Viral respiratory infections are the most common trigger of severe asthma exacerbations in children and adults. Unexpectedly, large epidemiological studies of the COVID-19 pandemic in China did not identify asthma as a risk factor of severe COVID19 related illnesses.(2) Here, we report that respiratory allergy and controlled allergen exposures are each associated with significant reductions in ACE2 expression. ACE2 expression was lowest in those with both high levels of allergic sensitization and asthma. Importantly, non-atopic asthma was not associated with reduced ACE2 expression. Given that ACE2 serves as the receptor for SARS-CoV-2, our findings suggest a potential mechanism of reduced COVID-19 severity in patients with respiratory allergies. However, it is likely that additional factors beyond ACE2 expression modulate the response to COVID-19 in allergic individuals, and elucidation of these factors may also provide important insights into COVID-19 disease pathogenesis. Strengths of our study include carefully phenotyped cohorts of children and adults. Further, the allergen challenge studies included both upper and lower airway samples, with each demonstrating a consistent impact on ACE2 expression. Limitations include lack of clinical information to directly link ACE2 expression to SARS-CoV-2 infection and illness severity in our study populations. In addition, we do not have data on the ACE2 protein levels to confirm the gene expression data, though previous work suggests a direct association between ACE2 mRNA levels and ACE2 protein levels in the lung.(8)
Thursday, April 30, 2020
As data continues to stream in regarding possible risk factors for COVID 19, one missing population besides children in general seems to be .... asthma. COVID 19 and other SARS type viruses are known to enter lung cells (type 2 pneumocytes) through a cell surface receptor known as ACE2. According to this study, there appears to be reduced cell surface expression in people with allergic diseases. This is of course, not enough to clear children with asthma from significant risk, but warrants investigation. Incidentally, nonatopic individuals did NOT have reduced ACE2 expression.