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Immunopathogenesis of 2009 pandemic influenza
Three years after the pandemic, major advances have been made in our understanding of the innate and adaptive immune responses to the influenza A(H1N1)pdm09 virus and those responses’ contribution to the immunopathology associated with this infection. Severe disease is characterized by early secreti...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier España, S.L.
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7130369/ https://www.ncbi.nlm.nih.gov/pubmed/23116788 http://dx.doi.org/10.1016/S0213-005X(12)70100-3 |
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author | Almansa, Raquel Bermejo-Martín, Jesús F. de Lejarazu Leonardo, Raúl Ortiz |
author_facet | Almansa, Raquel Bermejo-Martín, Jesús F. de Lejarazu Leonardo, Raúl Ortiz |
author_sort | Almansa, Raquel |
collection | PubMed |
description | Three years after the pandemic, major advances have been made in our understanding of the innate and adaptive immune responses to the influenza A(H1N1)pdm09 virus and those responses’ contribution to the immunopathology associated with this infection. Severe disease is characterized by early secretion of proinflammatory and immunomodulatory cytokines. This cytokine secretion persisted in patients with severe viral pneumonia and was directly associated with the degree of viral replication in the respiratory tract. Cytokines play important roles in the antiviral defense, but persistent hypercytokinemia may cause inflammatory tissue damage and participate in the genesis of the respiratory failure observed in these patients. An absence of pre-existing protective antibodies was the rule for both mild and severe cases. A role for pathogenic immunocomplexes has been proposed for this disease. Defective T cell responses characterize severe cases of infection caused by the influenza A(H1N1)pdm09 virus. Immune alterations associated with accompanying conditions such as obesity, pregnancy or chronic obstructive pulmonary disease may interfere with the normal development of the specific response to the virus. The role of host immunogenetic factors associated with disease severity is also discussed in this review. In conclusion, currently available information suggests a complex immunological dysfunction/alteration that characterizes the severe cases of 2009 pandemic influenza. The potential benefits of prophylactic/therapeutic interventions aimed at preventing/correcting such dysfunction warrant investigation. |
format | Online Article Text |
id | pubmed-7130369 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Elsevier España, S.L. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71303692020-04-08 Immunopathogenesis of 2009 pandemic influenza Almansa, Raquel Bermejo-Martín, Jesús F. de Lejarazu Leonardo, Raúl Ortiz Enferm Infecc Microbiol Clin Article Three years after the pandemic, major advances have been made in our understanding of the innate and adaptive immune responses to the influenza A(H1N1)pdm09 virus and those responses’ contribution to the immunopathology associated with this infection. Severe disease is characterized by early secretion of proinflammatory and immunomodulatory cytokines. This cytokine secretion persisted in patients with severe viral pneumonia and was directly associated with the degree of viral replication in the respiratory tract. Cytokines play important roles in the antiviral defense, but persistent hypercytokinemia may cause inflammatory tissue damage and participate in the genesis of the respiratory failure observed in these patients. An absence of pre-existing protective antibodies was the rule for both mild and severe cases. A role for pathogenic immunocomplexes has been proposed for this disease. Defective T cell responses characterize severe cases of infection caused by the influenza A(H1N1)pdm09 virus. Immune alterations associated with accompanying conditions such as obesity, pregnancy or chronic obstructive pulmonary disease may interfere with the normal development of the specific response to the virus. The role of host immunogenetic factors associated with disease severity is also discussed in this review. In conclusion, currently available information suggests a complex immunological dysfunction/alteration that characterizes the severe cases of 2009 pandemic influenza. The potential benefits of prophylactic/therapeutic interventions aimed at preventing/correcting such dysfunction warrant investigation. Elsevier España, S.L. 2012-10 2012-10-29 /pmc/articles/PMC7130369/ /pubmed/23116788 http://dx.doi.org/10.1016/S0213-005X(12)70100-3 Text en Copyright © 2012 Elsevier España, S.L. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Almansa, Raquel Bermejo-Martín, Jesús F. de Lejarazu Leonardo, Raúl Ortiz Immunopathogenesis of 2009 pandemic influenza |
title | Immunopathogenesis of 2009 pandemic influenza |
title_full | Immunopathogenesis of 2009 pandemic influenza |
title_fullStr | Immunopathogenesis of 2009 pandemic influenza |
title_full_unstemmed | Immunopathogenesis of 2009 pandemic influenza |
title_short | Immunopathogenesis of 2009 pandemic influenza |
title_sort | immunopathogenesis of 2009 pandemic influenza |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7130369/ https://www.ncbi.nlm.nih.gov/pubmed/23116788 http://dx.doi.org/10.1016/S0213-005X(12)70100-3 |
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