Abstract
Coronavirus disease 2019 (COVID-19) is caused by a novel zoonotic coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has been identified as a pandemic by the World Health Organization. Several risk factors have been identified for severe COVID-19–associated pneumonia including increased age and the presence of comorbidities, in particular diabetes, cardiovascular disease, and tobacco smoking.1 However, a number of reports have failed to identify excess risk in patients with respiratory airway diseases such as asthma.
Highlights
We thank the 2 clinical research associates, Gaelle Cavillon and Salima Merazga, for their excellent work
SARS-CoV-2 infects people by binding to the angiotensinconverting enzyme 2 (ACE2) receptor, a transmembrane endopeptidase that cleaves both angiotensin 1 and 2, and which is expressed by epithelial cells in several organs including the airways
There were no differences in ACE2, TMPRSS2, or furin gene expression between healthy volunteers and people with mild to moderate and severe asthma (Fig 1, A-C)
Summary
We thank the 2 clinical research associates, Gaelle Cavillon and Salima Merazga, for their excellent work. ACE2, TMPRSS2, and furin gene expression in the airways of people with asthma—implications for COVID-19
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