期刊
HEPATOLOGY
卷 63, 期 1, 页码 35-48出版社
WILEY
DOI: 10.1002/hep.28013
关键词
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资金
- Inserm
- University of Strasbourg
- European Union (EU-INTERREG-IV-Rhin Superieur-FEDER Hepato-Regio-Net) [ERC-2008-AdG-233130-HEPCENT, FP7 305600 HepaMab, EU Infect-Era hepBccc]
- ANRS [2012/318, 2013/108]
- French Cancer Agency [ARC IHU201301187]
- Canadian Institutes of Health Research [201411MFE-338606-245517]
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 and hepatitis delta virus use the sodium/taurocholate cotransporting polypeptide (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 hepatitis delta virus entry and infection. Using a targeted RNA interference entry screen, we identified glypican 5 as a common host cell entry factor for hepatitis B and delta viruses. Conclusion: These findings advance our understanding of virus cell entry and open new avenues for curative therapies. As glypicans have been shown to play a role in the control of cell division and growth regulation, virus-glypican 5 interactions may also play a role in the pathogenesis of virus-induced liver disease and cancer. (Hepatology 2016;63:35-48)
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