Although our results suggest that miR-484 and miR-744 possess antiviral activity, we also observed that both DENV infection and the expression of the 3′ UTR of DENV RNA can downregulate miR-484 and miR-744. Although it is still not clear how DENV promotes miR-484 and miR-744 downregulation, previous findings have identified the pathway by which DENV downregulates the expression of cellular miRNAs. Indeed, NS4B from all 4 DENV serotypes appears to inhibit the processing of Dicer, a protein involved in miRNA biogenesis of dsRNA (Kakumani et al. 2013). Similar behaviour has been reported for other viral proteins such as HIV-1 Nef, a regulatory and accessory protein that interacts with the RNAi pathway protein, Ago2, thereby suppressing miRNA silencing concentrated in the multivesicular bodies where HIV-1 actively replicates (Aqil et al. 2013). Interestingly, several recent reports have provided evidence that certain non-coding RNAs may function as competing endogenous RNAs (ceRNAs) in modulating the concentration and biological functions of miRNAs. These ceRNAs generally share miR-response elements with the transcripts of several important genes and prevent these mRNAs from being degraded. In accordance with these results, it was recently proposed that HBV mRNA acts as a ceRNA for miRNA-15a to regulate TGF-signalling, which contributes to the development of HBV-related hepatocellular carcinomas (HCCs) (Liu et al. 2015). Based on these results and because it was demonstrated that the West Nile virus (WNV) sfRNA suppresses the siRNA- and miR-induced RNAi pathway (Schnettler et al. 2012), we suggest a role for DENV RNA, through its 3′ UTR or sfRNA, that would act as a sponge for the hybridisation of endogenous miRNAs, and as a potential mechanism to reduce their expression; such a mechanism was demonstrated for HBV mRNAs possessing a miR-15a/16-complementary site that acts as a sponge to bind and sequester endogenous miR-15a/16 (Liu et al. 2013).