Tafforeau(Université Claude Bernard Lyon 1), Marie–Sophie Hiet(Université Claude Bernard Lyon 1), Anne Aublin‐Gex(Université Claude Bernard Lyon 1), Sophie Agaugué(Université Claude Bernard Lyon 1), Grégory Meiffren(Université Claude Bernard Lyon 1), Fabrine Pradezynski(Université Claude Bernard Lyon 1), B F Faria(Université Claude Bernard Lyon 1), T Chantier(Université Claude Bernard Lyon 1), Marc Breton(Université Claude Bernard Lyon 1), Johann Pellet(Université Claude Bernard Lyon 1), Nathalie Davoust(Université Claude Bernard Lyon 1), Philippe Mangeot(Université Claude Bernard Lyon 1), Annie Chaboud(Université Claude Bernard Lyon 1), François Pénin(Université Claude Bernard Lyon 1), Yves Jacob(Institut Pasteur), Pierre‐Olivier Vidalain(Centre National de la Recherche Scientifique), Marc Vidal(Harvard University), Patrice André(Université Claude Bernard Lyon 1), Chantal Rabourdin‐Combe(Université Claude Bernard Lyon 1), Vincent Lotteau(Université Claude Bernard Lyon 1)
Molecular Systems Biology
November 4, 2008
Cited by 384Open Access
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Abstract

A proteome-wide mapping of interactions between hepatitis C virus (HCV) and human proteins was performed to provide a comprehensive view of the cellular infection. A total of 314 protein-protein interactions between HCV and human proteins was identified by yeast two-hybrid and 170 by literature mining. Integration of this data set into a reconstructed human interactome showed that cellular proteins interacting with HCV are enriched in highly central and interconnected proteins. A global analysis on the basis of functional annotation highlighted the enrichment of cellular pathways targeted by HCV. A network of proteins associated with frequent clinical disorders of chronically infected patients was constructed by connecting the insulin, Jak/STAT and TGFbeta pathways with cellular proteins targeted by HCV. CORE protein appeared as a major perturbator of this network. Focal adhesion was identified as a new function affected by HCV, mainly by NS3 and NS5A proteins.


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