TRIM25, as a significant member of the TRIM family, has been frequently demonstrated in regulating the host's antiviral response by activating innate immunity. Ducks are often asymptomatic carriers of influenza A viruses, but the beneficial roles of TRIM25 in modulating the immune response remain largely unknown in ducks. In this study, we characterized the TRIM25, which contains a 16 bp 5'-UTR, a 279 bp 3'-UTR and a 2052 bp ORF that encodes 683 amino acid residues. In addition, we found that duTRIM25 transcripts were widely expressed in the 10 tissues tested, with higher expression levels in the kidney, liver, muscle and spleen and lower expression levels in the duodenum and blood. In addition, the six kinds of virus- or bacteria-mimicking stimuli were transfected into DEFs, and duTRIM25 was induced significantly with 5'ppp dsRNA stimulation. Furthermore, overexpression of duTRIM25 followed by treatment with 5'ppp dsRNA resulted in an increase in IFN-β. The SPRY domain of duTRIM25 contributed to promoting IFN-β activity in DEFs challenged with 5'ppp dsRNA. Taken together, our findings suggest that duck TRIM25 can induce the production of IFN-β against double-stranded RNA virus stimuli and that the SPRY domain of duTRIM25 was critical for the infection.
Keywords: IFN-β; TRIM25; duck; innate immune.