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African swine fever virus pB318L suppresses inflammatory response by inhibiting NF-κB activation and NLRP3 inflammasome formation

文献类型： 外文期刊

作者： Xiaohong Liu;Guangqiang Ye;Yi Zeng;Hanyu Wu;Siqi Dong;Xiaoping He;Qiongqiong Zhou;Hongyang Liu;Zhaoxia Zhang;Jiangnan Li;Changjiang Weng;Li Huang

作者机构：

期刊名称： PLOS Pathogens

ISSN： 1553-7374

年卷期： 2025 年 21 卷 10 期

页码：

收录情况： SCIE（2025版）

摘要： African swine fever (ASF) is an acute, hemorrhagic, and severe infectious disease caused by African swine fever virus (ASFV), posing significant threats to global swine production. ASFV pathogenesis is closely associated with its sophisticated immune evasion strategies. In this study, we demonstrate that ASFV pB318L, a trans-geranylgeranyl-diphosphate synthase (GGPPS) homolog inhibited both the NF-κB signaling pathway and the formation of the NLRP3 inflammasome. Infection with ASFVintB318L (a recombinant ASFV with pB318L expression inhibition) induced significantly higher levels of IL-1β compared to its parent strain ASFV HLJ/18. Mechanically, pB318L interacts with NEMO to inhibit the interaction between IKKα and NEMO, and suppresses the K63-linked ubiquitination of NEMO mediated by TRIM21. In addition, pB318L interacts with the NACHT and LRR domains of NLRP3, which prevents the oligomerization of NLRP3 by suppressing the interaction between NEK7 and NLRP3. Crucially, the immunosuppressive functions of pB318L on both NF-κB signaling pathway and NLRP3 inflammasome activation are independent of its GGPPS enzymatic activity. In conclusion, we presented evidence that ASFV pB318L negatively regulates NF-κB signaling pathway and NLRP3 inflammasome. This study provides critical mechanistic insights into the role of pB318L in ASFV pathogenesis and highlights its potential as a target for the development of antiviral strategies or live-attenuated vaccines against ASF.

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