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。血管紧张素转化酶2（ACE2）是肾素-血管紧张素系统（RAS）的组成部分，是严重急性呼吸系统综合症冠状病毒2（SARS-CoV-2）的人类细胞受体，COVID-19的病原体。由于肥胖，吸烟和空气污染，ACE2在肺泡上皮细胞和脂肪组织上的表达增加。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。肥胖或异位脂肪过多引起的合并症是严重COVID-19的潜在危险因素，这强烈鼓励了病毒/ ACE2受体-配体相互作用的概念。确实，肥胖 空气污染和吸烟相关的危险因素共有与SARS-CoV-2感染中的肾素-血管紧张素系统有关的潜在病理生理。这篇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感染导致死亡风险增加的影响。