| Literature DB >> 33208231 |
Yutaro Yamaoka1, Satoko Matsunaga2, Sundararaj S Jeremiah2, Mayuko Nishi2, Kei Miyakawa2, Takeshi Morita2, Hajera Khatun2, Hideaki Shimizu3, Nobuhiko Okabe3, Hirokazu Kimura4, Hideki Hasegawa5, Akihide Ryo6.
Abstract
The association of Zika virus (ZIKV) infection with a congenital malformation in fetuses, neurological, and other systemic complications in adults have brought significant global health emergency. ZIKV targets nerve cells in the brain and causes cell death, such as pyroptosis, leading to neuroinflammation. Here we described a novel mechanism of pyroptosis caused by ZIKV protease. We found that ZIKV protease directly cleaved the GSDMD into N-terminal fragment (1-249) leading to pyroptosis in a caspase-independent manner, suggesting a direct mechanism of ZIKV-induced cell death and subsequent inflammation. Our findings might shed new light to explore the pathogenesis of ZIKV infections where ZIKV protease might be a suitable target for the development of antiviral agents.Entities:
Keywords: GSDMD; NS2B3 protease; Pyroptosis; ZIKV
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Year: 2020 PMID: 33208231 DOI: 10.1016/j.bbrc.2020.11.023
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575