Infectious hematopoietic necrosis (IHN), caused by IHN virus, is a highly contagious and lethal disease that seriously hampers the development of rainbow trout (Oncorhynchus mykiss) aquaculture. However, the immune response mechanism of rainbow trout underlying IHNV infection remains largely unknown. MicroRNAs act as post-transcriptional regulators of gene expression and perform a crucial role in fish immune response. Herein, the regulatory mechanism and function of miR-206 in rainbow trout resistance to IHNV were investigated by overexpression and silencing. The expression analysis showed that miR-206 and its potential target receptor-interacting serine/threonine-protein kinase 2 (RIP2) exhibited significant time-dependent changes in headkidney, spleen and rainbow trout primary liver cells infected with IHNV and their expression displayed a negative correlation. In vitro, the interaction between miR-206 and RIP2 was verified by luciferase reporter assay, and miR-206 silencing in rainbow trout primary liver cells markedly increased RIP2 and interferon (IFN) expression but significantly decreased IHNV copies, and opposite results were obtained after miR-206 overexpression or RIP2 knockdown. In vivo, overexpressed miR-206 with agomiR resulted in a decrease in the expression of RIP2 and IFN in liver, headkidney and spleen. This study revealed the key role of miR-206 in anti-IHNV, which provided potential for anti-viral drug screening in rainbow trout.

传染性造血组织坏死(IHN)是由IHN病毒引起的一种高度传染性、致死性的疾病，严重阻碍虹鳟鱼( Oncorhynchus mykiss )养殖业的发展。然而，虹鳟鱼 IHNV 感染的免疫反应机制仍然很大程度上未知。 MicroRNA 作为基因表达的转录后调节因子，在鱼类免疫反应中发挥着至关重要的作用。本文通过过表达和沉默研究了 miR-206 在虹鳟鱼 IHNV 抗性中的调控机制和功能。表达分析显示，miR-206及其潜在靶受体相互作用丝氨酸/苏氨酸蛋白激酶2（RIP2）在感染IHNV的头肾、脾脏和虹鳟鱼原代肝细胞中表现出显着的时间依赖性变化，且其表达呈阴性。相关性。在体外，通过荧光素酶报告基因实验验证了miR-206和RIP2之间的相互作用，虹鳟原代肝细胞中miR-206沉默显着增加了RIP2和干扰素（IFN）的表达，但显着降低了IHNV拷贝，并且在虹鳟鱼原代肝细胞中沉默miR-206后得到了相反的结果。 miR-206 过表达或RIP2敲低。在体内，用agomiR过表达miR-206导致肝脏、头肾和脾脏中RIP2和IFN的表达降低。这项研究揭示了 miR-206 在抗 IHNV 中的关键作用，为虹鳟鱼的抗病毒药物筛选提供了潜力。