Latest findings by scientists from Cold Spring Harbor Laboratory (CSHL) may explain why smokers are at a higher risk of contracting fatal diseases such as COVID-19.
The New study, reported in the journal Developmental Cell, suggests that cigarette smoke spurs the lungs to make more ACE2 (angiotensin-converting enzyme 2), the protein that the coronavirus responsible for COVID-19 grabs and uses to enter human cells that make them more vulnerable to severe infections.
The WHO recently issued a strong warning statement about amplifying claims that tobacco or nicotine could reduce the risk of COVID-19. “Smoking impairs lung function making it harder for the body to fight off coronaviruses and other diseases,” the statement said. The statement came after several studies showing that the number of non-smokers was higher among COVID-19 patients compared to smokers.
From the early stages of the current pandemic, scientists and clinicians have noted dramatic differences in how people respond to infection with SARS-CoV-2. Most infected individuals suffer only mild illness, if they experience any at all. But others require intensive care when the sometimes-fatal virus attacks. Three groups, in particular, have been significantly more likely than others to develop severe illness: men, the elderly, and smokers.
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With most laboratory experiments on hold due to the pandemic, CSHL Fellow Jason Sheltzer and Joan Smith, an engineer at Google, turned to previously published data to seek possible explanations for these disparities. They were curious whether the vulnerable groups might share some key feature related to the human proteins that the coronavirus relies on for infection.
"We started gathering all the data we could find," Sheltzer says, explaining that he and Smith focused first on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers. "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."
While they found no evidence that age or sex impacts ACE2 levels in the lungs, the influence of smoke exposure was surprisingly strong, Sheltzer says. The change appears to be temporary, however: the data revealed that the level of ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.
Sheltzer, Smith, and colleagues also found that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells. Smoking is known to increase the prevalence of such cells, a change that can protect the airways from irritants but--by amplifying the amount of ACE2 in the lungs--may also increase vulnerability to SARS-CoV-2.
