We propose that the interaction of viral RNA with the deregulated RNA-induced silencing complex (RISC) containing the mature miRNAs could prevent genome circularisation, thus affecting viral RNA translation. This could explain the reduction in the percentage of infected cells observed at 72 hpi, compared to that in the control (scrambled) cells, but only when either miR-744 or miR-484 were first overexpressed, whereas no significant effect was observed when the cells were first infected, and at 24 hpi either miRNA was overexpressed with no reduction in DENV RNA in either strategy. This is interesting since the expression of miR-744 and miR-484 was decreased during the first 48 hpi but later, their expression was increased mainly at 72 hpi in Vero cells infected with DENV-1 or DENV-3. Why the expression of these two miRNAs increases with a delay only in response to DENV infection but not when the 3′ UTR fused downstream of the GFP ORF was overexpressed, is unknown. We suggest that this effect is due to an immune interaction caused by DENV infection; e.g., in natural killer cells, TLR7 stimulation was reported to induce the expression of miR-744 (Voynova et al. 2015). Further related studies are being performed in our laboratory to examine and confirm these possible mechanisms of miR-484 and miR-744 action in DENV infection, using primary human cells, such as macrophages/dendritic cells, or in patients with dengue. However, further studies will be required to lend weight to this possibility and to determine whether miR-484 and miR-744 are possible therapeutic targets for all DENV serotypes, even more so if we consider that the present study was carried out in monkey cells. In summary, we propose that DENV can escape the antiviral activity of miR-484 and miR-744, downregulating their expression, and simultaneously, that miRNAs target an unknown cellular factor that promotes DENV replication. Therefore, our results imply that DENV infection modulates host miR expression for their own benefit.