Fiche publication
Date publication
juillet 2015
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas
,
Dr HABERSETZER François
,
Dr VERRIER Eloi
Tous les auteurs :
Verrier ER, Colpitts CC, Bach C, Heydmann L, Weiss A, Renaud M, Durand SC, Habersetzer F, Durantel D, Abou-Jaoude G, Lopez Ledesma MM, Felmlee DJ, Soumillon M, Croonenborghs T, Pochet N, Nassal M, Schuster C, Brino L, Sureau C, Zeisel MB, Baumert TF
Lien Pubmed
Résumé
Chronic hepatitis B and D infections are major causes of liver disease and hepatocellular carcinoma worldwide. Efficient therapeutic approaches for cure are absent. Sharing the same envelope proteins, hepatitis B virus (HBV) and hepatitis D virus (HDV) use the sodium taurocholate co-transporting polypeptide (NTCP, a bile acid transporter) as a receptor to enter hepatocytes. However, the detailed mechanisms of the viral entry process are still poorly understood. Here, we established a high-throughput infectious cell culture model enabling functional genomics of HDV entry and infection. Using a targeted RNAi entry screen we identified glypican 5 (GPC5) as a common host cell entry factor for HBV and HDV. CONCLUSION: These findings advance our understanding of virus cell entry and open new avenues for curative therapies. Since glypicans have been shown to play a role in the control of cell division and growth regulation, virus-GPC5 interactions may also play a role in the pathogenesis of virus-induced liver disease and cancer. This article is protected by copyright. All rights reserved.
Référence
Hepatology. 2015 Jul 29
