nterferon alpha (IFNα)-induced TRIM22 interrupts HCV 'eplication by ubiquitinating NS5A  被引量:15

nterferon alpha (IFNα)-induced TRIM22 interrupts HCV 'eplication by ubiquitinating NS5A

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作  者:Chen Yang Xinhao Zhao Dakang Sun Leilei Yang Chang Chong Yu Pan Xiumei Chi Yanhang Gao Moli Wang Xiaodong Shi Haibo Sun Juan Lv Yuanda Gao Jin Zhong Junqi Niu Bing Sun 

机构地区:[1]State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China [2]Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China [3]Hepatology Section, First Hospital, University of Jilin, Changchun, China [4]Infectious Diseases Department, Fourth Hospital, University of Jilin, Changchun, China [5]Experiment Center of Clinical Medicine, Affiliated Hospital of Binzhou Medical University, Binzhou, China

出  处:《Cellular & Molecular Immunology》2016年第1期94-102,共9页中国免疫学杂志(英文版)

摘  要:TRIM22, a tripartite-motif (TRIM) protein, is upregulated upon interferon alpha (IFNa) administration to hepatitis C virus (HCV)-infected patients. However, the physiological role of TRIM22 upregulation remains unclear. Here, we describe a potential antiviral function of TRI M22's targeting of the HCV NSSA protein. NS5A is important for HCV replication and for resistance to I FNa therapy. During the first 24 h following the initiation of I FNa treatment, upregulation of TRIM22 in the peripheral blood mononuclear cells (PBMCs) of HCV patients correlated with a decrease in viral titer. This phenomenon was confirmed in the hepatocyte-derived cell line Huh-7, which is highly permissive for HCV infection. TRIM22 over-expression inhibited HCV replication, and Small interfering RNA (siRNA)-mediated knockdown of TRIM22 diminished IFNα-induced anti-HCV function. Furthermore, we determined that TRIM22 ubiquitinates NS5A in a concentration-dependent manner. In summary, our results suggest that TRIM22 upregulation is associated with HCV decline during IFNα treatment and Dlavs an important role in controlling HCV replication in vitro.TRIM22, a tripartite-motif (TRIM) protein, is upregulated upon interferon alpha (IFNa) administration to hepatitis C virus (HCV)-infected patients. However, the physiological role of TRIM22 upregulation remains unclear. Here, we describe a potential antiviral function of TRI M22's targeting of the HCV NSSA protein. NS5A is important for HCV replication and for resistance to I FNa therapy. During the first 24 h following the initiation of I FNa treatment, upregulation of TRIM22 in the peripheral blood mononuclear cells (PBMCs) of HCV patients correlated with a decrease in viral titer. This phenomenon was confirmed in the hepatocyte-derived cell line Huh-7, which is highly permissive for HCV infection. TRIM22 over-expression inhibited HCV replication, and Small interfering RNA (siRNA)-mediated knockdown of TRIM22 diminished IFNα-induced anti-HCV function. Furthermore, we determined that TRIM22 ubiquitinates NS5A in a concentration-dependent manner. In summary, our results suggest that TRIM22 upregulation is associated with HCV decline during IFNα treatment and Dlavs an important role in controlling HCV replication in vitro.

关 键 词:HCV IFNΑ NS5A TRIM22 UBIQUITIN 

分 类 号:Q78[生物学—分子生物学] TN946[电子电信—信号与信息处理]

 

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