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143 - Hemorrhagic Fevers: Endothelial Cells and Ebola-Virus Hemorrhagic Fever
- from PART III - VASCULAR BED/ORGAN STRUCTURE AND FUNCTION IN HEALTH AND DISEASE
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- By Tatiana A. Afanasieva, Institute of Physiology, Technical University, Dresden, Germany;, Victoria Wahl-Jensen, National Microbiology Laboratory, Public Health, Agency of Canada, Winnipeg, Manitoba;, University of Manitoba, Winnipeg, Manitoba, Canada;, Jochen Seebach, Institute of Physiology, Technical University, Dresden, Germany;, Herrmann Schillers, Institute of Physiology, Westfalia Wilhelms University, Muenster, Germany, Dessy Nikova, Institute of Physiology, Westfalia Wilhelms University, Muenster, Germany, Ute Ströher, National Microbiology Laboratory, Public Health, Agency of Canada, Winnipeg, Manitoba;, University of Manitoba, Winnipeg, Manitoba, Canada;, Heinz Feldmann, National Microbiology Laboratory, Public Health, Agency of Canada, Winnipeg, Manitoba;, University of Manitoba, Winnipeg, Manitoba, Canada;, Hans-Joachim Schnittler, Institute of Physiology, Technical University, Dresden, Germany;
- Edited by William C. Aird, Harvard University, Massachusetts
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- Book:
- Endothelial Biomedicine
- Published online:
- 04 May 2010
- Print publication:
- 03 September 2007, pp 1311-1319
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Summary
Viral hemorrhagic fever (VHF) is a severe multiorgan disease with strong immune involvement and diffuse vascular dysregulation, particularly of the vascular endothelium. Several families of RNA viruses are regularly associated with a VHF syndrome in humans: Arenaviridae (Lassa virus, Machupo virus, Junin virus, Guanarito virus, and Sabia virus), Bunyaviridae (Rift Valley fever virus, Crimean-Congo hemorrhagic fever virus, hantaviruses), Flaviviridae (Yellow fever virus, Dengue virus, Omsk hemorrhagic fever virus, and Kyasanur forest disease virus), and Filoviridae (Marburg virus and Ebola virus). The clinical manifestations of VHF vary and are dependent on the causative agent (see CDC homepage http://www.cdc.gov). However, some common clinical features include fever, various degrees of vascular dysregulation with bleeding tendency and shock development, and the vascular endothelium seems to be affected in most cases (1–3). Some of the VHF-causing pathogens target the endothelium directly, whereas others induce primarily indirect alterations through proinflammatory mediators released from infected target cells (e.g., monocytes/macrophages). Marburg (MARV) and Ebola viruses (EBOV) cause the most severe form of VHF and, thus, serve as important model pathogens for studying the pathogenesis and management of VHFs. Filoviruses, as well as some other hemorrhagic fever (HF) viruses, are biological safety level 4 (BSL4) agents, which somewhat complicates investigations. Filoviruses seem to target both the vascular system and the immune system, leading to the opinion that filovirus HF fever is a vascular disease as well as an immune syndrome (2–5). Although our understanding of the molecular mechanisms of VHF pathogenesis is still limited, some important scientific achievements have been made in the past decade.
12 - Structure and function of the proteins of Marburg and Ebola viruses
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- By Hans-Dieter Klenk, Institut für Virologie, Philipps-Universität Marburg, Postfach 2360, 35011 Marburg, Germany, Heinz Feldmann, Institut für Virologie, Philipps-Universität Marburg, Postfach 2360, 35011 Marburg, Germany, Viktor E. Volchkov, Institut für Virologie, Philipps-Universität Marburg, Postfach 2360, 35011 Marburg, Germany, Valentian A. Volchkova, Institut für Virologie, Philipps-Universität Marburg, Postfach 2360, 35011 Marburg, Germany, Winfried Weissenhorn, European Molecular Biology Laboratory (EMBL) Grenoble Outstation, 6 rue Jules Horowitz, 38000, Grenoble, France
- Edited by G. L. Smith, Imperial College of Science, Technology and Medicine, London, W. L. Irving, University of Nottingham, J. W. McCauley, Institute for Animal Health, Compton, Berkshire, D. J. Rowlands, University of Leeds
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- Book:
- New Challenges to Health
- Published online:
- 06 July 2010
- Print publication:
- 19 April 2001, pp 233-246
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Summary
INTRODUCTION
Filoviruses cause fulminant haemorrhagic fever in humans and non-human primates, killing up to 90 % of the infected patients. Since the discovery of Marburg virus (MBGV) in 1967 and the emergence of Ebola virus (EBOV), its better known cousin, a few years later, these infections have therefore been a matter of high public and scientific concern. Although it is clear from the recorded history of filovirus outbreaks that all of them have so far been self-limiting and that the total number of human infections hitherto documented scarcely exceeds a thousand cases, EBOV by now ranges among the most ill-famed human viruses. For a long time, research on filoviruses has been impeded by their high pathogenicity, but with the advent of recombinant DNA technology our knowledge of the genome structures and the replication strategies of these agents has increased significantly.
PATHOPHYSIOLOGY OF FILOVIRUS INFECTIONS
The pathophysiological changes that make filovirus infections so devastating are just beginning to be unravelled. Pathogenesis in fatal infections in human and non-human primates is similar, suggesting the primate system is a reasonable model for studying filovirus haemorrhagic fever (Simpson et al., 1968; Murphy et al., 1971; Ellis et al., 1978; Fisher- Hoch et al., 1985; Ryabchikova et al., 1994). Clinical and biochemical findings support the anatomical observations of extensive liver involvement, renal damage, changes in vascular permeability, including endothelial damage, and activation of the clotting cascade. The visceral organ necrosis is a consequence of virus replication in parenchymal cells. However, no organ, not even the liver, shows sufficient damage to account for death.
Fluid distribution problems and platelet abnormalities are dominant clinical manifestations, reflecting damage of endothelial cells and decrease of platelets.