The Roles of Epinephelus coioides miR-122 in SGIV Infection and Replication

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-kappa B, and miR-122 can bind the target gene p38 alpha 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-kappa B, and cell apoptosis to regulate viral replication and proliferation.

Automated summary

The study revealed that SGIV infection can up-regulate the expression of E. coioides miR-122, and the up-regulation of miR-122 can affect the activation of inflammatory factors, the activity of AP-1 and NF-kappa B, as well as cell apoptosis to regulate viral replication and proliferation.