It is becoming increasingly clear that STING is a crucial adaptor in immune cells after infection with different viruses, such as HIV and DENV, among others [35, 45, 46] . These viruses require activation of their target cells in order to establish infection, or in the case of DENV to induce viremia in the host. Nevertheless, all viruses need to limit or inhibit the production of type I IFN in infected cells to avoid the establishment of an antiviral state in those cells. STING could be instrumental in these types of virus infections, since it can discriminate between the induction of type I IFN and the activation of the NFkB pathway. Along those lines, this report shows a novel mechanism of inhibition of IFN production by an RNA virus, namely DENV targeting STING. By inhibiting only type I IFN but not the NF-kB pathway, DENV induces a specific profile in infected human MDDCs and other susceptible primary cells that allow the virus to efficiently reach the lymph nodes and spread in the infected host, culminating in the production of viremia. All our experiments were performed in the context of primary infections with DENV, since we believe that the early events in primary infections dictate the quality of adaptive immune responses and the outcome of the infection. By targeting DCs and inhibiting the production of type I IFN in those cells, DENV may be able to efficiently modulate the generation of adaptive immune responses and establish infection in the host [24, 25] .