Why smokers are more likely to have COVID-19 than non-smokers

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In a new study, researchers found that cigarette smokers are more likely to have health complications.

One possible reason is that smoking causes a big increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells.

The study suggests that prolonged smoking could cause an increase in the ACE2 protein in the lungs, possibly resulting in a higher rate of morbidity in patients.

The research was conducted by a team at Cold Spring Harbor Laboratory.

ACE2, or Angiotensin-Converting Enzyme 2, is a regulatory protein that has been linked to vulnerability to the 2003 SARS (2003) virus.

Evidence has shown that higher levels of ACE2 make individuals more susceptible to SARS.

More recent work with SARS-CoV-2 found that when human ACE2 was highly expressed in mice infected with COVID-19, they died more quickly.

In humans, the lungs act as one of the primary locations of ACE2 production.

To assess the direct impact of smoking on ACE2 expression in the lungs, the team compared ACE2 gene expression from the lung epithelial tissue of people who smoked cigarettes regularly to those who had never smoked.

They found that smoking caused a big increase in the expression of ACE2. Smokers produced 30%-55% more ACE2 than their non-smoking counterparts.

This change was also dose-dependent, with heavy smokers having the greatest ACE2 values.

The effects of smoking on ACE2 may be tied to the goblet cells in the lungs—one of the few lung cell types that the team found to actively express the ACE2 gene.

Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers’ lungs could be a byproduct of smoking-induced secretory cell hyperplasia.

An uptick in ACE2 was also associated with the inflammatory pulmonary diseases COPD and idiopathic pulmonary fibrosis.

Additionally, the team’s results indicate that other viral infections, such as influenza, as well as interferon signaling—the part of the body’s virus defense system—increase ACE2 expression.

While the impact of cigarette smoke and ACE2 expression is compelling, it is not permanent.

By comparing the lungs of current smokers to those who quit smoking for at least 12 months, the team found a big decrease in ACE2 expression, demonstrating that the effects of smoking on ACE2 can be reversed.

One author of the study is  Jason Sheltzer, a cancer geneticist.

The study is published in the journal Developmental Cell.

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