Journal
AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
Volume 90, Issue 6, Pages 993-1002Publisher
AMER SOC TROP MED & HYGIENE
DOI: 10.4269/ajtmh.13-0382
Keywords
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Funding
- Department of Pathology, University of Texas Medical Branch
- National Institutes of Health [T32 AI060549]
- John Sealy Foundation, University of Texas Medical Branch
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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.
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