Molecular pathogenesis of viral hemorrhagic fever

The clinical syndrome referred to as viral hemorrhagic fever (VHF) can be caused by several different families of RNA viruses, including select members of the arenaviruses, bunyaviruses, filoviruses, and flaviviruses. VHF is characterized by malaise, fever, vascular permeability, decreased plasma vo...

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Veröffentlicht in:Seminars in immunopathology Jg. 39; H. 5; S. 551 - 561
1. Verfasser: Basler, Christopher F.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Berlin/Heidelberg Springer Berlin Heidelberg 01.07.2017
Springer Nature B.V
Schlagworte:
Adaptive Immunity
Animal models
Animals
Antigen-presenting cells
Biomarkers
Biomedical and Life Sciences
Biomedicine
Blood Coagulation - immunology
Capillary Permeability - immunology
Coagulation
Cytokines
Cytokines - metabolism
Dendritic cells
Disease Susceptibility
Ebola virus
Epidemics
Hemorrhage
Hemorrhagic fever
Hemorrhagic Fevers, Viral - immunology
Hemorrhagic Fevers, Viral - metabolism
Hemorrhagic Fevers, Viral - virology
Host-Pathogen Interactions - genetics
Host-Pathogen Interactions - immunology
Humans
Immunity, Innate
Immunology
Inflammation
Inflammation Mediators - metabolism
Internal Medicine
Lassa fever
Leakage
Macrophages
Molecular modelling
Monocytes
Pathogenesis
Permeability
Replication
Review
RNA viruses
T cell receptors
Viruses
Ebola virus
Hemorrhagic fever
yellow fever virus
Lassa virus
ISSN:1863-2297, 1863-2300, 1863-2300
Online-Zugang:Volltext
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Zusammenfassung:The clinical syndrome referred to as viral hemorrhagic fever (VHF) can be caused by several different families of RNA viruses, including select members of the arenaviruses, bunyaviruses, filoviruses, and flaviviruses. VHF is characterized by malaise, fever, vascular permeability, decreased plasma volume, coagulation abnormalities, and varying degrees of hemorrhage. Study of the filovirus Ebola virus has demonstrated a critical role for suppression of innate antiviral defenses in viral pathogenesis. Additionally, antigen-presenting cells are targets of productive infection and immune dysregulation. Among these cell populations, monocytes and macrophages are proposed to produce damaging inflammatory cytokines, while infected dendritic cells fail to undergo proper maturation, potentially impairing adaptive immunity. Uncontrolled virus replication and accompanying inflammatory responses are thought to promote vascular leakage and coagulopathy. However, the specific molecular pathways that underlie these features of VHF remain poorly understood. The arenavirus Lassa virus and the flavivirus yellow fever virus exhibit similar molecular pathogenesis suggesting common underlying mechanisms. Because non-human primate models that closely mimic VHF are available for Ebola, Lassa, and yellow fever viruses, we propose that comparative molecular studies using these models will yield new insights into the molecular underpinnings of VHF and suggest new therapeutic approaches.
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ISSN:1863-2297
1863-2300
1863-2300
DOI:10.1007/s00281-017-0637-x