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Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution

With the rising prevalence of obesity has come an increasing awareness of its impact on communicable disease. As a consequence of the 2009 H1N1 influenza A virus pandemic, obesity was identified for the first time as a risk factor for increased disease severity and mortality in infected individuals....

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Autores principales: Honce, Rebekah, Schultz-Cherry, Stacey
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6523028/
https://www.ncbi.nlm.nih.gov/pubmed/31134099
http://dx.doi.org/10.3389/fimmu.2019.01071
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author Honce, Rebekah
Schultz-Cherry, Stacey
author_facet Honce, Rebekah
Schultz-Cherry, Stacey
author_sort Honce, Rebekah
collection PubMed
description With the rising prevalence of obesity has come an increasing awareness of its impact on communicable disease. As a consequence of the 2009 H1N1 influenza A virus pandemic, obesity was identified for the first time as a risk factor for increased disease severity and mortality in infected individuals. Over-nutrition that results in obesity causes a chronic state of meta-inflammation with systemic implications for immunity. Obese hosts exhibit delayed and blunted antiviral responses to influenza virus infection, and they experience poor recovery from the disease. Furthermore, the efficacy of antivirals and vaccines is reduced in this population and obesity may also play a role in altering the viral life cycle, thus complementing the already weakened immune response and leading to severe pathogenesis. Case studies and basic research in human cohorts and animal models have highlighted the prolonged viral shed in the obese host, as well as a microenvironment that permits the emergence of virulent minor variants. This review focuses on influenza A virus pathogenesis in the obese host, and on the impact of obesity on the antiviral response, viral shed, and viral evolution. We comprehensively analyze the recent literature on how and why viral pathogenesis is altered in the obese host along with the impact of the altered host and pathogenic state on viral evolutionary dynamics in multiple models. Finally, we summarized the effectiveness of current vaccines and antivirals in this populations and the questions that remain to be answered. If current trends continue, nearly 50% of the worldwide population is projected to be obese by 2050. This population will have a growing impact on both non-communicable and communicable diseases and may affect global evolutionary trends of influenza virus.
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spelling pubmed-65230282019-05-27 Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution Honce, Rebekah Schultz-Cherry, Stacey Front Immunol Immunology With the rising prevalence of obesity has come an increasing awareness of its impact on communicable disease. As a consequence of the 2009 H1N1 influenza A virus pandemic, obesity was identified for the first time as a risk factor for increased disease severity and mortality in infected individuals. Over-nutrition that results in obesity causes a chronic state of meta-inflammation with systemic implications for immunity. Obese hosts exhibit delayed and blunted antiviral responses to influenza virus infection, and they experience poor recovery from the disease. Furthermore, the efficacy of antivirals and vaccines is reduced in this population and obesity may also play a role in altering the viral life cycle, thus complementing the already weakened immune response and leading to severe pathogenesis. Case studies and basic research in human cohorts and animal models have highlighted the prolonged viral shed in the obese host, as well as a microenvironment that permits the emergence of virulent minor variants. This review focuses on influenza A virus pathogenesis in the obese host, and on the impact of obesity on the antiviral response, viral shed, and viral evolution. We comprehensively analyze the recent literature on how and why viral pathogenesis is altered in the obese host along with the impact of the altered host and pathogenic state on viral evolutionary dynamics in multiple models. Finally, we summarized the effectiveness of current vaccines and antivirals in this populations and the questions that remain to be answered. If current trends continue, nearly 50% of the worldwide population is projected to be obese by 2050. This population will have a growing impact on both non-communicable and communicable diseases and may affect global evolutionary trends of influenza virus. Frontiers Media S.A. 2019-05-10 /pmc/articles/PMC6523028/ /pubmed/31134099 http://dx.doi.org/10.3389/fimmu.2019.01071 Text en Copyright © 2019 Honce and Schultz-Cherry. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Honce, Rebekah
Schultz-Cherry, Stacey
Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution
title Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution
title_full Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution
title_fullStr Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution
title_full_unstemmed Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution
title_short Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution
title_sort impact of obesity on influenza a virus pathogenesis, immune response, and evolution
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6523028/
https://www.ncbi.nlm.nih.gov/pubmed/31134099
http://dx.doi.org/10.3389/fimmu.2019.01071
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