DENV is believed to cross the blood-brain barrier (BBB) through infection of endothelial cells or a “Trojan horse” mechanism, where infected monocytes or dendritic cells act as vectors into the CNS.18 Once in the CNS, viral replication can lead to neuronal dysfunction primarily through mechanisms like oxidative stress and excitotoxicity.19 The excessive release of pro-inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-6, and interferon-gamma, is central to neuroinflammation during dengue infection. The gene discussed is IL6; the disease is infection.