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Published on: November 5, 2021
SARS-CoV-2 infection in alpha1-antitrypsin deficiency
Carolin V Schneider1, Pavel Strnad2
1Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Aachen, Germany.
Alpha1-antitrypsin deficiency (AATD) did not increase the risk of SARS-CoV-2 infection or death in a large UK study. Mild AATD genotypes showed no association, but severe cases were too few for firm conclusions.
Area of Science:
- Genetics
- Pulmonology
- Infectious Diseases
Background:
- Alpha1-antitrypsin deficiency (AATD) is a genetic disorder linked to chronic obstructive pulmonary disease (COPD) and emphysema.
- Alpha1-antitrypsin (AAT) has immunomodulatory and tissue-protective functions, with potential roles in viral infections.
- Previous suggestions indicated AAT might offer protection against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Purpose of the Study:
- To investigate the association between alpha1-antitrypsin deficiency (AATD) and SARS-CoV-2 infection and fatality rates.
- To evaluate the impact of different AATD genotypes on COVID-19 outcomes.
Main Methods:
- Utilized data from the UK Biobank, a large community-based cohort exceeding 500,000 participants.
- Assessed correlations between common and severe alpha1-antitrypsin deficiency genotypes and SARS-CoV-2 infection and mortality data.
Main Results:
- Mild or common alpha1-antitrypsin deficiency genotypes were not associated with higher rates of SARS-CoV-2 infection.
- Mild AATD genotypes did not correlate with increased SARS-CoV-2 related fatalities.
- The study cohort had insufficient cases of severe AATD to draw definitive conclusions regarding their association with COVID-19 outcomes.
Conclusions:
- Common alpha1-antitrypsin deficiency genotypes do not appear to increase susceptibility or severity of SARS-CoV-2 infection.
- Further research is needed to ascertain the impact of severe AATD on COVID-19 outcomes due to limited data.
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