| First Author | Cheng JJ | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 21808 | PubMed ID | 26898231 |
| Mgi Jnum | J:254076 | Mgi Id | MGI:6101618 |
| Doi | 10.1038/srep21808 | Citation | Cheng JJ, et al. (2016) CD36 is a co-receptor for hepatitis C virus E1 protein attachment. Sci Rep 6:21808 |
| abstractText | The cluster of differentiation 36 (CD36) is a membrane protein related to lipid metabolism. We show that HCV infection in vitro increased CD36 expression in either surface or soluble form. HCV attachment was facilitated through a direct interaction between CD36 and HCV E1 protein, causing enhanced entry and replication. The HCV co-receptor effect of CD36 was independent of that of SR-BI. CD36 monoclonal antibodies neutralized the effect of CD36 and reduced HCV replication. CD36 inhibitor sulfo-N-succinimidyl oleate (SSO), which directly bound CD36 but not SR-BI, significantly interrupted HCV entry, and therefore inhibited HCV replication. SSO''s antiviral effect was seen only in HCV but not in other viruses. SSO in combination with known anti-HCV drugs showed additional inhibition against HCV. SSO was considerably safe in mice. Conclusively, CD36 interacts with HCV E1 and might be a co-receptor specific for HCV entry; thus, CD36 could be a potential drug target against HCV. |
