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*
2   Department of Microbiology, Faculty of Medicine, University of Buenos Aires, CONICET, Argentina
,
Roberto Gabriel Pozner*
1   Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina
,
Maria Angela Lazzari
1   Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina
,
Lina Paola D’Atri
1   Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina
,
Soledad Negrotto
1   Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina
,
Ana Marisa Chudzinski-Tavassi
3   Laboratory of Biochemistry and Biophysics, Butantan Institute, São Paulo, Brazil
,
María Isabel Berría
2   Department of Microbiology, Faculty of Medicine, University of Buenos Aires, CONICET, Argentina
,
Mirta Schattner
1   Department of Thrombosis and Hemostasis, Hematological Research Institute, National Academy of Medicine, National Research Council (CONICET), Buenos Aires, Argentina
› Author Affiliations

Financial support: This work was supported by grants from the René Baron Foundation, CONICET, SECyT, ministry of Health and Antorchas Foundation. *Ricardo Martin Gomez and Roberto Gabriel Pozner contributed equally to this work.
Further Information

Publication History

Received 09 September 2002

Accepted after revision 12 May 2003

Publication Date:
06 December 2017 (online)

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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.

* Ricardo Martin Gomez and Roberto Gabriel Pozner contributed equally to this work.