Asthma-associated risk for COVID-19 development

Abstract

The newly described severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for a pandemic (coronavirus disease 2019 [COVID-19]). It is now well established that certain comorbidities define high-risk patients. They include hypertension, diabetes, and coronary artery disease. In contrast, the context with bronchial asthma is controversial and shows marked regional differences. Because asthma is the most prevalent chronic inflammatory lung disease worldwide and SARS-CoV-2 primarily affects the upper and lower airways leading to marked inflammation, the question arises about the possible clinical and pathophysiological association between asthma and SARS-CoV-2/COVID-19. Here, we analyze the global epidemiology of asthma among patients with COVID-19 and propose the concept that patients suffering from different asthma endotypes (type 2 asthma vs non–type 2 asthma) present with a different risk profile in terms of SARS-CoV-2 infection, development of COVID-19, and progression to severe COVID-19 outcomes. This concept may have important implications for future COVID-19 diagnostics and immune-based therapy developments.

Risk factors for severe and critically ill COVID‐19 patients: A review

“…Further research is warranted to improve our current understanding of the type 2 immune response in COVID‐19 as it is targeted by biologicals in the treatment of asthma and atopic dermatitis 100,101 . In addition, deeper insight into phenotypes and endotypes of asthma might provide more understanding of the pathophysiology of COVID‐19 in asthma 102 …”

Interrelations between COVID-19 and other disorders

“…It would therefore appear that exacerbation of asthma is not the primary determinant of a severe disease requiring hospitalization but rather suggests that asthmatics may experience asthma exacerbations following the SARS-CoV-2 infection. More recently, different risks associated with SARS-CoV-2 infection and the disease development, progression, and severity have been connected differently across Th2 vs. non-Th2 asthma endotypes [ 123 ].…”

The type 2 asthma mediator IL-13 inhibits SARS-CoV-2 infection of bronchial epithelium

“…Our studies reveal that IL-13 stimulation of HBECs affects expression of many SARS-CoV (13)(14)(15)(16). We also found significant associations of many IL-13-induced SARS-CoV-2associated genes with type 2 inflammation in a large group of smokers with and without COPD, suggesting that the effects of IL-13 on SARS-CoV-2 risk may also be relevant in some individuals without asthma.…”

“…Subsequent studies have failed to find consistent evidence of increased risk of COVID-19 diagnosis, hospitalization, or mortality due to asthma (1,9,10), and some studies concluded that risk of acquiring and being hospitalized for COVID-19 are lower in those with asthma (10,11). Factors that might provide protection against COVID-19 in individuals with asthma (12)(13)(14)(15) include increased attention to limiting viral exposure, younger age, absence of co-morbidities, use of inhaled corticosteroids, and a variety of biological features of asthma, including chronic airway inflammation, mucus hypersecretion, and altered expression of SARS-CoV-2 receptor (12). However, direct evidence that these features alter SARS-CoV-2 infection has been lacking.…”