| Virus Name | Hepatitis C virus |
| Virus Short Name | HCV |
| Order | Unassigned |
| Virus Family | Flaviviridae |
| Virus Subfamily | N.A. |
| Genus | Hepacivirus |
| Species | Hepatitis C virus |
| Host | Human |
| Cell Tropism | Hepatocytes |
| Associated Disease | Hepatitis, hepatocellular carcinoma |
| Mode of Transmission | Sexual contact, blood |
| VIPR DB link | http://www.viprbrc.org/brc/home.spg?decorator=flavi |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_online_report/positive-sense-rna-viruses/w/flaviviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Flaviviridae |
| Paper Title | EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy |
| Author's Name | Joachim Lupberger, Mirjam B Zeisel, Fei Xiao, Christine Thumann, Isabel Fofana, Laetitia Zona, Christopher Davis, Christopher J Mee, Marine Turek, Sebastian Gorke, Cathy Royer, Benoit Fischer, Muhammad N Zahid, Dimitri Lavillette, Judith Fresquet, François-Lolc Cosset, S Michael Rothenberg, Thomas Pietschmann, Arvind H Patel, Patrick Pessaux, Michel Doffoël, Wolfgang Raffelsberger, Olivier Poch, Jane A McKeating, Laurent Brino & Thomas F Baumert |
| Journal Name | Nature Medicine |
| Pubmed ID | 21516087 |
| Abstract | Hepatitis C virus (HCV) is a major cause of liver disease, but therapeutic options are limited and there are no prevention strategies. Viral entry is the first step of infection and requires the cooperative interaction of several host cell factors. Using a functional RNAi kinase screen, we identified epidermal growth factor receptor and ephrin receptor A2 as host cofactors for HCV entry. Blocking receptor kinase activity by approved inhibitors broadly impaired infection by all major HCV genotypes and viral escape variants in cell culture and in a human liver chimeric mouse model in vivo. The identified receptor tyrosine kinases (RTKs) mediate HCV entry by regulating CD81-claudin-1 co-receptor associations and viral glycoprotein-dependent membrane fusion. These results identify RTKs as previously unknown HCV entry cofactors and show that tyrosine kinase inhibitors have substantial antiviral activity. Inhibition of RTK function may constitute a new approach for prevention and treatment of HCV infection. |
| Used Model | Huh7.5.1 cells |
| DOI | 10.1038/nm.2341 |
