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. 2022 Nov 29;9:953084. doi: 10.3389/fmed.2022.953084

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Copyright © 2022 Sansone, Valencise, Bredariol, Peixoto and Marson.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Physiopathology hypothesis on asthma’s protective mechanisms for death on coronavirus disease (COVID-19) infections. Atopic patients have a low production of interferons alpha (represented in red), beta (represented in orange), and gamma (represented in purple), which constitutes an inadequate antiviral defense (section 1 of the figure). In this scenario, lower interferon productions (mainly alpha) lead to a predominance of the Th2 response over the Th1 in patients with asthma (section 2 of the figure). This predominance may be protective, as it can downregulate the late phase of hyperinflammation in patients with asthma, which is a hallmark of severe respiratory viral infections (section 3 of the figure). Moreover, the inflammatory environment of the bronchoalveolar system in patients with asthma could result in a decrease in the expression of the angiotensin-converting enzyme 2 (ACE-2) (represented in blue), a known severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binding receptor, due to interleukin-13 eosinophil recruitment (section 4 of the figure).