Retracted: MicroR‐9‐5p suppresses EV 71 replication through targeting NF κB of the RIG ‐I‐mediated innate immune response

Accumulating evidence demonstrates that there is a causative link between hsa‐micro RNA ‐9‐5p (miR‐9) and pathophysiological processes. Enterovirus 71 ( EV 71) has been found to contribute to numerous severe clinical symptoms which result in death. The exact mechanism by which EV 71 influences miR‐9 expression is unknown, and the relationship between miR‐9 and EV 71 is still unclear. Here, miR‐9 expression was found to be impaired upon EV 71 infection in several cell lines and in an EV 71 infection mouse model. Additionally, we confirmed that EV 71 infection induces robust expression of pro‐inflammatory cytokines ( TNF ‐α, IL ‐6, and IL ‐1) and interferons ( IFN ‐α and IFN ‐β). Overexpression of miR‐9 attenuated EV 71 proliferation and reduced protein and gene expressions of virion protein 1 ( VP 1) of EV 71. Furthermore, we observed that the inflammation caused by EV 71 infection was restored to a moderate level via miR‐9 overexpression. Nuclear factor kappa B ( NF κB) in the retinoic acid‐induced gene 1 ( RIG ‐I) signaling pathway, but not interferon regulating factor 3 ( IRF 3), was significantly decreased and inactivated by ectopic miR‐9 expression. Moreover, in mouse infection experiments, administration of miR‐9 agomirs caused a significant decrease in VP 1 levels and pro‐inflammatory cytokine production after viral inoculation. Taken together, the present data demonstrate that miR‐9 exerts an anti‐ EV 71 effect in cells and a mouse model via mediating NF κB activity of the RIG ‐I signal pathway, thereby suggesting a new candidate for antiviral drug development.