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Immunopathology of highly virulent pathogens: insights from Ebola virus

Ebola virus is a highly virulent pathogen capable of inducing a frequently lethal hemorrhagic fever syndrome. Accumulating evidence indicates that the virus actively subverts both innate and adaptive immune responses and triggers harmful inflammatory responses as it inflicts direct tissue damage. Th...

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Detalles Bibliográficos
Autores principales: Zampieri, Carisa A, Sullivan, Nancy J, Nabel, Gary J
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group US 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7097212/
https://www.ncbi.nlm.nih.gov/pubmed/17952040
http://dx.doi.org/10.1038/ni1519
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author Zampieri, Carisa A
Sullivan, Nancy J
Nabel, Gary J
author_facet Zampieri, Carisa A
Sullivan, Nancy J
Nabel, Gary J
author_sort Zampieri, Carisa A
collection PubMed
description Ebola virus is a highly virulent pathogen capable of inducing a frequently lethal hemorrhagic fever syndrome. Accumulating evidence indicates that the virus actively subverts both innate and adaptive immune responses and triggers harmful inflammatory responses as it inflicts direct tissue damage. The host immune system is ultimately overwhelmed by a combination of inflammatory factors and virus-induced cell damage, particularly in the liver and vasculature, often leading to death from septic shock. We summarize the mechanisms of immune dysregulation and virus-mediated cell damage in Ebola virus–infected patients. Future approaches to prevention and treatment of infection will be guided by answers to unresolved questions about interspecies transmission, molecular mechanisms of pathogenesis, and protective adaptive and innate immune responses to Ebola virus.
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spelling pubmed-70972122020-03-26 Immunopathology of highly virulent pathogens: insights from Ebola virus Zampieri, Carisa A Sullivan, Nancy J Nabel, Gary J Nat Immunol Article Ebola virus is a highly virulent pathogen capable of inducing a frequently lethal hemorrhagic fever syndrome. Accumulating evidence indicates that the virus actively subverts both innate and adaptive immune responses and triggers harmful inflammatory responses as it inflicts direct tissue damage. The host immune system is ultimately overwhelmed by a combination of inflammatory factors and virus-induced cell damage, particularly in the liver and vasculature, often leading to death from septic shock. We summarize the mechanisms of immune dysregulation and virus-mediated cell damage in Ebola virus–infected patients. Future approaches to prevention and treatment of infection will be guided by answers to unresolved questions about interspecies transmission, molecular mechanisms of pathogenesis, and protective adaptive and innate immune responses to Ebola virus. Nature Publishing Group US 2007-10-19 2007 /pmc/articles/PMC7097212/ /pubmed/17952040 http://dx.doi.org/10.1038/ni1519 Text en © Nature Publishing Group 2007 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
Zampieri, Carisa A
Sullivan, Nancy J
Nabel, Gary J
Immunopathology of highly virulent pathogens: insights from Ebola virus
title Immunopathology of highly virulent pathogens: insights from Ebola virus
title_full Immunopathology of highly virulent pathogens: insights from Ebola virus
title_fullStr Immunopathology of highly virulent pathogens: insights from Ebola virus
title_full_unstemmed Immunopathology of highly virulent pathogens: insights from Ebola virus
title_short Immunopathology of highly virulent pathogens: insights from Ebola virus
title_sort immunopathology of highly virulent pathogens: insights from ebola virus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7097212/
https://www.ncbi.nlm.nih.gov/pubmed/17952040
http://dx.doi.org/10.1038/ni1519
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