gga-miR-27b-3p enhances type I interferon expression and suppresses infectious bursal disease virus replication via targeting cellular suppressors of cytokine signaling 3 and 6 (SOCS3 and 6).

MicroRNAs are small noncoding RNAs playing an important role in host response to pathogenic infection. Here we show that IBDV infection induced the demethylation of the pre-miR-27 promoter and upregulated gga-miR-27b-3p expression. We found that ectopic expression of miR-27b-3p in DF-1 cells enhanced the expression of chicken IFN-β, IRF3 and NF-κB, via directly targeting cellular suppressors of cytokine signaling 3 and 6 (SOCS3 and 6), inhibiting IBDV replication in host cells, while inhibition of endogenous miR-27b-3p by its inhibitors suppressed the expression of IFN-β, IRF3 and NF-κB, enhancing SOCS3 and 6 expressions and facilitating IBDV replication. Furthermore, transfection of DF-1 cells with miR-27b-3p markedly increased phosphorylation of STAT1 on Tyr701 in cells post chIFN-γ treatment. On the contrary, inhibition of endogenous miR-27b-3p reduced phosphorylation of STAT1 on Tyr701 in cells with chIFN-γ treatment. These findings indicate that gga-miR-27b-3p serves as an inducible antiviral mediator in host response to IBDV infection.