To study the effect of DENV-2 on modulating innate immune response, we determined the levels of type I IFN and cytokines in DENV-2-infected mouse BMDCs by quantitative RT-PCR. The TLR3 ligand polyI:C and the TLR9 ligand CpG greatly stimulated the mRNA expression of IFN-b (124-fold induction at 2 h by polyI:C and 531-fold induction at 6 h by CpG), IL-10 (77-fold at 12 h by polyI:C and 74-fold at 36 h by CpG), IL-12p40 (381-fold at 24 h by polyI:C and 1551-fold at 6 h by CpG), and TNFa (64-fold at 2 h by polyI:C and 180-fold at 6 h by CpG) ( Figure 1A -D, left panels). However, levels of IFN-b and these cytokines were much lower in cells with DENV-2 infection (Figure 1 , left and right panels): especially, IL-10 was not induced by DENV-2 infection. The kinetic of DENV-2 replication in BMDCs was measured by qPCR with primers specific for DENV-2 59-UTR ( Figure 1E ) and by immunofluorescence staining with antibody specific against DENV-2 NS3 ( Figure 1F ). DENV-2 replication peaked around 12-24 h post infection, in consistence with cytokine induction peaked around 12-36 h post infection. Therefore, infection with DENV-2 inefficiently triggered type I IFN expression and that of other cytokines. Since DENV-2 infection would produce intracellular viral RNA to turn on RLR and TLR signaling cascades for cytokine production, weak induction of DENV-2 for these cytokine genes ( Figure 1 ) implies that DENV-2 may interfere with a common signaling pathway for inducing type I IFN and other inflammatory cytokines.