| Literature DB >> 23237992 |
Run-Xuan Shao1, Leiliang Zhang, Zhi Hong, Kaku Goto, Du Cheng, Wen-Chi Chen, Nikolaus Jilg, Kattareeya Kumthip, Dahlene N Fusco, Lee F Peng, Raymond T Chung.
Abstract
Suppressor of cytokine signaling 1 (SOCS1) and suppressor of cytokine signaling 3 (SOCS3) have been thought to block type I interferon (IFN) signaling. We have previously reported that SOCS3 suppresses HCV replication in an mTOR-dependent manner. However, the relationship between SOCS1 and HCV replication remains unclear. Here, we found that overexpression of SOCS1 alone did not have an effect on HCV RNA replication. However, suppression of HCV replication by IFN-α was rescued by SOCS1 overexpression. The upregulation of HCV replication by SOCS1 overexpression in the presence of IFN is likely a result of the impairment of IFN signaling by SOCS1 and subsequent induction of ISGs. Knockdown of SOCS1 alone with specific shRNA enhanced the antiviral effect of IFN compared with negative control. Thus, SOCS1 acts as a suppressor of type I IFN function against HCV.Entities:
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Year: 2012 PMID： 23237992 PMCID： PMC3764487 DOI： 10.1016/j.antiviral.2012.12.001
Source DB: PubMed Journal: Antiviral Res ISSN： 0166-3542 Impact factor: 5.970