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Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution.
Front Immunol. 2019; 10:1071.FI

Abstract

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.

Authors+Show Affiliations

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, United States. Integrated Program in Biomedical Sciences, Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, United States.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

31134099

Citation

Honce, Rebekah, and Stacey Schultz-Cherry. "Impact of Obesity On Influenza a Virus Pathogenesis, Immune Response, and Evolution." Frontiers in Immunology, vol. 10, 2019, p. 1071.
Honce R, Schultz-Cherry S. Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution. Front Immunol. 2019;10:1071.
Honce, R., & Schultz-Cherry, S. (2019). Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution. Frontiers in Immunology, 10, 1071. https://doi.org/10.3389/fimmu.2019.01071
Honce R, Schultz-Cherry S. Impact of Obesity On Influenza a Virus Pathogenesis, Immune Response, and Evolution. Front Immunol. 2019;10:1071. PubMed PMID: 31134099.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution. AU - Honce,Rebekah, AU - Schultz-Cherry,Stacey, Y1 - 2019/05/10/ PY - 2019/03/11/received PY - 2019/04/26/accepted PY - 2019/5/29/entrez PY - 2019/5/28/pubmed PY - 2020/6/2/medline KW - evolution KW - immunity KW - influenza KW - obesity KW - pathogenesis SP - 1071 EP - 1071 JF - Frontiers in immunology JO - Front Immunol VL - 10 N2 - 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. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/31134099/Impact_of_Obesity_on_Influenza_A_Virus_Pathogenesis_Immune_Response_and_Evolution_ L2 - https://doi.org/10.3389/fimmu.2019.01071 DB - PRIME DP - Unbound Medicine ER -