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)

Abstract

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.

Keywords: IBDV; SOCS; STAT; Type I IFN; miR-27b-3p.