Fig. 1

Monocytes participate in inflammation and viral propagation and produce TNF-α upon JEV infection. (1) TNF-α is implicated in the activation and differentiation of monocytes as well as (2) the expression of adhesion molecules on endothelial cell surface constituting the BBB which participates in (3) the transmigration of inflammatory monocytes through the BBB. (4) In the brain, inflammatory monocytes, macrophages, microglia and neuronal cells contribute to viral propagation and neuroinflammation. (5) TNF-α and CCL2 lead to microglial activation and astrocytic expansion. (6) Ultimately, neuronal cell death results of direct cytotoxicity of JEV and indirect effects of inflammatory mediators. (in black) Chemokines (CCL2) and pattern recognition receptors (TLR3, TLR7) inhibit cellular and virus neuroinvasion and miRNAs (miR-155b, miR-146a) suppress microglia-derived inflammatory responses during JE. (in red) Promising therapeutic candidates inhibit neuroinflammation in JE