In mammals, mature miR-122 is 22 nucleotides long and can be involved in regulating a variety of physiological and biological pathways. In this study, the expression profile and effects of grouper Epinephelus coioides miR-122 response to Singapore grouper iridovirus (SGIV) infection were investigated. The sequences of mature microRNAs (miRNAs) from different organisms are highly conserved, and miR-122 from E. coioides exhibits high similarity to that from mammals and other fish. The expression of miR-122 was up-regulated during SGIV infection. Up-regulation of miR-122 could significantly enhance the cytopathic effects (CPE) induced by SGIV, the transcription levels of viral genes (MCP, VP19, LITAF and ICP18), and viral replication; reduce the expression of inflammatory factors (TNF-a, IL-6, and IL-8), and the activity of AP-1 and NF-κB, and miR-122 can bind the target gene p38α MAPK to regulate the SGIV-induced cell apoptosis and the protease activity of caspase-3. The results indicated that SGIV infection can up-regulate the expression of E. coioides miR-122, and up-regulation of miR-122 can affect the activation of inflammatory factors, the activity of AP-1 and NF-κB, and cell apoptosis to regulate viral replication and proliferation.

在哺乳动物中，成熟的 miR-122 长 22 个核苷酸，可参与调节多种生理和生物学途径。在这项研究中，研究了石斑鱼Epinephelus coioides miR-122 对新加坡石斑鱼虹彩病毒 (SGIV) 感染的表达谱和影响。来自不同生物体的成熟 microRNAs (miRNAs) 的序列高度保守，来自E. coioides 的miR-122表现出与哺乳动物和其他鱼类的高度相似。miR-122的表达在SGIV感染期间上调。上调miR-122可显着增强SGIV诱导的细胞病变效应（CPE）、病毒基因（MCP、VP19、LITAF和ICP18）的转录水平和病毒复制；降低炎症因子（TNF-a、IL-6和IL-8）的表达，以及AP-1和NF-κB的活性，miR-122可以结合靶基因p38α MAPK调节SGIV诱导的细胞凋亡和 caspase-3 的蛋白酶活性。结果表明SGIV感染可上调E. coioides的表达 miR-122 和 miR-122 的上调可以影响炎症因子的激活、AP-1 和 NF-κB 的活性以及细胞凋亡以调节病毒复制和增殖。