Investigations into endothelial cell permeability and adherens junction disruption induced by Junín virus infection.

Junín virus is found in the fertile Pampas of Argentina and is maintained in nature by the rodent host, Calomys musculinus. Junín is the causative agent of Argentine hemorrhagic fever (AHF) characterized by vascular dysfunction and fluid distribution abnormalities. Clinical, as well as experimental studies, have implicated involvement of the endothelium in pathogenesis of AHF, although the role it may play is poorly understood. Junín virus has been shown to produce productive infection of endothelial cells in vitro with no visible cytopathic effects which provides a unique opportunity to study the cells while they are infected. Here, we show that direct Junín virus infection of primary human endothelial cells (EC) corresponds to increased vascular permeability as measured by electric cell-substrate impedance sensing (ECIS) and transwell assays. We also show that EC adherens junctions are disrupted during infection which may provide insight into the role of the endothelium in the pathogenesis of AHF and possibly other viral hemorrhagic fevers (VHFs).