Dengue virus (DENV) infection of cells including macrophages and endothelial cells (EC) result in release of inflammatory and innate factors. Many of these factors are vasoactive and can act on EC lining the vasculature to alter endothelial barrier function that may be manifested as vascular leak syndrome as observed in patients with severe dengue1. Cellular microRNAs (miRNA) that function to regulate gene expression by cleaving mRNA or through translational repression have a role in regulating innate inflammatory responses and vascular function. Here we explore the role of the miRNA miR-155-5p (known to regulate factors associated with inflammation) in the context of DENV infection. Our results show that in DENV infected macrophages and human umbilical vein endothelial cells (HUVEC), the levels of miR-155-5p increases. In HUVECs, overexpression of miR-155-5p using miR-155-5p mimics did not alter DENV replication or virus release in infected cells but DENV release was diminished in miR-155-5p inhibitor treated HUVEC. Further miR-155-5p mimics decreased DENV-induced mRNA for TNF-α, IFN-β, ICAM-1 (cell adhesion molecule) and the interferon stimulated gene viperin. In contrast, miR-155-5p inhibitors augmented DENV induced TNF-α and IFN-β transcripts, although no significant change in ICAM-1 or viperin was observed. Further studies are underway to confirm these observations and extend the investigation to macrophages. Our studies may define novel miRNA therapeutic to treat DENV-induced vascular leak by targeting exacerbated inflammation in EC.