Summary: Smoking remodels the gene expression of lung cells so that the ACE2 gene is more highly expressed in goblet cells. The effects of smoking on ACE2 pulmonary expression indicates an increase in the overall entry points for coronavirus and increases the risk for viral binding and entry of COVID-19 into the lungs.
Source: Baylor College of Medicine
Researchers at Baylor College of Medicine, the University of South Carolina and other institutions have identified tobacco smoking as a potential risk factor for infection of the COVID-19 virus.
Co-corresponding authors Dr. Christopher I. Amos, director of the Institute of Clinical and Translational Research at Baylor, Dr. Guoshuai Cai, assistant professor at the University of South Carolina, and their colleagues analyzed datasets of the RNA expressed by various types of lung tissue, comparing current and former smokers and non-smokers.
They looked at the expression of ACE2, the molecule in the respiratory tract that the COVID-19 virus uses to attach to and infect human cells. They also looked at the expression of FURIN and TMPRSS2, human enzymes known to facilitate COVID-19 virus infection.
The researchers report in the American Journal of Respiratory and Critical Care Medicine a 25 percent 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. Smoking also increased the presence of FURIN, but to a lower extent compared to ACE2. TMRPSS2 expression in lungs was not associated with smoking. They also found that smoking remodeled the gene expression of cells in the lungs so that the ACE2 gene was more highly expressed in goblet cells, cells that secrete mucus in order to protect the mucous membranes in the lungs.
The significant smoking effect on ACE2 pulmonary expression identified in this 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 findings 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,” Amos said. “Studies of COVID-19 patients would help resolve the influence of smoking on COVID-19 outcomes.”
About this coronavirus research article
Source:
Baylor College of Medicine
Media Contacts:
Molly Chiu – Baylor College of Medicine
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The image is in the public domain.
Original Research: Open access (PDF)
“Tobacco Smoking Increases the Lung Gene Expression of ACE2, the Receptor of SARS-CoV-2”. by Guoshuai Cai, Yohan Bossé, Feifei Xiao, Farrah Kheradmand, and Christopher I. Amos.
American Journal of Respitatory and Critical Care Medicine doi:10.1164/rccm.202003-0693LE
Abstract
Tobacco Smoking Increases the Lung Gene Expression of ACE2, the Receptor of SARS-CoV-2
On March 11, 2020, the World Health Organization declared the Coronavirus Disease 2019 (COVID-19) outbreak a pandemic. As of April 20th, 2020, laboratories
have confirmed 2,470,410 COVID-19 cases and caused 169,794 deaths in 213 counties, areas, or territories. COVID-19 is caused by a new type of pathogenic
coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is phylogenetically similar to SARS-CoV, with approximately 80% identity between genomes (1). SARS viruses affect the respiratory tract and cause acute respiratory response through the same cell-entry receptor, angiotensin-converting enzyme 2 (ACE2), which is the only experimentally confirmed SARS-CoV-2 receptor. SARSCoV-2 infection also employs activation of the spike proteins found on the surface of the virus for cellular entry. The best candidates for priming spike proteins are two host-cell enzymes called Furin and TMPRSS2 (1). In the current severe global emergency, it is imperative to identify potential risk factors for effective prevention and care, such as cigarette smoking, which is a substantial risk factor for various important bacterial and viral infections.
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