Is Asthma a Risk Factor for Coronavirus Disease-2019 Worse Outcomes?

The Answer Is No, But...

Priscila A. Franco; Sergio Jezler; Alvaro A. Cruz


Curr Opin Allergy Clin Immunol. 2021;21(3):223-228. 

In This Article

A Possible Protection Related to Atopy in Asthma and Rhinitis

SARS-CoV-2 enters the host cell through large spikes projecting from its envelope, which recognizes angiotensin-converting enzyme 2 (ACE2) receptors, particularly in the human respiratory epithelial cells. This process is dependent on the host serine protease TMPRSS2, which cleaves viral spike protein and allow viral and cellular membranes fusion.[25,26] Kimura et al.[27] demonstrated that IL-13, a cytokine associated with type 2 asthma, suppresses ACE2 expression in airway epithelial cells from patients with atopic asthma. According to these findings, it was hypothesized that ACE2 expression is modulated by type 2 inflammation in upper and lower airways. Allergic sensitization was inversely related to ACE2 expression on nasal epithelium, independently of asthma. Greater reductions in ACE2 expression in asthmatic children with moderate or severe allergic sensitization were noted when compared with children with asthma but without or with minimal allergic sensitization.[13] Furthermore, ACE2 expression was inversely associated with type 2 inflammation markers as allergen-specific IgE, total IgE, FeNO and IL13 expression in nasal epithelia. All of these observations support the hypothesis that the airways of patients with allergic asthma and atopic diseases express less ACE2 receptors, possibly leading to reduced entry of the virus in the host cells and being protective against SARS-CoV-2 infection and may indicate a pathway for the development of options for prevention. Furthermore, some studies reported inhaled corticosteroids are associated with decreased expression of ACE2 in induced sputum,[14,28] which may also benefit patients with asthma and rhinitis on regular treatment.