Smoking stimulates the production of ACE2 in the lungs, the enzyme used by the new coronavirus to enter human cells.
Research by the Cold Spring Harbor Laboratory in the United States suggests that cigarette smoke stimulates the lungs to produce more ACE2, the enzyme used by the new coronavirus to enter human cells. The discovery, reported last Saturday (16) in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to Covid-19.
Since the early stages of the new coronavirus pandemic, scientists have observed dramatic differences in the way Covid-19 targets smokers and non-smokers. According to a study published in early April, for example, smokers are 14 times more likely to develop severe infections.
With this in mind, the Cold Spring Harbor Laboratory team decided to investigate the relationship between smoking and more severe cases of the disease. “We started gathering all the data we could find,” said Jason Sheltzer, co-author of the study, in a statement. “When we put it all together and started analyzing it, we saw that both mice that had been exposed to smoke in a laboratory and humans who were current smokers had significant upregulation of ACE2.”
According to the scientists, the main producers of ACE2 in the airways are mucus-producing cells, called goblet cells. It is known that smoking increases the prevalence of these particles, which consequently produce more ACE2 in the lungs and increase the vulnerability to Sars-CoV-2.
The good news is that this condition changes when you quit smoking. According to the researchers, the study shows that the level of ACE2 in the lungs of people who stopped smoking was similar to that of non-smokers.