Pathogenesis of vascular leak in dengue virus infection.

摘要: Endothelial dysfunction leading to vascular leak is the hallmark of severe dengue. Vascular typically becomes clinically evident 3-6 days after onset illness, which known as critical phase. This phase follows period peak viraemia, and lasts for 24-48 hr usually shows rapid complete reversal, suggesting that it likely occur a result inflammatory mediators, rather than infection endothelium. Cytokines such tumour necrosis factor-α, are be elevated in dengue, contributing factors. Dengue NS1, soluble viral protein, has also been shown disrupt endothelial glycocalyx thus contribute leak, although there appears discordance between timing NS1 antigenaemia occurrence leak. In addition, many lipid mediators acute dengue platelet activating factor (PAF) leukotrienes. Furthermore, other growth angiopoietin-2 have patients with haemorrhagic fever, exerting their action part by inducing activity phospholipases, diverse effects including generation PAF. Platelets significantly production interleukin-1β through activation NLRP3 inflammasome cytokines monocytes. Drugs block down-stream immunological mediator pathways PAF may beneficial treatment disease.