FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity.

ABSTRACT: RIG-I like receptors (RLRs) recognize RNA viruses and induce an innate immune response. Although many host factors strictly regulate the signal transduction of the RLR pathway, the mechanisms remain unclear. In the present study, we demonstrated that virus infection slightly increased the expression of programmed cell death protein 10 (PDCD10). PDCD10 overexpression inhibited interferon beta (IFN-β) promoter activation after Sendai virus (SeV) infection. Moreover, PDCD10 negatively regulated RNA virus-induced IFN-β secretion. These effects were reversed following PDCD10 gene knockout. PDCD10 also interacted with virus-induced signaling adaptor (VISA) and disrupted the formation of the VISA-IRF3 complex to inhibit IFN-β production. Additionally, PDCD10 promoted foot-and-mouth disease virus

SUBMITTER: Li Q 

PROVIDER: S-EPMC12724370 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature