| 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 | A functional genomic screen identifies cellular cofactors of hepatitis C virus replication |
| Author's Name | Tai AW, Benita Y, Peng LF, Kim SS, Sakamoto N, Xavier RJ, Chung RT |
| Journal Name | Cell Host Microbe |
| Pubmed ID | 19286138 |
| Abstract | Hepatitis C virus (HCV) chronically infects 3% of the worlds population, and complications from HCV are the leading indication for liver transplantation. Given the need for better anti-HCV therapies, one strategy is to identify and target cellular cofactors of the virus lifecycle. Using a genome-wide siRNA library, we identified 96 human genes that support HCV replication, with a significant number of them being involved in vesicle organization and biogenesis. Phosphatidylinositol 4-kinase PI4KA and multiple subunits of the COPI vesicle coat complex were among the genes identified. Consistent with this, pharmacologic inhibitors of COPI and PI4KA blocked HCV replication. Targeting hepcidin, a peptide critical for iron homeostasis, also affected HCV replication, which may explain the known dysregulation of iron homeostasis in HCV infection. The host cofactors for HCV replication identified in this study should serve as a useful resource in delineating new targets for anti-HCV therapies. |
| Used Model | Huh-7 cells |
| DOI | 10.1016/j.chom.2009.02.001 |
