Atopic endotypes as a modulating factor for SARS-CoV-2 infection: mechanisms and implications

Area of Science:

• Respiratory viral infections
• Immunology
• COVID-19 pathogenesis

Background:

• Asthma patients face higher risks from viral infections.
• Asthma and atopy are not overrepresented in COVID-19 patients, contrary to expectations.
• Understanding COVID-19 outcomes in asthma patients is crucial for clinical guidance.

Purpose of the Study:

• To investigate the relationship between asthma, atopy, and COVID-19 outcomes.
• To explore hypotheses explaining the observed prevalence of asthma/atopy in COVID-19.
• To guide patient care by clarifying disease influences in this population.

Main Methods:

• Review of epidemiological and experimental findings.
• Analysis of the roles of Angiotensin-converting enzyme 2 (ACE2) and Transmembrane protease serine 2 (TMRSS2).
• Exploration of models linking atopic endotypes to ACE2 and TMRSS2 expression.

Main Results:

• Atopic endotypes may reduce ACE2 and increase TMRSS2 expression in respiratory epithelia.
• Alterations in ACE2 expression appear to correlate with COVID-19 clinical disease.
• Current evidence is limited for drawing direct conclusions on the ACE2-TMRSS2 interplay.

Conclusions:

• Atopic endotypes likely modulate COVID-19 susceptibility.
• It is too early to classify the association as protective or harmful.
• Further clinical and experimental studies are required to understand the complex interactions affecting viral entry and disease outcomes.