Tobacco smoking could be a potential risk factor for infection with the novel COVID-19, according to a study which suggests that there is an increased risk for the virus binding and gaining entry into the lungs of smokers than non-smokers.
Researchers, including those from the University of South Carolina in the US, analysed datasets of the molecule ribonucleic acid (RNA) expressed by various types of lung tissue, comparing current and former smokers and non-smokers.
In the study, published in the American Journal of Respiratory and Critical Care Medicine, they looked at the expression of ACE2, the molecule in the respiratory tract that the novel coronavirus, SARS-CoV-2, uses to attach to and infect human cells.
The scientists also looked at the expression of FURIN and TMPRSS2, which are human enzymes known to facilitate the viral infection.
According to the researchers, there is a 25 per cent increase in the expression of ACE2 in lung tissues from ever-smokers — people who have smoked at least 100 cigarettes during their lives, when compared with nonsmokers.
They said smoking also increased the presence of FURIN, but to a lower extent compared to ACE2.
However, the scientists said the expression of the enzyme TMRPSS2 in the lungs was not associated with smoking.
They also noted that smoking remodeled the expression of genes in lung cells so that the ACE2 gene was more highly expressed in goblet cells, which are cells that secrete mucus in order to protect the mucous membranes in the respiratory organ.
The effect of smoking on ACE2 pulmonary expression identified in the study indicates not only an increase in the entry points for the COVID-19 virus but also may suggest an increased risk for viral binding and entry of the virus in the lungs of smokers, the researchers said.
They added that the findings may provide valuable information for identifying potentially susceptible populations.
“We hypothesized that the worse outcomes of COVID-19 infections in regions of the world with high levels of cigarette smoking may reflect host factors,” said study co-author Christopher I. Amos, the director of the Institute of Clinical and Translational Research at Baylor College of Health in the US.
However, the scientists noted that more studies are needed to identify the mechanism by which ACE2 expression is increased due to tobacco smoking in the lungs.
“The mechanisms underlying tobacco-related upregulation of ACE2 pulmonary expression are unknown, among many others, the degrees of smoking effects to the infection susceptibility and clinical manifestations are unknown, and further mechanistic studies are needed,” they wrote in the study.