TY -的T1 -小airwa ACE-2表达式y epithelia of smokers and COPD patients: implications for COVID-19 JF - European Respiratory Journal JO - Eur Respir J DO - 10.1183/13993003.00688-2020 VL - 55 IS - 5 SP - 2000688 AU - Leung, Janice M. AU - Yang, Chen X. AU - Tam, Anthony AU - Shaipanich, Tawimas AU - Hackett, Tillie-Louise AU - Singhera, Gurpreet K. AU - Dorscheid, Delbert R. AU - Sin, Don D. Y1 - 2020/05/01 UR - //www.qdcxjkg.com/content/55/5/2000688.abstract N2 - The World Health Organization (WHO) has declared coronavirus disease 2019 (COVID-19) 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 18 April 2020, there have been 2 280 945 cases of COVID-19 worldwide and 156 354 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 >55 years of age and with significant comorbidities, such as COPD [7]. Here, we determined whether patients with COPD have increased expression of ACE-2 in bronchial epithelial cells in the lower respiratory tract.Smokers and those 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 the importance of smoking cessation. https://bit.ly/3bC29es ER -