Extract
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.
Abstract
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
Footnotes
Data availability: Raw data available from the authors upon request. The data are also posted on GEO (Gene Expression Omnibus).
Conflict of interest: J.M. Leung has nothing to disclose.
Conflict of interest: C.X. Yang has nothing to disclose.
Conflict of interest: A. Tam has nothing to disclose.
Conflict of interest: T. Shaipanich has nothing to disclose.
Conflict of interest: T.L. Hackett has nothing to disclose.
Conflict of interest: G.K. Singhera has nothing to disclose.
Conflict of interest: D.R. Dorschied has nothing to disclose.
Conflict of interest: D.D. Sin reports grants from Merck, personal fees for advisory board work from Sanofi-Aventis and Regeneron, grants and personal fees for research from Boehringer Ingelheim, grants and personal fees for advisory board work and lectures from AstraZeneca, personal fees for advisory board work and lectures from Novartis, outside the submitted work.
Support statement: This work is supported by the Canadian Institutes of Health Research, the British Columbia Lung Association, and de Lazzari Family Chair at HLI. J.M. Leung is supported by the Michael Smith Foundation for Health Research (MSFHR)/Providence Health Care Health Professional Investigator (HPI) Award and by the Canadian Institutes of Health Research (CIHR)/AstraZeneca Early Career Investigator Award. T-L. Hackett is supported by the MSFHR scholar and CIHR Early Career Investigator awards. D. Dorscheid is supported by the MSFHR/PHC HPI Award. D.D. Sin is a Tier 1 Canada Research Chair (CRC) in COPD and the de Lazzari Family Chair at HLI. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received March 2, 2020.
- Accepted March 25, 2020.
- Copyright ©ERS 2020
This version is distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.
