Smoking increases the SARS-CoV-2 receptor in the lungs | Instant News


New research from CSHL scientists shows that cigarette smoke stimulates the lungs to make more ACE2 (angiotensin-converting enzyme 2), the protein that the corona virus is responsible for COVID-19 to use and enter human cells. The findings, reported May 16, 2020 in the journal Cell Development, can explain why smokers seem to be very vulnerable to severe infections. This analysis also shows that these changes can be reversed, showing that stopping smoking can reduce the risk of severe coronavirus infection.

From the initial stages of the current pandemic, scientists and doctors have noted dramatic differences in how people respond to infection with SARS-CoV-2. Most people who are infected only suffer from minor ailments, if they experience anything. But others need intensive care when sometimes fatal virus attacks. Three groups, in particular, are significantly more likely than others to develop severe illness: men, the elderly, and smokers.

With most laboratory experiments being held because of a pandemic, CSHL Associates Jason Sheltzer and Joan Smith, an engineer at Google, turned to previously published data to look for possible explanations for this difference. They wondered whether vulnerable groups might share some key features related to human proteins that the corona virus relied on for infection.

“We are starting to gather all the data we can find,” Sheltzer said, explaining that he and Smith first focused on comparing gene activity in the lungs at various ages, between genders, and between smokers and nonsmokers. “When we combined everything and began to analyze it, we saw that both mice that had been exposed to smoke in the laboratory and humans who were smokers now had a significant increase in ACE2 regulation.”

While they found no evidence that age or gender affected ACE2 levels in the lungs, the effect of smoke exposure turned out to be very strong, Sheltzer said. However, the change seems to be temporary: data reveal that ACE2 levels in the lungs of people who quit smoking are the same as nonsmokers.

Sheltzer, Smith, and colleagues also found that the most productive ACE2 producers in the airways were mucous-producing cells called trophy cells. Smoking is known to increase the prevalence of these cells, a change that can protect the airways from irritation but – by strengthening the amount of ACE2 in the lungs – can also increase susceptibility to SARS-CoV-2.



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