Impaired interferon response in senecavirus A infection and identification of 3C^pro as an antagonist.

ABSTRACT: Senecavirus A (SVA), a picornavirus, causes vesicular diseases and epidemic transient neonatal losses in swine, resulting in a multifaceted economic impact on the swine industry. SVA counteracts host antiviral response through multiple strategies facilitatng viral infection and transmission. However, the mechanism of how SVA modulates interferon (IFN) response remains elusive. Here, we demonstrate that SVA 3C protease (3C^pro) blocks the transduction of Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway to antagonize type I IFN response. Mechanistically, 3C^pro selectively cleaves and degrades STAT1 and STAT2 while does not target JAK1, JAK2, and IRF9, through its protease activity. Notably, SVA 3C^pro cleaves human and

SUBMITTER: Zhang X 

PROVIDER: S-EPMC11265225 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature