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Virologica Sinica, 33 (6) : 515, 2018
Research Article
Japanese Encephalitis Virus NS1' Protein Antagonizes Interferon Beta Production
Dengyuan Zhou1,2,3, Fan Jia4, Qiuyan Li1,2,3, Luping Zhang1,2,3, Zheng Chen1,2,3, Zikai Zhao1,2,3, Min Cui1,2,3, Yunfeng Song1,2,3, Huanchun Chen1,2,3, Shengbo Cao1,2,3, Jing Ye1,2,3  
1 State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China
2 Key Laboratory of Preventive Veterinary Medicine in Hubei Province, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
3 The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan 430070, China
4 Wuhan Institute of Physics and Mathematics (WIPM), Chinese Academy of Sciences, Wuhan 430070, China
 Correspondence: yej@mail.hzau.edu.cn
(1639.19KB)  (127.34KB)  
Abstract
Japanese encephalitis virus (JEV) is a mosquito-borne virus and the major cause of viral encephalitis in Asia. NS1', a 52-amino acid C-terminal extension of NS1, is generated with a -1 programmed ribosomal frameshift and is only present in members of the Japanese encephalitis serogroup of flaviviruses. Previous studies demonstrated that NS1' plays a vital role in virulence, but the mechanism is unclear. In this study, an NS1' defected (rG66A) virus was generated. We found that rG66A virus was less virulent than its parent virus (pSA14) in wild-type mice. However, similar mortality caused by the two viruses was observed in an IFNAR knockout mouse model. Moreover, we found that rG66A virus induced a greater type I interferon (IFN) response than that by pSA14, and JEV NS1' significantly inhibited the production of IFN-β and IFN-stimulated genes. Taken together, our results reveal that NS1' plays a vital role in blocking type I IFN production to help JEV evade antiviral immunity and benefit viral replication.
Received: 27 Sep 2018  Accepted: 7 Nov 2018  Published online: 12 Dec 2018
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