The effects of cigarette smoke and COPD on SARS-CoV-2 infection

The coronavirus disease (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to wreak havoc across the globe. As the pandemic evolves, more information about the virus and its effect on the body emerges.

A team of researchers from Harvard Medical School, USA, the University of Arizona, USA, and other major institutions, have revealed some of the effects of cigarette smoke and chronic obstructive pulmonary disease (COPD) on SARS-CoV-2 infection.

They found that the angiotensin-converting enzyme 2 (ACE2) protein and messenger RNA (mRNA) levels were decreased in the peripheral airways in patients with COPD. However, the levels were the same in central airways in smokers and those who never smoked.

ACE2 and SARS-CoV-2

The coronavirus pandemic first emerged in Wuhan City, China, in December 2019. Since then, it has spread to more than 190 countries, infecting over 68.34 million people.

SARS-CoV-2 primarily spreads through respiratory droplets and aerosols suspended in the air when an infected person coughs, sneezes, breathes and speaks. The virus Spike (S) protein binds to the cell's angiotensin-converting enzyme 2 (ACE2) receptor to enter and cause infection.

The ACE receptor acts as a cellular gateway. It can be found in many parts of the body, including cells and tissues in the lungs, heart, blood vessels, liver, kidneys, and gastrointestinal tract. COVID-19 affects the respiratory tract and causes a systemic illness.

The exchange of oxygen and carbon dioxide between the lungs and blood vessels happens across an epithelial lining in the lung. The lining found in the nose, mouth, and lungs contains ACE2 receptors. In the lungs, ACE2 is highly prevalent on type 2 pneumocytes, an essential cell type present in the chambers in the lungs called alveoli, where gas exchange occurs.

Cigarette smoke and COPD

How cigarette smoke (CS) and COPD affect the vulnerability and outcomes of SARS-CoV-2 infection is controversial. Some studies showed that smoking could heighten the risk of infection and severe illness. Studies have also demonstrated the up-regulation of ACE2 in clinical and experimental models of smoke-induced lung illness.

In the study, published in the pre-print journal bioRxiv*, the researchers evaluated the ACE21 and Transmembrane serine protease 2 (TMPRSS2) expression in smokers' airways with COPD, compared to smokers and those who never smoked. TMPRSS2 is a cell surface protein primarily expressed by endothelial cells across the respiratory and digestive tracts. It is involved in the cleaving peptide bonds of proteins.

The team studied the ACE2 expression in the lungs of mice acutely and chronically exposed to cigarette smoke, as well as the effect of cigarettes smoke on SARS-CoV-2 infection of bronchial epithelial cells in vitro.

To arrive at the study findings, lung tissue from two separate COPD cohorts and controls were evaluated to validate the results. The first cohort included smokers with pulmonary nodules who had lung resection at Ferrara University Hospital in Italy. The second cohort included patients who underwent surgery for lung nodules or lung transplant at the University of Arizona. Control lungs were used, which were from non-smokers who died of extrapulmonary causes.

The researchers also studied the effects of cigarette smoke on SARS-CoV-2 infection after 72 hours of in vitro cell infection.

The team has found that in both human cohorts, ACE2 protein and mRNA levels were reduced in the peripheral airways from COPD patients compared to smokers and neve smoker controls. However, all the groups had similar levels in the airways.

TMPRSS2 levels were similar across the groups. When evaluating the mice exposed to cigarette smoke, they found that the mice had decreased ACE2 protein levels in their bronchial and alveolar epithelia.


The team concluded reduced ACE2 levels in both bronchial and alveolar epithelial cells from uninfected COPD patients versus controls. This means that there are fewer receptors for the virus to enter. Also, cigarette smoke pre-treatment did not affect ACE2 levels but potently inhibited SARS-CoV-2 replication in the in vitro model.

The researchers recommend further investigating the effects of cigarette smoke and COPD on SARS-CoV-2 infection.

*Important Notice

bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

Journal reference:
Angela Betsaida B. Laguipo

Written by

Angela Betsaida B. Laguipo

Angela is a nurse by profession and a writer by heart. She graduated with honors (Cum Laude) for her Bachelor of Nursing degree at the University of Baguio, Philippines. She is currently completing her Master's Degree where she specialized in Maternal and Child Nursing and worked as a clinical instructor and educator in the School of Nursing at the University of Baguio.


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