ArticleJournal of virology2025
FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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 (FMDV) replication by inhibiting IFN-β production. FMDV is the causative pathogen of foot-and-mouth disease, one of the most destructive and contagious animal diseases in the world. The FMDV 3A protein plays important roles in viral replication, host tropism, and immune regulation. Our experimental results also showed that full-length 3A cooperated with PDCD10 to inhibit IFN-β production by promoting the binding of PDCD10 to VISA. Collectively, the study findings revealed that PDCD10, as a new negative regulator, cooperated with 3A to inhibit viral-induced IFN-β production. IMPORTANCE: Foot-and-mouth disease virus (FMDV) is a pathogen that causes a highly contagious and destructive foot-and-mouth disease in animals with cloven hooves. Although the 3A protein of FMDV is involved in viral replication and host tropism, its function remains unclear. PDCD10 plays critical roles in normal cardiovascular development, cell proliferation, and normal structure and assembly of the Golgi complex. The present study showed that PDCD10 expression was slightly increased by virus infection, while PDCD10 promoted FMDV replication. Our results also demonstrated that PDCD10 inhibited Sendai virus-induced interferon beta (IFN-β) production through interaction with virus-induced signaling adaptor (VISA). PDCD10 also disrupted VISA-IRF3 complex formation to impair IFN-β production induced by RNA virus. The FMDV 3A protein bound with PDCD10 to synergistically promote FMDV replication. This study helped to reveal the potential mechanism of FMDV 3A protein and PDCD10 impact on viral replication.
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