CD36 is a co-receptor for hepatitis C virus E1 protein attachment

  • Sci Rep. 2016 Feb 22;6:21808. doi: 10.1038/srep21808.
Jun-Jun Cheng  1  2 ,  Jian-Rui Li  1 ,  Meng-Hao Huang  1 ,  Lin-Lin Ma  1 ,  Zhou-Yi Wu  1 ,  Chen-Chen Jiang  1 ,  Wen-Jing Li  1 ,  Yu-Huan Li  1 ,  Yan-Xing Han  2 ,  Hu Li  1 ,  Jin-Hua Chen  1 ,  Yan-Xiang Wang  1 ,  Dan-Qing Song  1 ,  Zong-Gen Peng  1 ,  Jian-Dong Jiang  1  2
Affiliations
  • 1. Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, 100050, China.
  • 2. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, 100050, China.
PMID: 26898231 DOI: 10.1038/srep21808
Abstract

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.

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