MicroRNA-30e* suppresses dengue virus replication by promoting NF-?B-dependent IFN production.

ABSTRACT: 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?B? 3'-UTR and disrupted the NF-?B/I?B? negative feedback loop, leading to hyperactivation of NF-?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-? and the downstream IFN-stimulated genes (ISGs) such as OAS1, MxA and IFITM1, and suppressed DENV replication. Furthermore, suppression of I?B? mediates the enhancing effect of miR-30e* on IFN-?-induced antiviral response. Collectively, our findings suggest a modulatory role of miR-30e* in DENV induced IFN-? signaling via the NF-?B-dependent pathway. Further investigation is needed to evaluate whether miR-30e* has an anti-DENV effect in vivo.

SUBMITTER: Zhu X 

PROVIDER: S-EPMC4133224 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature