To determine STING's impact on DENV replication in primary human MDDCs, we used RNA interference (RNAi) to silence its endogenous expression. A decrease of STING mRNA level was observed when specific siRNAs were used compared to two scrambled control siRNAs ( Figure 7A ). As expected, the previously observed upregulation of STING after DENV infection was controlled by the STING siRNAs ( Figure 7A ). As a consequence, the reduction in STING expression resulted in an increase of DENV replication, illustrated in Figure 7B . When the viral progeny released by those infected MDDCs was quantified by plaque assay, the six donors treated with STING specific siRNA, showed viral production under this experimental conditions, however when scrambled siRNA was used, only three out of the six donors released detectable viral progeny in the supernatant ( Figure 7C ). Data shown in figures 7A and 7B correspond to donor 4 in figure 7C . Taken together, these data confirm that STING is a crucial restriction factor of DENV replication in human dendritic cells, since its silencing increases the levels of DENV replication in those cells.