Skin microRNA transcriptome of rainbow trout infected with infectious hematopoietic necrosis virus revealed novel-m0065-3p regulating antiviral immune responses via targeting interferon regulatory factor 7.

miRNAs are small non-coding RNA that instrumental in host immune response to pathogen infection. However, studies on the involvement of miRNAs in rainbow trout antiviral response are still lacking. In this study, miRNA profiles of 48 hpi (T48SKs) compared to control (C48SKs), novel-m0065-3p and interferon regulatory factor 7 (IRF7) expression, and novel-m0065-3p-IRF7 functions were examined in rainbow trout skin following infectious hematopoietic necrosis virus (IHNV) challenge through RNA-seq, qRT-PCR, and overexpression and inhibition assays. Transcriptome analysis identified 23 up-regulated and 25 down-regulated differentially expressed miRNAs (DEMs). Enrichment analysis revealed that target genes were enriched in MAPK, RIG-I-like receptor, and Toll-like receptor signaling pathways. The DEMs (miR-205-z, novel-m0065-3p, novel-m0215-5p, novel-m0384-5p, and novel-m0397-3p) were identified, which can target key immune-related genes. Expression patterns suggested that novel-m0065-3p and IRF7 were potential regulators in immune responses of rainbow trout. Functional analysis revealed that the overexpression of novel-m0065-3p reduced significantly IRF7 expression in liver cells, which was attenuated by the introduction of IRF7, whereas the opposite result was obtained by silencing novel-m0065-3p. Overexpressed novel-m0065-3p promoted liver cell proliferation and inhibited apoptosis, and co-transfection of IRF7 attenuated the effect of novel-m0065-3p. Furthermore, IRF7 overexpression inhibited significantly IHNV replication. In vivo, the injection of agomiR-m0065-3p inhibited significantly the expression of IRF7. This study provided valuable information for drug-targeted diseases research and directed breeding efforts.

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Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.