Fig. 2

Pathophysiology of Dengue-Induced Inflammation and Shock. The pathophysiological mechanisms triggered by Dengue virus infection that lead to inflammation and potentially to cytokine storm and shock. Upon infection, the virus activates platelets and monocytes, leading to the release of inflammatory cytokines (IL-6, IL-10, IL-12, IL-18) and TNF-α. Macrophages produce nitric oxide, while mast cells release VEGF and secretory Phospholipase A2 (sPLA2). These mediators contribute to endothelial activation and NF-κB production, further promoting inflammation. The combined effects result in increased vascular permeability (plasma leakage), contributing to the development of shock