Endothelial cell function alteration after Junin virus infection

Ricardo Martin Gomez; Roberto Gabriel Pozner; Maria Angela Lazzari; Lina Paola D’Atri; Soledad Negrotto; Ana Marisa Chudzinski-Tavassi; María Isabel Berría; Mirta Schattner

doi:10.1160/TH02-09-0043

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 2003; 90(02): 326-334
DOI: 10.1160/TH02-09-0043

Wound Healing and Inflammation/Infection

Schattauer GmbH

Endothelial cell function alteration after Junin virus infection

Ricardo Martin Gomez^*

²Department of Microbiology, Faculty of Medicine, University of Buenos Aires, CONICET, Argentina

,

Roberto Gabriel Pozner^*

¹Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina

,

Maria Angela Lazzari

¹Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina

,

Lina Paola D’Atri

¹Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina

,

Soledad Negrotto

¹Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina

,

Ana Marisa Chudzinski-Tavassi

³Laboratory of Biochemistry and Biophysics, Butantan Institute, São Paulo, Brazil

,

María Isabel Berría

²Department of Microbiology, Faculty of Medicine, University of Buenos Aires, CONICET, Argentina

,

Mirta Schattner

¹Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina

› Institutsangaben

Abstract

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-infected 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.

Keywords

Cell adhesion molecules - von Willebrand factor - prostacyclin - nitric oxide

Volltext

Referenzen

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