Activated TLR3 triggered the production of proinflammatory cytokines during ZIKV infection, which upregulated the STAT3 pathway and reduced the STAT1 phosphorylation in a suppressor of cytokine signaling (SOCS)-3 dependent manner, thereby inhibiting interferon response triggered by RIG-I-like receptors (RLR) and reducing the antiviral effect (139). Here, TLR3 is linked to Zika virus infectious disease.