The pathogenesis mechanism of severe DHF/DSS with DENV infection is not well understood, but evidence suggests that the magnitude of DENV replication and its regulation of innate and adaptive immunity may both contribute [34] . The incidence of DHF/DSS is higher in people with previous exposure to different serotypes of DENV, and antibody-dependent enhancement (ADE) may be a mechanism for DHF/DSS [1] . Enhancing antibodies may increase viral entry and increase the number of infected cells. DENV infection via the ADE route has also been shown to downregulate several genes of the innate immunity system, resulting in suppression of the innate response and increase of DENV replication [35, 36, 37] . In this study, we further demonstrate that DENV per se is a weak cytokine inducer because IL-10, IL-12, and TNFa were induced to a lower extent in DENV-2infected BMDCs. Furthermore, even in the absence of enhancing antibody, DENV could block NF-kB activation and cytokine induction triggered by TLR signaling. Downregulation of the cytokine system may provide a growth advantage for DENV to propagate in host macrophages and DCs.