Suppressor of cytokine signaling 1 (SOCS1) inhibits antiviral responses to facilitate Senecavirus A infection by regulating the NF-κB signaling pathway

Abstract

Senecavirus A (SVA) is a new virus inducing porcine idiopathic vesicular disease that causes significant economic losses. Although some progress has been made in etiological research, the role of host factors in SVA infection remains unclear. This study investigated the role of the host factor, suppressor of cytokine signaling 1 (SOCS1), in SVA infection. The expression of SOCS1 was significantly upregulated with infection of SVA in a dose-dependent manner, and SOCS1 inhibited the expression of type I interferons (IFN-α, IFN-β) and the production of interferon stimulating genes (ISGs) (ISG56, ISG54, PKR), thereby facilitating viral replication. Further results showed that inhibition of antiviral responses of SOCS1 was achieved by regulating the NF-κB signaling pathway, which attenuates the production of IFNs and pro-inflammatory cytokines. These findings provide a new perspective of SVA pathogenesis and may partially explain the persistence of this infection. Moreover, the data indicate that targeting SOCS1 can help in developing new agents against SVA infection.

Keywords: IFN; NF-κB; Proliferation; SOCS1; SVA.