SOCS1 abrogates IFN's antiviral effect on hepatitis C virus replication

被引：21

作者：

Shao, Run-Xuan ^{[3
]}

Zhang, Leiliang ^{[1
,2
,3
]}

Hong, Zhi ^{[1
,2
]}

Goto, Kaku ^{[3
]}

Cheng, Du ^{[3
]}

Chen, Wen-Chi ^{[3
]}

Jilg, Nikolaus ^{[3
]}

Kumthip, Kattareeya ^{[3
]}

Fusco, Dahlene N. ^{[3
]}

Peng, Lee F. ^{[3
]}

Chung, Raymond T. ^{[3
]}

机构：

[1] Chinese Acad Med Sci, Inst Pathogen Biol, MOH Key Lab Syst Biol Pathogens, Beijing 100730, Peoples R China

[2] Peking Union Med Coll, Beijing 100730, Peoples R China

[3] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit,Dept Med, Boston, MA 02114 USA

来源：

ANTIVIRAL RESEARCH | 2013年 / 97卷 / 02期

基金：

美国国家卫生研究院;

关键词：

Hepatitis C virus; SOCS1; Interferon; ISG; JFH1; JAK-STAT PATHWAY; INTERFERON-ALPHA; RIBAVIRIN; CYTOKINE; ACTIVATION; SUPPRESSOR; EXPRESSION; INHIBITOR; INFECTION; PROTEINS;

D O I：

10.1016/j.antiviral.2012.12.001

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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-alpha, 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. (C) 2012 Elsevier B.V. All rights reserved.

引用

页码：101 / 107

页数：7

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