Thromb Haemost 2009; 102(06): 1024-1029
DOI: 10.1160/TH09-06-0357
Theme Issue Article
Schattauer GmbH

The role of the vascular endothelium in arenavirus haemorrhagic fevers

Stefan Kunz
1   Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland
› Author Affiliations
Further Information

Publication History

Received: 08 June 2009

Accepted after minor revision: 13 August 2009

Publication Date:
28 November 2017 (online)

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Summary

Viral haemorrhagic fevers (VHF) caused by arenaviruses are among the most devastating emerging human diseases.The most important pathogen among the arenaviruses is Lassa virus (LASV), the causative agent of Lassa fever that is endemic to West Africa. On the South American continent, the New World arenavirus Junin virus (JUNV), Machupo (MACV), Guanarito (GTOV), and Sabia virus (SABV) have emerged as causative agents of severe VHFs. Clinical and experimental studies on arenavirus VHF have revealed a crucial role of the endothelium in their pathogenesis. However, in contrast to other VHFs, haemorrhages are not a salient feature of Lassa fever and fatal cases do not show overt destruction of vascular tissue.The functional alteration of the vascular endothelium that precede shock and death in fatal Lassa fever may be due to more subtle direct or indirect effects of the virus on endothelial cells. Haemorrhagic disease manifestations and vascular involvement are more pronounced in the VHF caused by the South American haemorrhagic fever viruses. Recent studies on JUNV revealed perturbation of specific endothelial cell function, including expression of cell adhesion molecules, coagulation factors, and vasoactive mediators as a consequence of productive viral infection.These studies provided first possible links to some of the vascular abnormalities observed in patients; however, their relevance in vivo remains to be investigated.