Division of Pulmonary and Critical Care Medicine, Department of Medicine, and.
Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Stony Brook University Hospital/Renaissance School of Medicine, Stony Brook, New York.
Am J Respir Cell Mol Biol. 2021 Jul;65(1):13-21. doi: 10.1165/rcmb.2020-0236TR.
Coronavirus disease (COVID-19), the clinical syndrome caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is currently a global health pandemic with substantial morbidity and mortality. COVID-19 has cast a shadow on nearly every aspect of society, straining health systems and economies across the world. Although it is widely accepted that a close relationship exists between obesity, cardiovascular disease, and metabolic disorders on infection, we are only beginning to understand ways in which the immunological sequelae of obesity functions as a predisposing factor related to poor clinical outcomes in COVID-19. As both the innate and adaptive immune systems are each primed by obesity, the alteration of key pathways results in both an immunosuppressed and hyperinflammatory state. The present review will discuss the cellular and molecular immunology of obesity in the context of its role as a risk factor for severe COVID-19, discuss the role of cytokine storm, and draw parallels to prior viral epidemics such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and 2009 H1N1.
冠状病毒病（COVID-19），由严重急性呼吸系统综合征冠状病毒 2（SARS-CoV-2）引起的临床综合征，目前是一种具有较高发病率和死亡率的全球健康大流行疾病。COVID-19几乎给社会的各个方面都蒙上了阴影，使世界各地的卫生系统和经济都承受着压力。尽管人们普遍认为肥胖、心血管疾病和代谢紊乱与感染之间存在密切关系，但我们才刚刚开始了解肥胖的免疫后遗症如何作为一个易患因素，与 COVID-19 的不良临床结局相关。由于固有免疫和适应性免疫系统都被肥胖所激活，关键途径的改变导致免疫抑制和过度炎症状态。本综述将讨论肥胖在作为 COVID-19 严重风险因素的细胞和分子免疫学中的作用，讨论细胞因子风暴的作用，并与先前的病毒流行（如严重急性呼吸系统综合征（SARS）、中东呼吸系统综合征（MERS）和 2009 年 H1N1）进行类比。
