The Cellular Antiviral Protein Viperin Is Attenuated by Proteasome-Mediated Protein Degradation in Japanese Encephalitis Virus-Infected Cells

被引:79
作者
Chan, Yi-Lin [1 ,2 ,3 ]
Chang, Tsung-Hsien [1 ,2 ]
Liao, Ching-Len [3 ,4 ]
Lin, Yi-Ling [1 ,2 ,3 ,5 ]
机构
[1] Acad Sinica, Inst Biomed Sci, Taipei 115, Taiwan
[2] Acad Sinica, Natl Def Med Ctr, Taipei 115, Taiwan
[3] Acad Sinica, Grad Inst Life Sci, Taipei 115, Taiwan
[4] Acad Sinica, Dept Microbiol & Immunol, Taipei 115, Taiwan
[5] Acad Sinica, Genom Res Ctr, Taipei 115, Taiwan
关键词
D O I
10.1128/JVI.00438-08
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Viperin is identified as an antiviral protein induced by interferon (IFN), viral infections, and pathogen-associated molecules. In this study, we found that viperin is highly induced at the RNA level by Japanese encephalitis virus (JEV) and Sindbis virus (SIN) and that viperin protein is degraded in JEV-infected cells through a proteasome-dependent mechanism. Promoter analysis revealed that SIN induces viperin expression in an IFN-dependent manner but that JEV by itself activates the viperin promoter through IFN regulatory factor-3 and AP-1. The overexpression of viperin significantly decreased the production of SIN, but not of JEV, whereas the proteasome inhibitor MG132 sustained the protein level and antiviral effect of viperin in JEV-infected cells. Knockdown of viperin expression by RNA interference also enhanced the replication of SIN, but not that of JEV. Our results suggest that even though viperin gene expression is highly induced by JEV, it is negatively regulated at the protein level to counteract its antiviral effect. In contrast, SIN induces viperin through the action of IFN, and viperin exhibits potent antiviral activity against SIN.
引用
收藏
页码:10455 / 10464
页数:10
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