| Literature DB >> 30530224 |
Shaoli Lin1, Shixing Yang2, Jia He1, Johnathan D Guest3, Zexu Ma1, Liping Yang1, Brian G Pierce3, Qiyi Tang4, Yan-Jin Zhang5.
Abstract
Zika virus (ZIKV) is a mosquito-borne positive-sense single-stranded RNA virus in the family of Flaviviridae. Unlike other flaviviruses, ZIKV infection of pregnant women may result in birth defects in their newborns, such as microcephaly or vision problem. ZIKV is known to antagonize the interferon (IFN) production in infected cells. However, the exact mechanism of this interference is not fully understood. Here, we demonstrate that NS5 protein of ZIKV MR766 strain antagonizes IFN production through inhibiting the activation of TANK-binding kinase 1 (TBK1), which phosphorylates the transcription activator IFN regulatory factor 3 (IRF3). Mechanistically, NS5 interacts with the ubiquitin-like domain of TBK1 and results in less complex of TBK1 and TNF (tumor necrosis factor) receptor-associated factor 6 (TRAF6), leading to dampened TBK1 activation and IRF3 phosphorylation. Our study provides insights into the mechanism of ZIKV evasion of IFN-mediated innate immunity.Entities:
Keywords: IRF3; Interferon; NS5; TBK1; ZIKV; Zika virus
Mesh:
Substances:
Year: 2018 PMID: 30530224 PMCID: PMC6340140 DOI: 10.1016/j.virol.2018.11.009
Source DB: PubMed Journal: Virology ISSN: 0042-6822 Impact factor: 3.616