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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Vydáno v:	Seminars in immunopathology Ročník 39; číslo 5; s. 551 - 561
Hlavní autor:	Basler, Christopher F.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Berlin/Heidelberg Springer Berlin Heidelberg 01.07.2017 Springer Nature B.V
Témata:	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
On-line přístup:	Získat plný text
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Popis
Shrnutí:	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.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23
ISSN:	1863-2297 1863-2300 1863-2300
DOI:	10.1007/s00281-017-0637-x