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The association of APOE genotype with COVID-19 disease severity
COVID-19 has caused the recent pandemic of respiratory infection, which threatened global health. The severity of the symptoms varies among affected individuals, from asymptotic or mild signs to severe or critical illness. Genetic predisposition explains the variation in disease severity among patie...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9356041/ https://www.ncbi.nlm.nih.gov/pubmed/35931737 http://dx.doi.org/10.1038/s41598-022-17262-4 |
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author | Safdari Lord, Javad Soltani Rezaiezadeh, Javad Yekaninejad, Mir Saeed Izadi, Pantea |
author_facet | Safdari Lord, Javad Soltani Rezaiezadeh, Javad Yekaninejad, Mir Saeed Izadi, Pantea |
author_sort | Safdari Lord, Javad |
collection | PubMed |
description | COVID-19 has caused the recent pandemic of respiratory infection, which threatened global health. The severity of the symptoms varies among affected individuals, from asymptotic or mild signs to severe or critical illness. Genetic predisposition explains the variation in disease severity among patients who suffer from severe symptoms without any known background risk factors. The present study was performed to show the association between APOE genotype and the severity of COVID-19 disease. The APOE genotype of 201 COVID-19 patients (101 patients with asymptomatic to mild form of the disease as the control group and 100 patients with severe to critical illness without any known background risk factors as the case group) were detected via multiplex tetra-primer ARMS-PCR method. Results showed that the e4 allele increased the risk of the COVID-19 infection severity more than five times and the e4/e4 genotype showed a 17-fold increase in the risk of severe disease. In conclusion, since our study design was based on the exclusion of patients with underlying diseases predisposing to severe form of COVID-19 and diseases related to the APOE gene in the study population, our results showed that the e4 genotype is independently associated with the severity of COVID-19 disease. However, further studies are needed to confirm these findings in other nations and to demonstrate the mechanisms behind the role of these alleles in disease severity. |
format | Online Article Text |
id | pubmed-9356041 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-93560412022-08-07 The association of APOE genotype with COVID-19 disease severity Safdari Lord, Javad Soltani Rezaiezadeh, Javad Yekaninejad, Mir Saeed Izadi, Pantea Sci Rep Article COVID-19 has caused the recent pandemic of respiratory infection, which threatened global health. The severity of the symptoms varies among affected individuals, from asymptotic or mild signs to severe or critical illness. Genetic predisposition explains the variation in disease severity among patients who suffer from severe symptoms without any known background risk factors. The present study was performed to show the association between APOE genotype and the severity of COVID-19 disease. The APOE genotype of 201 COVID-19 patients (101 patients with asymptomatic to mild form of the disease as the control group and 100 patients with severe to critical illness without any known background risk factors as the case group) were detected via multiplex tetra-primer ARMS-PCR method. Results showed that the e4 allele increased the risk of the COVID-19 infection severity more than five times and the e4/e4 genotype showed a 17-fold increase in the risk of severe disease. In conclusion, since our study design was based on the exclusion of patients with underlying diseases predisposing to severe form of COVID-19 and diseases related to the APOE gene in the study population, our results showed that the e4 genotype is independently associated with the severity of COVID-19 disease. However, further studies are needed to confirm these findings in other nations and to demonstrate the mechanisms behind the role of these alleles in disease severity. Nature Publishing Group UK 2022-08-05 /pmc/articles/PMC9356041/ /pubmed/35931737 http://dx.doi.org/10.1038/s41598-022-17262-4 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Safdari Lord, Javad Soltani Rezaiezadeh, Javad Yekaninejad, Mir Saeed Izadi, Pantea The association of APOE genotype with COVID-19 disease severity |
title | The association of APOE genotype with COVID-19 disease severity |
title_full | The association of APOE genotype with COVID-19 disease severity |
title_fullStr | The association of APOE genotype with COVID-19 disease severity |
title_full_unstemmed | The association of APOE genotype with COVID-19 disease severity |
title_short | The association of APOE genotype with COVID-19 disease severity |
title_sort | association of apoe genotype with covid-19 disease severity |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9356041/ https://www.ncbi.nlm.nih.gov/pubmed/35931737 http://dx.doi.org/10.1038/s41598-022-17262-4 |
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