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COVID-19 risk may differ by asthma phenotype

Published online: June 9, 2020

As the COVID-19 pandemic continues to evolve, increasing data have shed light on patients that are at greatest risk. Epidemiological studies consistently identify chronic lung disease as a risk factor, though the relationship between asthma and infection with SARS-CoV-2 remains highly controversial, perhaps due to the long-appreciated heterogeneity of asthma as a disease. In their study in The Journal of Allergy and Clinical Immunology (JACI), Camiolo et al. show that the underlying type of inflammation in asthma patients could be an indicator of risk for SARS-CoV-2 infection as it may correlate with the amount of viral receptor present in the lung.  

To investigate the link between the type of asthma inflammation and COVID-19 risk, the authors turned to data collected from multiple large, independent cohorts of asthma patients and healthy controls. They analyzed gene expression from epithelial cells of bronchial airways, the predominant site of inflammation in asthma, to define patterns that may confer risk to infection by SARS-CoV-2. These findings were related to immune cells in the lung and blood, as well as commonly available clinical parameters such as resting blood pressure, allowing for identification of potentially at-risk patients.

Asthma phenotype refers to differences in the signaling pathways and mechanisms driving airway inflammation in patients. The authors found an inverse relationship between the number of circulating blood eosinophils and levels of the SARS-CoV-2 viral receptor, angiotensin converting enzyme 2 (ACE2), in airway cells. Asthma patients with low blood eosinophils, and therefore low Type-2 inflammation (T2-low), showed increased levels of ACE2 expression.  This could indicate a greater portal for SARS-CoV-2 cell entry and thus increased susceptibility to infection. ACE2 level was closely tied to a signature of viral response in airway epithelial cells and a corresponding Type-1 gene signature in immune cells, suggesting a possible link in T2-low patients. Pathways active in these individuals overlapped with those currently being targeted in clinical trials for catastrophic lung injury in COVID-19. Surprisingly, these T2-low asthma patients demonstrated several additional risk factors for severe COVID-19 despite being infection-free at the time of assessment, including propensity towards male sex and higher blood pressure. These data suggest that information such as differential blood cell count and other commonly obtained clinical parameters may help clinicians triage vulnerable asthma patients.  

Though we have much to learn in our ongoing fight against COVID-19, the information presented by Camiolo et al. sheds light on why risk imparted by a diagnosis of asthma may vary and why asthma, per se, may not be a risk factor. T2-low asthma patients, identified by low blood eosinophils, may be more susceptible to SARS-CoV-2 infection via increased ACE2 in their lungs. They may be recognizable based on baseline levels of peripheral blood eosinophils and other clinical parameters which may help triage them to a higher level of care. Confirmation of increased susceptibility requires further study of asthma patients who contract the disease.

The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.

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