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

ABSTRACT: 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 ASFV-intB318L (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 TRIM2

SUBMITTER: Liu X 

PROVIDER: S-EPMC12543117 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature