| Literature DB >> 30542978 |
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 Ye5,6,7.
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.Entities:
Keywords: Immune evasion; Japanese encephalitis virus (JEV); NS1′; Type I interferon (IFN-I)
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Year: 2018 PMID： 30542978 PMCID： PMC6335221 DOI： 10.1007/s12250-018-0067-5
Source DB: PubMed Journal: Virol Sin ISSN： 1995-820X Impact factor: 4.327