The effects of obesity and smoking in the coronavirus disease 2019 (COVID-19) pandemic remain controversial. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system (RAS), is the human cell receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19. ACE2 expression increases on lung alveolar epithelial cells and adipose tissue due to obesity, smoking and air pollution. A significant relationship exists between air pollution and SARS-CoV-2 infection, as more severe COVID-19 symptoms occur in smokers; comorbid conditions due to obesity or excess ectopic fat accumulation as underlying risk factors for severe COVID-19 strongly encourage the virus/ACE2 receptor-ligand interaction concept. Indeed, obesity, air pollution and smoking associated risk factors share underlying pathophysiologies that are related to the Renin-Angiotensin-System in SARS-CoV-2 infection. The aim of this review is to emphasize the mechanism of receptor-ligand interaction and its impact on the enhanced risk of death due to SARS-CoV-2 infection.

肥胖和吸烟对 2019 年冠状病毒病 (COVID-19) 大流行的影响仍然存在争议。血管紧张素转换酶 2 (ACE2) 是肾素-血管紧张素系统 (RAS) 的组成部分，是严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2)（COVID-19 的病原体）的人体细胞受体。由于肥胖、吸烟和空气污染，肺泡上皮细胞和脂肪组织中的 ACE2 表达增加。空气污染与 SARS-CoV-2 感染之间存在显着关系，因为吸烟者会出现更严重的 COVID-19 症状；肥胖或过度异位脂肪积累引起的共病是严重 COVID-19 的潜在危险因素，强烈鼓励病毒/ACE2 受体-配体相互作用的概念。事实上，肥胖、空气污染和吸烟相关的危险因素具有与 SARS-CoV-2 感染中的肾素血管紧张素系统相关的潜在病理生理学特征。本综述的目的是强调受体-配体相互作用的机制及其对 SARS-CoV-2 感染导致的死亡风险增加的影响。