As shown in figure 5 , the lack of STING cleavage was sufficient to increase the expression of type I IFN in MEFs infected with DENV. To validate these results in primary human cells, we transduced MDDCs from three different donors with the STINGexpressing lentiviruses and the GFP-only control ( Figure 5G ). STING transduced DCs were then infected with DENV-2 at an MOI of 5 and we assessed the production of IFNb in those cells. As shown in Figure 6A (showing one representative donor out of three), there were no significant differences between the levels of STING-WT and STING-MUT mRNA. This demonstrates that any difference in antiviral effect observed with the two different versions of STING is independent of the expression levels for these proteins. Upon DENV-2 infection, DCs expressing STING-MUT produced higher levels of IFNb when compared with STING-WT or GFP controls (showing statistical significance at 2 and 12 hpi). The induction of IFNb messenger RNA was detected as early as 2 hpi, which is in agreement with the results described with MEFs ( Figures 4, 5 and 6B ). These data confirm that detection of DENV infection by DCs takes place at early times post infection and that STING cleavage by DENV NS2B3 is fundamental to inhibit the signaling mediated by this adaptor in human cells. We next measured DENV replication kinetics and we found that viral RNA levels were significantly lower in DCs over-expressing STING-MUT when compared with STING-WT and GFP control ( Figure 6C ). Suggesting that the inability of DENV to cleave mutant STING and inhibit the induction of type I IFN has a direct impact on its replication kinetic and the accumulation of viral RNA in those cells.