IRF7
内部收益率3
坦克结合激酶1
生物
干扰素
蛋白酶体
小干扰RNA
RNA干扰
非洲猪瘟病毒
自噬
Ⅰ型干扰素
病毒学
猪流行性腹泻病毒
基因敲除
基因沉默
细胞生物学
病毒
先天免疫系统
免疫系统
核糖核酸
细胞培养
信号转导
基因
免疫学
细胞凋亡
遗传学
MAPK/ERK通路
MAP激酶激酶激酶
作者
Kaidian Yang,Ying Xue,Tianming Niu,Xinyang Li,Mingyang Cheng,Meiying Bao,Bo-Shi Zou,Chunwei Shi,Jianzhong Wang,Wentao Yang,Nan Wang,Yanlong Jiang,Guilian Yang,Yan Zeng,Xin Cao,Chunfeng Wang
出处
期刊:Virus Research
[Elsevier]
日期:2022-12-01
卷期号:322: 198931-198931
被引量:14
标识
DOI:10.1016/j.virusres.2022.198931
摘要
African swine fever virus (ASFV) employs diverse strategies to confront or evade host type I interferon (IFN-I)-induced antiviral responses. Moreover, the mechanisms of this process are largely unknown. Here, we assessed 27 ASFV proteins to determine whether any of them suppressed the cGAS-STING pathway to facilitate immune evasion. Using dual-luciferase assays, we found that ASFV MGF505-7R suppressed the activity of the IFN-β and ISRE promoters and the expression of IFN-I and ISGs. MGF505-7R interacted with IRF7 and TBK1, degrading IRF7 by autophagy, cysteine, and proteasome pathways and TBK1 by the proteasome pathway. Moreover, TBK1 and IRF3 were phosphorylated by cGAS-STING stimulation. Finally, small interfering RNA (siRNA)-based silencing of MGF505-7R enhanced IFN-I antiviral activity. Taken together, these results preliminarily clarified the immune escape mechanism of ASFV MGF505-7R, which provides a potential target for developing antiviral agents.
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