MicroRNA-30e* Suppresses Dengue Virus Replication by Promoting NF-κB-Dependent IFN Production

MicroRNAs have been shown to contribute to a repertoire of host-pathogen interactions during viral infection. Our previous study demonstrated that microRNA-30e* (miR-30e*) directly targeted the I kappa B alpha 3'-UTR and disrupted the NF-kappa B/I kappa B alpha negative feedback loop, leading to hyperactivation of NF-kappa B. This current study investigated the possible role of miR-30e* in the regulation of innate immunity associated with dengue virus (DENV) infection. We found that DENV infection could induce miR-30e* expression in DENV-permissive cells, and such an overexpression of miR-30e* upregulated IFN-beta and the downstream IFN-stimulated genes (ISGs) such as OAS1, MxA and IFITM1, and suppressed DENV replication. Furthermore, suppression of I kappa B alpha mediates the enhancing effect of miR-30e* on IFN-beta-induced antiviral response. Collectively, our findings suggest a modulatory role of miR-30e* in DENV induced IFN-beta signaling via the NF-kappa B-dependent pathway. Further investigation is needed to evaluate whether miR-30e* has an anti-DENV effect in vivo.