It has been proposed that during DENV infection IPS-1 may be responsible for controlling early viral replication and type I IFN production [47] , while the IFN signaling pathway (JAK/STAT) may control late viral replication and type I IFN production in DENV infected cells [48] . It is possible that interactions between STING and IPS-1 [46] may be disrupted by the DENV NS2B3 targeting of STING. This mayinhibit type I IFN production early during DENV infection in susceptible cells, although the NS2B3 has not been shown to directly interact with IPS-1. Further experiments are required to understand these complex interplays between different signaling molecules in human primary cells infected with DENV. Our experiments demonstrate that primary human cells implicated in dengue virus infection, such as dendritic cells, macrophages, monocytes and B cells can support DENV replication, although at different levels. Interestingly, DENV infection did not induce type I IFN production in any of those human primary cells tested (Figure 8) . These different blood cells may play different roles during DENV infection in humans, such as being involved in the initial infection or in the final stage of viremia. Also, since the mouse models that support DENV replication and recapitulate dengue symptoms are deficient in type I IFN responses or are reconstituted with human immune cells [6, 49] , the inhibition of type I IFN in infected cells seems to be crucial for the establishment of infection by DENV. Our data on different cells from blood also show that the inhibition of type I IFN production by DENV is not a DC specific phenomenon ( Figure 8) .