TRIM25 inhibits spring viraemia of carp virus replication by positively regulating RIG-I signaling pathway in common carp (Cyprinus carpio L.)

Common carp (Cyprinus carpio L.) is one of the most widely cultivated fish in China. Spring viraemia of carp virus (SVCV) is a highly pathogenic virus and has often caused excessive losses in carp pond fisheries. Innate immune play important roles against virus infection. To better understand the immune response of common carp against SVCV infection, transcriptome analysis was performed using the Illumina Novaseq 6000 platform. It was showed that a total of 3953 differentially expressed unigenes were identified, and the RLR signaling pathway were significantly enriched after SVCV infection. Subsequently, the role of RLR signaling pathway in SVCV infection was studied. The results showed that common carp RIG-I (CcRIG-I) and TRIM25 (CcTRIM25) significantly decreased the replication of SVCV by inducing the phosphorylation of TBK1, IRF3 and p65 and the expression of ifn-1, viperin, isg15 and mx. Further studies illustrated that CcTRIM25 could positive regulate CcRIG-I mediated downstream signaling pathway. Finally, the mechanism of CcTRIM25 promoting CcRIG-I-mediated signaling was investigated. CcTRIM25 could interact with the caspase activation and recruitment domain (CARD) of CcRIG-I and promoted K63-linked polyubiquitination of CcRIG-I. Altogether, the study revealed a mechanism of CcTRIM25 regulating CcRIG-I mediated immune response in SVCV infection.

Automated summary

In this study, transcriptome analysis was performed to investigate the immune response of common carp against SVCV infection. It was found that the RLR signaling pathway was significantly enriched after SVCV infection. Further investigation revealed that CcRIG-I and CcTRIM25 suppressed the replication of SVCV by inducing the phosphorylation of TBK1, IRF3, and p65, as well as the expression of ifn-1, viperin, isg15, and mx. Additionally, CcTRIM25 was shown to regulate CcRIG-I-mediated immune response through interaction with CARD and promoting K63-linked polyubiquitination of CcRIG-I.