Roles for endothelial cells in dengue virus infection.
Roles for endothelial cells in dengue virus infection.
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DOI：
10.1155/2012/840654
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发表时间：
2012
影响因子：
2.2
通讯作者：
Mackow ER
中科院分区：
文献类型：
--
作者：
Dalrymple NA;Mackow ER
登革热病毒导致两种严重的疾病，改变血管液体屏障功能，登革出血热(DHF)和登革休克综合征(DSS)。内皮是血管系统的主要液体屏障，最终导致毛细血管渗漏的登革病毒感染影响内皮细胞(EC)屏障功能。登革热病毒感染内皮细胞的能力为登革热提供了改变毛细血管通透性、允许病毒复制和诱导免疫细胞向内皮细胞募集的反应的直接手段。最近关于登革热病毒感染原代内皮细胞的研究表明，内皮细胞可以有效地感染，迅速产生病毒后代，并诱导免疫增强的细胞因子反应，这可能参与了发病机制。此外，感染的内皮细胞还与增强小鼠登革热模型中的病毒血症和免疫病理机制有关。因此，感染登革热的内皮细胞有可能直接促进免疫增强、毛细血管通透性、病毒血症和内皮细胞的免疫靶向。这些效应表明感染的内皮细胞在登革热发病机制中的反应，并使内皮细胞和EC反应的治疗靶点合理化，以此作为降低登革热病毒疾病严重程度的手段。
Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). The endothelium is the primary fluid barrier of the vasculature and ultimately the effects of dengue virus infection that cause capillary leakage impact endothelial cell (EC) barrier functions. The ability of dengue virus to infect the endothelium provides a direct means for dengue to alter capillary permeability, permit virus replication, and induce responses that recruit immune cells to the endothelium. Recent studies focused on dengue virus infection of primary ECs have demonstrated that ECs are efficiently infected, rapidly produce viral progeny, and elicit immune enhancing cytokine responses that may contribute to pathogenesis. Furthermore, infected ECs have also been implicated in enhancing viremia and immunopathogenesis within murine dengue disease models. Thus dengue-infected ECs have the potential to directly contribute to immune enhancement, capillary permeability, viremia, and immune targeting of the endothelium. These effects implicate responses of the infected endothelium in dengue pathogenesis and rationalize therapeutic targeting of the endothelium and EC responses as a means of reducing the severity of dengue virus disease.