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.

Keywords: COVID-19; SARS-CoV-2; asthma; endotypes; non–type 2 asthma; type 2 asthma.

Fig 1

Asthma prevalence. A, Countries with high prevalence of asthma among COVID-19 comorbidities in comparison with asthma prevalence in the general population (high asthma-COVID-19 zone) are marked in red color. Countries with low/equal prevalence of asthma among COVID-19 comorbidities in comparison with asthma prevalence in the general population (low asthma-COVID-19 zone) are marked in green. B, Asthma prevalence (%) among patients with COVID-19 in comparison with the general population in various countries.^,,, , , , , , ,

Fig 2

The impact of asthma endotypes on infection of airway epithelium with SARS-CoV-2, development and progression of COVID-19. The 2 major asthma endotypes, type 2 asthma and non–type 2 asthma, are defined by unique inflammatory patterns on the level of adaptive immunity and effector cell responses. Type 2 asthma is characterized by the presence of T_H2 cells secreting IL-4, IL-5, and IL-13. These cytokines have a strong impact on the regulation of helper-cell subsets, airway epithelial function, and regulation of effector cell responses, including eosinophils and mast cells. In contrast, non–type 2 asthma is defined by the presence of T_H1 cells and/or T_H17 cells among other effector T-cell responses. The subset of these patients shows vascular and metabolic comorbidities, which are underlined by the presence of subclinical chronic inflammatory responses (eg, activation of IL-1 signaling pathways). EDN, Eosinophil-derived neurotoxin; pDC, plasmacytoid dendritic cell; T2D, type 2 diabetes.