LncRNA transcriptome analysis of rainbow trout ( <i>Oncorhynchus mykiss</i> ) skin infected with IHNV reveals that lncRNA SARL/miR-205-z/ <i>SOCS3</i> axis negatively regulates antiviral immunity mechanisms

Long non-coding RNAs (lncRNAs) are new gene regulators involved in various biological processes. However, the regulatory effect of lncRNA on the rainbow trout (<i>Oncorhynchus mykiss</i>) antiviral immune response has not been reported. Here, we measured lncRNA profiles at 48 hpi compared to the control group, expression levels of lncRNA, miRNA, and gene, and lncRNA SARL/miR-205-z/<i>SOCS3</i> functions after rainbow trout skin infected with infectious haematopoietic necrosis virus (IHNV) by RNA-seq, qRT-PCR, and overexpression and inhibition assays. Transcriptome analysis identified twelve upregulated and four downregulated DElncRNAs. Twelve key immune-related competing endogenous RNA (ceRNA) networks were identified, and the target genes were enriched in the TLR, RLR, NLR, and p53 signalling pathways. Expression patterns suggested that changes in lncRNA SARL, miR-205-z, and <i>SOCS3</i> expression presented a ceRNA regulatory relationship. Further studies demonstrated that the lncRNA SARL was a ceRNA of <i>SOCS3</i> by sponging miR-205-z <i>in vitro</i>, thereby playing a negative regulatory role in the antiviral immune response of rainbow trout. We also found that miR-205-z was a positive regulator of rainbow trout liver cell proliferation, and this effect could be reversed by <i>SOCS3</i>. <i>In vivo</i>, <i>SOCS3</i> expression significantly increased after antagomiR-205-z injection. Furthermore, <i>SOCS3</i> overexpression significantly promoted the replication of IHNV. This study provides fundamental data for disease resistance breeding and targeted drug therapy in rainbow trout.