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SARS-CoV-2 infection in alpha1-antitrypsin deficiency

Alpha1-antitrypsin deficiency arises due to mutations in alpha1-antitrypsin (AAT) gene and represents the most prominent genetic predisposition to chronic obstructive pulmonary disease and emphysema. Since AAT plays important immunomodulatory and tissue-protective roles and since it was suggested to...

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Detalles Bibliográficos
Autores principales: Schneider, Carolin V., Strnad, Pavel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Ltd. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8116136/
https://www.ncbi.nlm.nih.gov/pubmed/34010739
http://dx.doi.org/10.1016/j.rmed.2021.106466
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author Schneider, Carolin V.
Strnad, Pavel
author_facet Schneider, Carolin V.
Strnad, Pavel
author_sort Schneider, Carolin V.
collection PubMed
description Alpha1-antitrypsin deficiency arises due to mutations in alpha1-antitrypsin (AAT) gene and represents the most prominent genetic predisposition to chronic obstructive pulmonary disease and emphysema. Since AAT plays important immunomodulatory and tissue-protective roles and since it was suggested to protect from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we assessed this association in United Kingdom Biobank, a community-based cohort with >500,000 participants. The most common, mild AATD genotypes were associated neither with increased SARS-CoV-2 infection rates nor with increased SARS-CoV-2 fatalities, while the numbers of severe AATD cases were too low to allow definitive conclusions.
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spelling pubmed-81161362021-05-13 SARS-CoV-2 infection in alpha1-antitrypsin deficiency Schneider, Carolin V. Strnad, Pavel Respir Med Original Research Alpha1-antitrypsin deficiency arises due to mutations in alpha1-antitrypsin (AAT) gene and represents the most prominent genetic predisposition to chronic obstructive pulmonary disease and emphysema. Since AAT plays important immunomodulatory and tissue-protective roles and since it was suggested to protect from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we assessed this association in United Kingdom Biobank, a community-based cohort with >500,000 participants. The most common, mild AATD genotypes were associated neither with increased SARS-CoV-2 infection rates nor with increased SARS-CoV-2 fatalities, while the numbers of severe AATD cases were too low to allow definitive conclusions. Elsevier Ltd. 2021-08 2021-05-13 /pmc/articles/PMC8116136/ /pubmed/34010739 http://dx.doi.org/10.1016/j.rmed.2021.106466 Text en © 2021 Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Original Research
Schneider, Carolin V.
Strnad, Pavel
SARS-CoV-2 infection in alpha1-antitrypsin deficiency
title SARS-CoV-2 infection in alpha1-antitrypsin deficiency
title_full SARS-CoV-2 infection in alpha1-antitrypsin deficiency
title_fullStr SARS-CoV-2 infection in alpha1-antitrypsin deficiency
title_full_unstemmed SARS-CoV-2 infection in alpha1-antitrypsin deficiency
title_short SARS-CoV-2 infection in alpha1-antitrypsin deficiency
title_sort sars-cov-2 infection in alpha1-antitrypsin deficiency
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8116136/
https://www.ncbi.nlm.nih.gov/pubmed/34010739
http://dx.doi.org/10.1016/j.rmed.2021.106466
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