ACE-2 Expression in the Small Airway Epithelia of Smokers and COPD Patients: Implications for COVID-19

Abstract

The World Health Organization (WHO) has declared coronavirus disease 2019 (COVID-19) as a pandemic [1]. COVID-19 is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). COVID-19 displays symptoms ranging from mild to severe (pneumonia) that can lead to death in some individuals [2–4]. As of March 24, 2020, there have been 422 566 cases of COVID-19 worldwide and 18 887 deaths [5]. SARS-CoV-2 uses the angiotensin converting enzyme II (ACE-2) as the cellular entry receptor [6]. While the virus can infect individuals of any age, to date, most of the severe cases have been described in those over the age of 55 years and with significant co-morbidities such as chronic obstructive pulmonary disease (COPD) [7]. Here, we determined whether patients with COPD have increased expression of ACE-2 in bronchial epithelial cells in lower respiratory tract.

Abstract

Smokers and individuals with COPD have increased airway expression of ACE-2, which is the entry receptor for the COVID-19 virus. This may explain the increased risk of severe COVID-19 in these subpopulations and highlight importance of smoking cessation.