Cellular microRNA-miR-548g-3p modulates the replication of dengue virus

•miR-548g-3p directly targets the SLA promoter element within the 5′UTR of DENV.•Overexpression of miR-548g-3p suppressed replication of DENV.•The anti-viral effect of miR-548g-3p is independent of interferon signaling.•The anti-viral effect of miR-548g-3p is not due to cell cycle arrest.

SummaryObjectiveIt has been well recognized that microRNA plays a role in the host-pathogen interaction network. The significance of microRNA in the regulation of dengue virus (DENV) replication, however, remains unknown. The objective of our study was to determine the biological function of miR-548g-3p in modulating the replication of dengue virus.MethodsHere we report that employment of a microRNA target search algorithm to analyze the 5′ untranslated region (5′UTR) consensus sequences of DENV (DENV serotypes 1-4) led to a discovery that miR-548g-3p directly targets the stem loop A promoter element within the 5′UTR, a region essential for DENV replication. Real-time PCR was used to measure the expression levels of miR-548g-3p under DENV infection. We performed overexpression and inhibition assays to test the role of miR-548g-3p on DENV replication. The protein and mRNA levels of interferon were measured by ELISA and real-time PCR respectively.ResultWe found that overexpression of miR-548g-3p suppressed multiplication of DENV 1, 2, 3 and 4, and that miR-548g-3p was also found to interfere with DENV translation, thereby suppressing the expression of viral proteins.ConclusionOur results suggest that miR-548g-3p directly regulates DENV replication and warrant further study to investigate the feasibility of microRNA-based anti-DENV approaches.