ACE-2 expression in the small airway epithelia of smokers and COPD patients: implications for COVID-19
By J. Leung, C. Yang, A. Tam, T. Shaipanich, T. Hackett, G. Singhera, D. Dorscheid, D. Sin. European Respiratory Journal, 2020
785 citations recorded by the source corpus.
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
Subfields: Physiology, Psychiatry and Mental health, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/55f87287f395edc08d8c7e69dd4e931b2ce5ed6c
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In Pulmonary and Respiratory Medicine
Citations in the corpus
- COVID-19: angiotensin-converting enzyme 2 (ACE2) expression and tissue susceptibility to SARS-CoV-2 infection (2021, background): “Smoking can increase ACE2 expression in the lungs and bronchial epithelium [63, 64], so that nicotine may also upregulate ACE2 in neurons and glia and endothelial cells through the nicotinic acetylcholine receptor activation [28].”
- Smell dysfunction: a biomarker for COVID‐19 (2020, background): “A recent study reported that smoking upregulated the expression of ACE-2 in the airways, potentially predisposing individuals to increased risk of coronavirus infection but, paradoxically, protecting the host against acute lung injury.(36) Interestingly, non-smokers appear to be much more susceptibl”
- SARS-CoV-2 Reverse Genetics Reveals a Variable Infection Gradient in the Respiratory Tract (2020, background): “…that seed infection into the deep lung, and the virus-host interaction networks that attenuate or augment intra-regional virus growth in the lung to produce severe disease, especially in vulnerable patients experiencing chronic lung or inflammatory diseases (Guan et al., 2020; Leung et al., 2020).”