Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-speci...

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Main Author: Hajar Fauzan, Ahmad
Format: Article
Language:English
Published: Springer Nature 2021
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Online Access:http://umpir.ump.edu.my/id/eprint/35374/3/Mapping%20the%20human%20genetic%20architecture%20of%20COVID.docx
http://umpir.ump.edu.my/id/eprint/35374/
https://www.nature.com/articles/s41586-021-03767-x#Sec5
https://doi.org/10.1038/s41586-021-03767-x
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spelling my.ump.umpir.353742022-10-07T05:11:31Z http://umpir.ump.edu.my/id/eprint/35374/ Mapping the human genetic architecture of COVID-19 Hajar Fauzan, Ahmad HV Social pathology. Social and public welfare RA Public aspects of medicine RA0421 Public health. Hygiene. Preventive Medicine The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease. Springer Nature 2021 Article PeerReviewed pdf en http://umpir.ump.edu.my/id/eprint/35374/3/Mapping%20the%20human%20genetic%20architecture%20of%20COVID.docx Hajar Fauzan, Ahmad (2021) Mapping the human genetic architecture of COVID-19. Nature, 600. pp. 472-477. ISSN ISSN 1476-4687 (online) ISSN 0028-0836 (print) https://www.nature.com/articles/s41586-021-03767-x#Sec5 https://doi.org/10.1038/s41586-021-03767-x
institution Universiti Malaysia Pahang
building UMP Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Malaysia Pahang
content_source UMP Institutional Repository
url_provider http://umpir.ump.edu.my/
language English
topic HV Social pathology. Social and public welfare
RA Public aspects of medicine
RA0421 Public health. Hygiene. Preventive Medicine
spellingShingle HV Social pathology. Social and public welfare
RA Public aspects of medicine
RA0421 Public health. Hygiene. Preventive Medicine
Hajar Fauzan, Ahmad
Mapping the human genetic architecture of COVID-19
description The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.
format Article
author Hajar Fauzan, Ahmad
author_facet Hajar Fauzan, Ahmad
author_sort Hajar Fauzan, Ahmad
title Mapping the human genetic architecture of COVID-19
title_short Mapping the human genetic architecture of COVID-19
title_full Mapping the human genetic architecture of COVID-19
title_fullStr Mapping the human genetic architecture of COVID-19
title_full_unstemmed Mapping the human genetic architecture of COVID-19
title_sort mapping the human genetic architecture of covid-19
publisher Springer Nature
publishDate 2021
url http://umpir.ump.edu.my/id/eprint/35374/3/Mapping%20the%20human%20genetic%20architecture%20of%20COVID.docx
http://umpir.ump.edu.my/id/eprint/35374/
https://www.nature.com/articles/s41586-021-03767-x#Sec5
https://doi.org/10.1038/s41586-021-03767-x
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