University of Massachusetts Medical School, Center for Infectious Diseases and Vaccine Research, Worcester, MA 01655-0002, USA.
Thromb Haemost. 2009 Dec;102(6):1042-9. doi: 10.1160/TH09-03-0208.
Dengue viruses (DENV), a group of four serologically distinct but related flaviviruses, are the cause of one of the most important emerging viral diseases. DENV infections result in a wide spectrum of clinical disease including dengue haemorrhagic fever (DHF), a viral haemorrhagic disease characterised by bleeding and plasma leakage. The characteristic feature of DHF is the transient period of plasma leakage and a haemorrhagic tendency. DHF occurs mostly during a secondary DENV infection. Serotype cross-reactive antibodies and mediators from serotype cross-reactive Dengue-specific T cells have been implicated in the pathogenesis. A complex interaction between virus, host immune response and endothelial cells likely impacts the barrier integrity and functions of endothelial cells leading to plasma leakage. Recently the role of angiogenic factors and the role of dengue virus on endothelial cell transcription and functions have been studied. Insights into the mechanisms that confer protection or cause disease are critical in the development of prophylactic and therapeutic modalities for this important disease.
登革病毒（DENV）属于黄病毒科黄病毒属，为 4 种血清型相关但血清学不同的虫媒病毒，是最重要的新发病毒性疾病之一。登革病毒感染可引起广泛的临床疾病，包括登革出血热（DHF），这是一种以出血和血浆渗漏为特征的病毒性出血性疾病。DHF 的特征是短暂的血浆渗漏和出血倾向。DHF 主要发生在二次登革病毒感染期间。血清型交叉反应性抗体和来自血清型交叉反应性登革特异性 T 细胞的介质被认为与发病机制有关。病毒、宿主免疫反应和内皮细胞之间的复杂相互作用可能会影响内皮细胞的屏障完整性和功能，导致血浆渗漏。最近，血管生成因子的作用以及登革病毒对内皮细胞转录和功能的作用已经得到研究。了解赋予保护或导致疾病的机制对于开发这种重要疾病的预防和治疗方法至关重要。
