内部收益率3
生物
病毒复制
基因敲除
MDA5型
干扰素
病毒学
细胞生物学
干扰素调节因子
先天免疫系统
病毒
基因沉默
RNA干扰
免疫系统
核糖核酸
基因
遗传学
作者
Shujuan Xu,Jingyuan Xie,Xiangbo Zhang,Lei Chen,Yingjie Bi,Xiangrong Li,Adi Idris,Ru Feng
标识
DOI:10.1016/j.vetmic.2021.109304
摘要
DEAD (Asp-Glu-Ala-Asp)-box RNA helicases (DDX) play important roles in viral infection, either as cytosolic viral nucleic acids sensors or as essential host factors for viral replication. In this study, we identified DDX56 as a positive regulator for encephalomyocarditis virus (EMCV) replication. EMCV infection promotes DDX56 expression via its viral proteins, VP3 and 3C. We showed that DDX56 overexpression promotes EMCV replication whereas its loss dampened EMCV replication. Consequently, knockdown of DDX56 increases type I interferon (IFN) expression during EMCV infection. We also showed that DDX56 interrupts IFN regulatory factor 3 (IRF3) phosphorylation and its nucleus translocation by directly targeting KPNA3 and KPNA4 in an EMCV-triggered MDA5 signaling activation cascade leading to the blockade of IFN-β production. Overall, we showed that DDX56 is a novel negative regulator of EMCV-mediated IFN-β responses and that DDX56 plays a critical role in EMCV replication. These findings reveal a novel strategy for EMCV to utilize a host factor to evade the host innate immune response and provide us new insight into the function of DDX56.
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