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) 是由严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 引起的临床综合征，目前是一种全球性的健康大流行病，具有很高的发病率和死亡率。COVID-19 几乎给社会的方方面面都蒙上了阴影，给世界各地的卫生系统和经济带来了压力。尽管人们普遍认为肥胖、心血管疾病和感染引起的代谢紊乱之间存在密切关系，但我们才刚刚开始了解肥胖的免疫后遗症如何作为与 COVID-19 临床结果不佳相关的诱发因素. 由于先天免疫系统和适应性免疫系统均由肥胖引发，因此关键途径的改变会导致免疫抑制和过度炎症状态。