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, Table of Contents

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

Authors

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

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

Full Text

References

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