miR-2188-5p promotes GCRV replication by the targeted degradation of klf2a in Ctenopharyngodon idellus.

Studies on host immunity evasion by aquatic viruses have largely focused on coding genes. There is accumulating evidence for the important biological functions of non-coding miRNAs in virus–host interactions. The regulatory functions of non-coding miRNAs in fish reovirus–host interactions remain unknown. Here, miR-2188-5p in grass carp (Ctenopharyngodon idellus), a miRNA specific to teleosts, was predicted to target the 3′ UTR of the transcription factor klf2a. A correlation analysis and dual-luciferase reporter assay revealed that miR-2188-5p could induce the degradation of klf2a. The expression of miR-2188-5p induced the degradation of klf2a in a dose-dependent manner, suppressing the type I interferon response and promoting grass carp reovirus (GCRV) replication. As determined by a co-expression analysis , klf2a inhibited viral infection when miR-2188-5p was overexpressed. The targeted degradation of klf2a by miR-2188-5p could inhibit the type I interferon response and promote the replication of GCRV; however, this targeted degradation ability was insufficient to fully inhibit GCRV infection. These results provide novel insights into the regulatory effects and biological functions of non-coding miRNAs in fish–virus interactions. • Grass carp miR-2188-5p targets the degradation of klf2a. • miR-2188-5p targets klf2a , suppresses IFN1 and promotes GCRV replication. • klf2a expression offsets the induced expression of the GCRV genome by miR-2188-5p. [ABSTRACT FROM AUTHOR]