Thromb Haemost 2009; 102(06): 1030-1041
DOI: 10.1160/TH09-09-0640
Theme Issue Article
Schattauer GmbH

Hantavirus regulation of endothelial cell functions

Erich R. Mackow
1   Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA
,
Irina N. Gavrilovskaya
2   Northport VAMC, Northport, New York, USA
› Author Affiliations
Further Information

Publication History

Received: 14 September 2009

Accepted after minor revision: 07 November 2009

Publication Date:
28 November 2017 (online)

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Summary

Hantaviruses cause two vascular permeability-based diseases and primarily infect endothelial cells which form the primary fluid barrier of the vasculature. Since hantavirus infections are not lytic, the mechanisms by which hantaviruses cause haemorrhagic fever with renal syndrome (HFRS) or Hantavirus Pulmonary Syndrome (HPS) are indeterminate. HPS is associated with acute pulmonary oedema and HFRS with moderate haemorrhage and renal sequelae, perhaps reflecting the location of vast microvascular beds and endothelial cell reservoirs available for hantavirus infection. Endothelial cells regulate capillary integrity, and hantavirus infection provides a primary means for alteing vascular permeability that contributes to pathogenesis. The central importance of endothelial cells in regulating oedema, vascular repair, angiogenesis, immune cell recruitment, platelet deposition as well as gas exchange and solute delivery suggest that a multitude of inputs and cellular responses may be influenced by hantavirus infection and contribute to pathogenic changes in vascular permeability. Here we focus on understanding hantavirus interactions with endothelial cells which are linked to vascular permeability, and provide insight into the contribution of endothelial cell responses in hantavirus pathogenesis.