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      Viperin inhibits hepatitis C virus replication by interfering with binding of NS5A to host protein hVAP-33.

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          Abstract

          Viperin is a type-I and -II interferon-inducible intracytoplasmic protein that mediates antiviral activity against several viruses. A previous study has reported that viperin could limit hepatitis C virus (HCV) replication in vitro. However, the underlying mechanism remains elusive. In the present study, we found that overexpression of viperin could inhibit HCV replication in a dose-dependent manner in both the replicon and HCVcc systems. Furthermore, through co-immunoprecipitation and laser confocal microscopic analysis, viperin was found to interact with the host protein hVAP-33. Mutagenesis analysis demonstrated that the anti-HCV activity of viperin was located to its C terminus, which was required for the interaction with the C-terminal domain of hVAP-33. Competitive co-immunoprecipitation analysis showed that viperin could interact competitively with hVAP-33, and could therefore interfere with its interactions with HCV NS5A. In summary, these findings suggest a novel mechanism by which viperin inhibits HCV replication, possibly through binding to host protein hVAP-33 and interfering with its interaction with NS5A.

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          Author and article information

          Journal
          J Gen Virol
          The Journal of general virology
          Microbiology Society
          1465-2099
          0022-1317
          Jan 2012
          : 93
          : Pt 1
          Affiliations
          [1 ] Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, PR China.
          [2 ] Key Laboratory of Medical Molecular Virology, Shanghai Medical College, Fudan University, Shanghai 200032, PR China.
          Article
          10.1099/vir.0.033860-0
          21957124
          682297b4-4ea3-4bb7-8e08-bdd96e3306d0

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