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The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection

BACKGROUND: Tumor necrosis factor-alpha (TNFɑ) is a cytokine that manages the host defense mechanism, which may play a role in the pathogenesis of COVID-19 patients. Several single-nucleotide polymorphisms, described in the promoter region of the TNFα gene, have a significant role on its transcripti...

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Autores principales: Sotomayor-Lugo, Francisco, Alemañy-Díaz Perera, Claudia, Roblejo-Balbuena, Hilda, Zúñiga-Rosales, Yaíma, Monzón-Benítez, Giselle, Suárez-Besil, Beatriz, González-Torres, María de los Ángeles, Torres-Rives, Bárbara, Álvarez-Gavilán, Yudelmis, Bravo-Ramírez, Maidalys, Pereira-Roche, Nayade, Benítez-Cordero, Yudelkis, Silva-Ayçaguer, Luis Carlos, Marcheco-Teruel, Beatriz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8900469/
https://www.ncbi.nlm.nih.gov/pubmed/37521833
http://dx.doi.org/10.1186/s43042-022-00274-0
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author Sotomayor-Lugo, Francisco
Alemañy-Díaz Perera, Claudia
Roblejo-Balbuena, Hilda
Zúñiga-Rosales, Yaíma
Monzón-Benítez, Giselle
Suárez-Besil, Beatriz
González-Torres, María de los Ángeles
Torres-Rives, Bárbara
Álvarez-Gavilán, Yudelmis
Bravo-Ramírez, Maidalys
Pereira-Roche, Nayade
Benítez-Cordero, Yudelkis
Silva-Ayçaguer, Luis Carlos
Marcheco-Teruel, Beatriz
author_facet Sotomayor-Lugo, Francisco
Alemañy-Díaz Perera, Claudia
Roblejo-Balbuena, Hilda
Zúñiga-Rosales, Yaíma
Monzón-Benítez, Giselle
Suárez-Besil, Beatriz
González-Torres, María de los Ángeles
Torres-Rives, Bárbara
Álvarez-Gavilán, Yudelmis
Bravo-Ramírez, Maidalys
Pereira-Roche, Nayade
Benítez-Cordero, Yudelkis
Silva-Ayçaguer, Luis Carlos
Marcheco-Teruel, Beatriz
author_sort Sotomayor-Lugo, Francisco
collection PubMed
description BACKGROUND: Tumor necrosis factor-alpha (TNFɑ) is a cytokine that manages the host defense mechanism, which may play a role in the pathogenesis of COVID-19 patients. Several single-nucleotide polymorphisms, described in the promoter region of the TNFα gene, have a significant role on its transcriptional activity. These include the − 308A > G polymorphism which increases the TNFα levels with the expression of the A allele. The aim of this study was to explore whether the TNFα.− 308A > G polymorphism affects the clinical state of COVID-19 patients. The study included a total of 1028 individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which were distributed in 3 groups: asymptomatic, mild symptomatic and severe symptomatic patients. The amplification-refractory mutation system was used to determine the genotype of the TNFα.− 308A > G polymorphism. RESULTS: Results show a higher tendency of being asymptomatic in individuals carrying the GG genotype (336 of 411; OR 1.24, 95% CI 0.91–1.70). The development of a severe form of SARS-CoV-2 infection was not found in subjects with the A allele compared to those with the G allele (OR 0.96, 95% CI 0.51–1.79), except in the eastern region of the country where the risk increased (OR 4.41, 95% CI 1.14–17.05). However, the subjects carrying the A allele had a higher chance of developing symptoms (OR 1.24, 95% CI 0.91–1.70) compared to those with the G allele. CONCLUSION: The TNFα.− 308A allele has an influence on developing symptoms of COVID-19 in Cuban patients, and that it particularly increases the risk of presenting severe forms of the disease in the eastern region of the country.
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spelling pubmed-89004692022-03-07 The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection Sotomayor-Lugo, Francisco Alemañy-Díaz Perera, Claudia Roblejo-Balbuena, Hilda Zúñiga-Rosales, Yaíma Monzón-Benítez, Giselle Suárez-Besil, Beatriz González-Torres, María de los Ángeles Torres-Rives, Bárbara Álvarez-Gavilán, Yudelmis Bravo-Ramírez, Maidalys Pereira-Roche, Nayade Benítez-Cordero, Yudelkis Silva-Ayçaguer, Luis Carlos Marcheco-Teruel, Beatriz Egypt J Med Hum Genet Research BACKGROUND: Tumor necrosis factor-alpha (TNFɑ) is a cytokine that manages the host defense mechanism, which may play a role in the pathogenesis of COVID-19 patients. Several single-nucleotide polymorphisms, described in the promoter region of the TNFα gene, have a significant role on its transcriptional activity. These include the − 308A > G polymorphism which increases the TNFα levels with the expression of the A allele. The aim of this study was to explore whether the TNFα.− 308A > G polymorphism affects the clinical state of COVID-19 patients. The study included a total of 1028 individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which were distributed in 3 groups: asymptomatic, mild symptomatic and severe symptomatic patients. The amplification-refractory mutation system was used to determine the genotype of the TNFα.− 308A > G polymorphism. RESULTS: Results show a higher tendency of being asymptomatic in individuals carrying the GG genotype (336 of 411; OR 1.24, 95% CI 0.91–1.70). The development of a severe form of SARS-CoV-2 infection was not found in subjects with the A allele compared to those with the G allele (OR 0.96, 95% CI 0.51–1.79), except in the eastern region of the country where the risk increased (OR 4.41, 95% CI 1.14–17.05). However, the subjects carrying the A allele had a higher chance of developing symptoms (OR 1.24, 95% CI 0.91–1.70) compared to those with the G allele. CONCLUSION: The TNFα.− 308A allele has an influence on developing symptoms of COVID-19 in Cuban patients, and that it particularly increases the risk of presenting severe forms of the disease in the eastern region of the country. Springer Berlin Heidelberg 2022-03-07 2022 /pmc/articles/PMC8900469/ /pubmed/37521833 http://dx.doi.org/10.1186/s43042-022-00274-0 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 Research
Sotomayor-Lugo, Francisco
Alemañy-Díaz Perera, Claudia
Roblejo-Balbuena, Hilda
Zúñiga-Rosales, Yaíma
Monzón-Benítez, Giselle
Suárez-Besil, Beatriz
González-Torres, María de los Ángeles
Torres-Rives, Bárbara
Álvarez-Gavilán, Yudelmis
Bravo-Ramírez, Maidalys
Pereira-Roche, Nayade
Benítez-Cordero, Yudelkis
Silva-Ayçaguer, Luis Carlos
Marcheco-Teruel, Beatriz
The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection
title The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection
title_full The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection
title_fullStr The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection
title_full_unstemmed The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection
title_short The role of tumor necrosis factor alpha − 308A > G polymorphism on the clinical states of SARS-CoV-2 infection
title_sort role of tumor necrosis factor alpha − 308a > g polymorphism on the clinical states of sars-cov-2 infection
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8900469/
https://www.ncbi.nlm.nih.gov/pubmed/37521833
http://dx.doi.org/10.1186/s43042-022-00274-0
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