Smoking Upregulates Angiotensin-Converting Enzyme-2 Receptor: A Potential Adhesion Site for Novel Coronavirus SARS-CoV-2 (Covid-19)

Abstract

The epicenter of the original outbreak in China has high male smoking rates of around 50%, and early reported death rates have an emphasis on older males, therefore the likelihood of smokers being overrepresented in fatalities is high. In Iran, China, Italy, and South Korea, female smoking rates are much lower than males. Fewer females have contracted the virus. If this analysis is correct, then Indonesia would be expected to begin experiencing high rates of Covid-19 because its male smoking rate is over 60% (Tobacco Atlas). Smokers are vulnerable to respiratory viruses. Smoking can upregulate angiotensin-converting enzyme-2 (ACE2) receptor, the known receptor for both the severe acute respiratory syndrome (SARS)-coronavirus (SARS-CoV) and the human respiratory coronavirus NL638. This could also be true for new electronic smoking devices such as electronic cigarettes and "heat-not-burn" IQOS devices. ACE2 could be a novel adhesion molecule for SARS-CoV-2 causing Covid-19 and a potential therapeutic target for the prevention of fatal microbial infections, and therefore it should be fast tracked and prioritized for research and investigation. Data on smoking status should be collected on all identified cases of Covid-19.

Keywords: ACE2 receptor; COPD; Covid-19; Electronic cigarettes; Heat-Not-Burn; IQOS; SARS-CoV-2; Smoking; Vaping.

Figure 1

Surgically resected lung tissue stained for the angiotensin-converting enzyme-2 (ACE2) receptor. Current smoker with chronic obstructive pulmonary disease (COPD-CS), (A) showing positive staining in the small airway epithelium but also apical including cilia (B) red arrows indicating positive staining in type-2 pneumocytes and black arrows showing alveolar macrophages positive for the ACE2 receptor. Normal lung function smoker (NLFS), (C) and (D) showing similar pattern for COPD-CS although a little less staining is observed. Normal controls (NC), (E) and (F) no staining observed in any of the areas. This is the first immunohistochemical human lung evidence for ACE2 receptor expression in smokers and patients with COPD.