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Pathogenesis of the viral hemorrhagic fevers.

Authors
  • Paessler, Slobodan
  • Walker, David H
Type
Published Article
Journal
Annual Review of Pathology Mechanisms of Disease
Publisher
Annual Reviews
Publication Date
Jan 24, 2013
Volume
8
Pages
411–440
Identifiers
DOI: 10.1146/annurev-pathol-020712-164041
PMID: 23121052
Source
Medline
License
Unknown

Abstract

Four families of enveloped RNA viruses, filoviruses, flaviviruses, arenaviruses, and bunyaviruses, cause hemorrhagic fevers. These viruses are maintained in specific natural cycles involving nonhuman primates, bats, rodents, domestic ruminants, humans, mosquitoes, and ticks. Vascular instability varies from mild to fatal shock, and hemorrhage ranges from none to life threatening. The pathogenic mechanisms are extremely diverse and include deficiency of hepatic synthesis of coagulation factors owing to hepatocellular necrosis, cytokine storm, increased permeability by vascular endothelial growth factor, complement activation, and disseminated intravascular coagulation in one or more hemorrhagic fevers. The severity of disease caused by these agents varies tremendously; there are extremely high fatality rates in Ebola and Marburg hemorrhagic fevers, and asymptomatic infection predominates in yellow fever and dengue viral infections. Although ineffective immunity and high viral loads are characteristic of several viral hemorrhagic fevers, severe plasma leakage occurs at the time of viral clearance and defervescence in dengue hemorrhagic fever.

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