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Endothelial cell function alteration after Junin virus infection

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
DOI: http://dx.doi.org/10.1160/TH02-09-0043
Issue: 2003: 90/2 (Aug) pp. 163-366
Pages: 326-334

Endothelial cell function alteration after Junin virus infection

Ricardo Martin Gomez (2) , Roberto Gabriel Pozner (1), Maria Angela Lazzari (1) , Lina Paola D’Atri (1) , Soledad Negrotto (1) , Ana Marisa Chudzinski-Tavassi (3) , María Isabel Berría (2) , Mirta Schattner (1)
(1) Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina (2) Department of Microbiology, Faculty of Medicine, University of Buenos Aires

Summary

Hematologic involvement is the main feature of Argentine hemorrhagic fever (AHF), an endemo-epidemic disease caused by Junin virus (JV). Since endothelial dysfunction could play a role in AHF-altered hemostasis, we studied human umbilical vein endothelial cell (HUVEC) infection with a virulent (JVv) and a non-virulent (JVa) JV strain. Cells were infected by the two JV variants with no detectable apoptosis or cytopathic effect. Both viral variants up-regulated ICAM-1 and VCAM-1 levels, while von Willebrand factor (VWF) production was decreased. Prostacyclin (PGI2 ) release and decay accelerating factor (DAF) expression were greater in JVv- than in JVa-infect-ed or control cells. Furthermore, nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) expression was only raised in JVv-infected supernatants. Significant NO and PGI2 values were also detected in AHF patient sera. These data demonstrate that endothelial cell responses are triggered subsequently by JV infection, suggesting that such alterations play a major role in the pathogenesis of AHF and perhaps in other viral-induced hemorrhagic diseases.