Avirutnan P, Malasit P, Seliger B, Bhakdi S, Husmann M
Institute of Medical Microbiology and Hygiene, Johannes Gutenberg University, Mainz, Germany.
J Immunol. 1998 Dec 1;161(11):6338-46.
Dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS) are severe complications of secondary dengue virus (DV) infection. Vascular leakage, hemorrhagic diathesis and complement activation are the hallmarks of the disease. The short-lived nature of the plasma leakage syndrome has led to the conclusion that altered permeability is most likely effected by a soluble mediator. In the present study, we show that infection of human endothelial cells with DV induces the transcriptional up-regulation and secretion of RANTES and IL-8 and, in the presence of anti-dengue Abs, the formation of nonlytic complement complexes. Extremely high levels of IL-8 were detected in plasma and pleural fluid samples from patients with DSS. Furthermore, DV infection of endothelial cells in vitro caused apoptosis. Complement activation, chemokine induction, and apoptotic cell death may act in concert to cause the fulminant but short-lived vascular leakage that is characteristic of DHF/DSS.
登革出血热和登革休克综合征（DHF/DSS）是继发性登革病毒（DV）感染的严重并发症。血管渗漏、出血素质和补体激活是该疾病的特征。血浆渗漏综合征的短暂性导致了这样的结论，即通透性改变很可能是由一种可溶性介质引起的。在本研究中，我们表明用DV感染人内皮细胞会诱导RANTES和IL-8的转录上调和分泌，并且在存在抗登革热抗体的情况下，会形成非溶细胞性补体复合物。在DSS患者的血浆和胸水样本中检测到极高水平的IL-8。此外，体外DV感染内皮细胞会导致细胞凋亡。补体激活、趋化因子诱导和凋亡性细胞死亡可能共同作用，导致DHF/DSS所特有的暴发性但短暂的血管渗漏。
