内部收益率3
生物
干扰素调节因子
干扰素
先天免疫系统
MDA5型
转录因子
病毒学
免疫系统
细胞生物学
免疫学
RNA干扰
核糖核酸
基因
生物化学
作者
Li Zi,Ya‐Wen Yang,Huijun Lu,Jing Zhang,Rongyi Xu,Junchao Shi,Yungang Lan,Jiyu Guan,Kui Zhao,Hongbin He,Feng Gao,Wenqi He
标识
DOI:10.1016/j.vetmic.2020.108918
摘要
Porcine haemagglutinating encephalomyelitis virus (PHEV) is a member of coronavirus that causes acute infectious disease and high mortality in piglets. The transcription factor IRF3 is a central regulator of type I interferon (IFN) innate immune signalling. Here, we report that PHEV infection of RAW264.7 cells results in strong suppression of IFN-β production in the early stage. A comparative analysis of the upstream effector of IFN-β transcription demonstrated that deactivation of IRF3, but not p65 or ATF-2 proteins, is uniquely attributed to failure of early IFN-β induction. Moreover, the RIG-I/MDA5/MAVS/TBK1-dependent protective response that regulates the IRF3 pathway is not disrupted by PHEV and works well underlying the deactivated IRF3-mediated IFN-β inhibition. After challenge with poly(I:C), a synthetic analogue of dsRNA used to stimulate IFN-β secretion in the TLR-controlled pathway, we show that PHEV and poly(I:C) regulate IFN-β-induction via two different pathways. Collectively, our findings reveal that deactivation of IRF3 is a specific mechanism that contributes to termination of type I IFN signalling during early infection with PHEV independent of the conserved RIG-I/MAVS/MDA5/TBK1-mediated innate immune response.
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