Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas
Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas.
Am J Trop Med Hyg. 2014 Jun;90(6):993-1002. doi: 10.4269/ajtmh.13-0382. Epub 2014 Apr 7.
Junín 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.
胡宁病毒（JUNV）是阿根廷肥沃的潘帕斯草原的地方病病原体，由啮齿动物宿主 Calomys musculinus 维持，是阿根廷出血热（AHF）的病原体，其特征是血管功能障碍和液体分布异常。临床和实验研究表明内皮细胞参与了 AHF 的发病机制，尽管其作用知之甚少。已经表明 JUNV 在体外能够使内皮细胞（ECs）产生感染，而没有明显的细胞病变效应。在这项研究中，我们表明，JUNV 直接感染原代人 ECs 会导致通过电细胞基质阻抗传感和 Transwell 通透性测定测量的血管通透性增加。我们还表明，在病毒感染过程中 EC 黏附连接被破坏，这可能为内皮细胞在 AHF 发病机制中的作用提供了一些见解，也可能为其他病毒性出血热提供了一些见解。
