Endothelial Cell Permeability and Adherens Junction Disruption Induced by Junín Virus Infection

Heather M. Lander Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas

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Ashley M. Grant Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas

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Thomas Albrecht Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas

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Terence Hill Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas

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Clarence J. Peters Departments of Pathology and Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas

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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.

Author Notes

* Address correspondence to Heather M. Lander, Sealy Center for Structural Biology and Molecular Biophysics, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555. E-mail: hmlander@utmb.edu

Financial support: This work was supported by the Department of Pathology, University of Texas Medical Branch; National Institutes of Health Biodefense Training Grant T32 AI060549; and the John Sealy Foundation, University of Texas Medical Branch.

Authors' addresses: Heather M. Lander, Sealy Center for Structural Biology and Molecular Biophysics, University of Texas Medical Branch, Galveston, TX, E-mail: hmlander@utmb.edu. Ashley M. Grant, United States Department of Defense, Washington, DC, E-mail: ashleymariegrant@gmail.com. Thomas Albrecht, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, E-mail: talbrecht731@yahoo.com. Terence Hill, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, E-mail: tehill@utmb.edu. Clarence J. Peters, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, E-mail: cjpeters@utmb.edu.

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