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.
Front Immunol. 2019 May 10;10:1071. doi: 10.3389/fimmu.2019.01071. eCollection 2019.
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.
随着肥胖症的患病率不断上升，人们越来越意识到它对传染病的影响。由于 2009 年甲型 H1N1 流感病毒大流行，肥胖首次被确定为感染个体疾病严重程度和死亡率增加的一个风险因素。导致肥胖的营养过剩会导致慢性代谢炎症，对免疫系统产生全身性影响。肥胖宿主对流感病毒感染的抗病毒反应延迟且减弱，并且从疾病中恢复不佳。此外，该人群中抗病毒药物和疫苗的疗效降低，肥胖症可能还会改变病毒的生命周期，从而补充已经减弱的免疫反应，并导致严重的发病机制。人类队列和动物模型的病例研究和基础研究强调了肥胖宿主中病毒的延长脱落，以及允许毒力较弱的变异体出现的微环境。这篇综述重点关注肥胖宿主中的甲型流感病毒发病机制，以及肥胖症对抗病毒反应、病毒脱落和病毒进化的影响。我们全面分析了最近关于肥胖宿主中病毒发病机制如何以及为何发生改变的文献，以及改变的宿主和发病状态对多种模型中病毒进化动态的影响。最后，我们总结了当前在该人群中疫苗和抗病毒药物的有效性，以及仍需要回答的问题。如果当前的趋势继续下去，到 2050 年，全球近 50%的人口预计将肥胖。这一人群将对非传染性和传染性疾病产生越来越大的影响，并可能影响流感病毒的全球进化趋势。
