title: Role of the endothelium in viral hemorrhagic fevers.
abstract: OBJECTIVE
  To describe endothelial participation in the pathogenesis of viral hemorrhagic fevers and certain other acute infectious diseases.
  
  
  METHODS
  Survey of published literature on viral hemorrhagic fevers interpreted in light of observations in patients and research on those diseases.
  
  
  CONCLUSIONS
  Endothelial involvement is an extremely important factor in the clinical syndrome termed viral hemorrhagic fever. Endothelial dysfunction is important in the genesis of bleeding, which is not universal and is commonly seen only in the presence of thrombocytopenia or severe platelet dysfunction. The pathogenesis of endothelial dysfunction varies in the different diseases. In some situations, direct endothelial infection is important in increased vascular permeability, changes in the procoagulant vs. anticoagulant balance, or cytokine production. In all the viral hemorrhagic fevers studied to date, cytokine induction is an important factor and also acts on the endothelium. Poor myocardial contractility is a very important issue in viral hemorrhagic fever and is not caused by direct viral infection of the heart; it is increasingly being recognized that these patients present with low cardiac output and high peripheral resistance and that they respond poorly to fluid infusion. The clinical findings in viral hemorrhagic fever differ from those in the sepsis syndrome and should be studied and interpreted separately; this approach will sharpen therapeutic approaches and could shed light on the problems of sepsis in general.
authors: John Sealy Distinguished University Chair in Tropical and Emerging Virology, University of Texas Medical Branch, Galveston 77555-0609, USA. cjpeters@utmb.edu
authors: Clarence J
authors: CJ
authors: Peters
authors: Sherif R
authors: SR
authors: Zaki
mesh_terms: D006477:Arenaviruses, New World / Q000472:pathogenicity*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006482:Hemorrhagic Fevers, Viral / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D006801:Humans