During severe infection, immature DENV particles are recognized by TLR2 (Toll-like Receptor 2) and DC-SIGN (Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin) on monocytes and immature dendritic cells, resulting in the release of inflammatory mediators like IL-1β (interleukin 1β) and TNF-α (tumour necrosis factor α), which increase endothelial cell permeability or dysfunction, contributing towards severe complications (30, 31). Here, TLR2 is linked to infection.