Japanese Encephalitis Virus NS1' Protein Antagonizes Interferon Beta Production.
Dengyuan ZhouFan JiaQiuyan LiLuping ZhangZheng ChenZikai ZhaoMin CuiYunfeng SongHuanchun ChenShengbo CaoJing YePublished in: Virologica Sinica (2018)
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.
Keyphrases
- dengue virus
- dendritic cells
- prostate cancer
- immune response
- mouse model
- amino acid
- disease virus
- escherichia coli
- staphylococcus aureus
- pseudomonas aeruginosa
- genome wide
- metabolic syndrome
- oxidative stress
- adipose tissue
- cardiovascular events
- coronary artery disease
- antimicrobial resistance
- radical prostatectomy
- diabetic rats
- binding protein