Endothelial Cell Permeability and Adherens Junction Disruption Induced by Junin Virus Infection
Endothelial Cell Permeability and Adherens Junction Disruption Induced by Junin Virus Infection
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DOI：
10.4269/ajtmh.13-0382
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发表时间：
2014-06-01
影响因子：
3.3
通讯作者：
Peters, Clarence J.
中科院分区：
文献类型：
--
作者：
Lander, Heather M.;Grant, Ashley M.;Peters, Clarence J.
Junin病毒（JUNV）是阿根廷肥沃的潘帕斯草原上的一种特有病毒，由啮齿动物宿主Calomys musculinus维持在自然界中，是阿根廷出血热（AHF）的病原体，其特征是血管功能障碍和体液分布异常。临床和实验研究暗示内皮细胞参与AHF的发病机制，尽管对其作用知之甚少。JUNV已被证明在体外导致内皮细胞（ECs）的生产性感染，而没有明显的细胞病变效应。在这项研究中，我们发现JUNV直接感染原代人内皮细胞导致血管通透性增加，这是通过细胞底物阻抗传感和透井渗透性测定来测量的。我们还发现EC粘附连接在病毒感染期间被破坏，这可能为内皮在AHF发病机制中的作用以及可能的其他病毒性出血热的发病机制提供洞见。
Junin virus (JUNV) is endemic to the fertile Pampas of Argentina, maintained in nature by the rodent host Calomys musculinus, and the causative agent of Argentine hemorrhagic fever (AHF), which is characterized by vascular dysfunction and fluid distribution abnormalities. Clinical as well as experimental studies implicate involvement of the endothelium in the pathogenesis of AHF, although little is known of its role. JUNV has been shown to result in productive infection of endothelial cells (ECs) in vitro with no visible cytopathic effects. In this study, we show that direct JUNV infection of primary human ECs results in increased vascular permeability as measured by electric cell substrate impedance sensing and transwell permeability assays. We also show that EC adherens junctions are disrupted during virus infection, which may provide insight into the role of the endothelium in the pathogenesis of AHF and possibly, other viral hemorrhagic fevers.