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Review
. 2020 Aug:78:103411.
doi: 10.1016/j.etap.2020.103411. Epub 2020 May 15.

Two important controversial risk factors in SARS-CoV-2 infection: Obesity and smoking

Ayse Basak Engin  1 , Evren Doruk Engin  2 , Atilla Engin  3
Affiliations
Review

Two important controversial risk factors in SARS-CoV-2 infection: Obesity and smoking

Ayse Basak Engin et al. Environ Toxicol Pharmacol. 2020 Aug.

Abstract

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.

Keywords: Air pollution; Angiotensin II; Angiotensin-converting-enzyme inhibitors; COVID-19; Obesity; Smoking.

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Conflict of interest statement

Declaration of Competing Interest The authors have no conflict of interest.

Figures

Fig. 1
Fig. 1
The mechanism of receptor-ligand interaction and its impact on the enhanced risk of death due to SARS-CoV-2 infection. In the renin angiotensin system, ACE cleaves Ang I to produce Ang II. Ang II action is mediated by the AT1R. SARS-CoV-2 uses the ACE2 as a receptor for entry into the cell. Coronaviruses use the surface spike (S) glycoprotein on the coronavirus envelope to attach host cells and mediate host cell membrane and viral membrane fusion during infection. The spike protein includes two regions, S1 and S2. The receptor binding domain is located in the S1 region. SARS-CoV attaches the human host cells through the binding of the receptor binding domain protein to ACE2. The expression of ACE2 and the balance of Ang II/Ang 1–7 influence the course of the disease. ACEI and ARBs cause the increase in the formation of Ang 1–7 from Ang II via increased ACE2. The loss of ACE2 function following binding by SARS-CoV-2 is driven by endocytosis and activation of proteolytic cleavage and processing. Accordingly, ACE2 may be upregulated due to the NO2 associated air pollution, and ACEIs. Nicotine has dual action by enhancing ACE and down-regulating ACE2 (Abbreviations. ACE: angiotensin-converting enzyme; ACE2: angiotensin-converting enzyme II; ACEI: angiotensin-converting enzyme inhibitors; Ang I: angiotensin I; Ang II: angiotensin II; ARB: angiotensin II type-I receptor blocker; AT1R: angiotensin II receptor type 1; NO2: Nitrogen dioxide; SARS-CoV-2: severe acute respiratory syndrome coronavirus-2).
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