There are a couple of theories to explain why smokers appear to be under represented in severe cases of COVID-19.
- Smoke appears to upregulate the expression of ACE2 receptors in the lung. We have both animal experiments that show that mice exposed to smoke increased the numbers of ACE2 receptors. More ACE2 receptors is thought to help prevent lung damage.
The team inspected tissue samples from mice that had been exposed to diluted cigarette smoke for zero, 2, 3 or 4 hours a day over the course of five months. They found that, the more smoke exposure, the more ACE2 receptors studded the animals' lungs. Compared with unexposed mice, the mice that received the highest dose of cigarette smoke accumulated about 80% more ACE2 receptors in their lungs. The researchers then compared the lungs of human smokers against those who never smoked, and again, they found a similar trend: Smokers’ lungs contained 40% to 50% more ACE2 receptors than those of nonsmokers.
Nicotine may bind to ACE2 receptors blocking the virus's infection
Nicotine may have an anti-inflammatory effect. It is known that cigarette smoking cessation is linked to the onset of ulcerative colitis. It may involve the nicotinic acetylcholine receptor (nAChR)
A potential protective effect of smoking and of nicotine on SARS-CoV-2 infection has been noted. Until recently , no firm conclusions could be drawn from studies evaluating the rates of current smokers in Covid-19. All these studies [40-48], although reporting low rates of current smokers, ranging from 1.4% to 12.5%, did not take into account the main potential confounders of smoking including age and sex. In the study that two of us are reporting , the rates of current smoking remain below 5 % even when main confounders for tobacco consumption, i.e. age and sex, in- or outpatient status, were considered. Compared to the French general population, the Covid-19 population exhibited a significantly weaker current daily smoker rate by 80.3 % for outpatients and by 75.4 % for inpatients. Thus, current smoking status appears to be a protective factor against the infection by SARS-CoV-2.
I have not seen any data to suggest carbon monoxide is important in the pathogenesis of COVID-19.
A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications. https://www.qeios.com/read/FXGQSB.2