Figure 1.

Events of immune response during Dengue virus (DENV) infection and DENV-antibody-dependent enhancement (ADE) infection. (A) DENV infection: (a) upon viral entry, pattern recognizing receptor (PRR) signaling activates RIG-1 and MDA-5, (b) IFN-α/β are produced, (c) NO production is upregulated, (d) phosphorylation of STAT1 is reduced, and (e) less viral progeny is produced. (B) DENV-ADE infection: (1) virus-antibody immune complex binds to FcγR and is trafficked inside the cell; (2) PRR signaling is not involved and RIG-1 and MDA-5 are suppressed; (3) IFN-α/β production is inhibited, (4) negative regulation of DAK and Atg5–Atg12; (5) disrupts the RIG-I/MDA-5 (PRRs) signaling cascade; (6) enhanced expression of p65 of NF-κB and degradation of I κB resulted in elevated levels of IL-6, IL-8, IL-1β, and TNF-α (pro-inflammatory cytokines); (7) IL-10 secretion enhances SOCS-3 and SOCS-1; (8) in turn attenuates STAT1 phosphorylation; (9) downregulation of IL-12 and IFN-γ; (10) NO production is suppressed; (11) autophagy is increased; and (12) more viral progeny is produced.