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GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19

Based on the close relationship between dysregulation of redox homeostasis and immune response in SARS-CoV-2 infection, we proposed a possible modifying role of ACE2 and glutathione transferase omega (GSTO) polymorphisms in the individual propensity towards the development of clinical manifestations...

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Autores principales: Djukic, Tatjana, Stevanovic, Goran, Coric, Vesna, Bukumiric, Zoran, Pljesa-Ercegovac, Marija, Matic, Marija, Jerotic, Djurdja, Todorovic, Nevena, Asanin, Milika, Ercegovac, Marko, Ranin, Jovan, Milosevic, Ivana, Savic-Radojevic, Ana, Simic, Tatjana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955736/
https://www.ncbi.nlm.nih.gov/pubmed/35330457
http://dx.doi.org/10.3390/jpm12030458
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author Djukic, Tatjana
Stevanovic, Goran
Coric, Vesna
Bukumiric, Zoran
Pljesa-Ercegovac, Marija
Matic, Marija
Jerotic, Djurdja
Todorovic, Nevena
Asanin, Milika
Ercegovac, Marko
Ranin, Jovan
Milosevic, Ivana
Savic-Radojevic, Ana
Simic, Tatjana
author_facet Djukic, Tatjana
Stevanovic, Goran
Coric, Vesna
Bukumiric, Zoran
Pljesa-Ercegovac, Marija
Matic, Marija
Jerotic, Djurdja
Todorovic, Nevena
Asanin, Milika
Ercegovac, Marko
Ranin, Jovan
Milosevic, Ivana
Savic-Radojevic, Ana
Simic, Tatjana
author_sort Djukic, Tatjana
collection PubMed
description Based on the close relationship between dysregulation of redox homeostasis and immune response in SARS-CoV-2 infection, we proposed a possible modifying role of ACE2 and glutathione transferase omega (GSTO) polymorphisms in the individual propensity towards the development of clinical manifestations in COVID-19. The distribution of polymorphisms in ACE2 (rs4646116), GSTO1 (rs4925) and GSTO2 (rs156697) were assessed in 255 COVID-19 patients and 236 matched healthy individuals, emphasizing their individual and haplotype effects on disease development and severity. Polymorphisms were determined by the appropriate qPCR method. The data obtained showed that individuals carrying variant GSTO1*AA and variant GSTO2*GG genotypes exhibit higher odds of COVID-19 development, contrary to ones carrying referent alleles (p = 0.044, p = 0.002, respectively). These findings are confirmed by haplotype analysis. Carriers of H2 haplotype, comprising GSTO1*A and GSTO2*G variant alleles were at 2-fold increased risk of COVID-19 development (p = 0.002). Although ACE2 (rs4646116) polymorphism did not exhibit a statistically significant effect on COVID-19 risk (p = 0.100), the risk of COVID-19 development gradually increased with the presence of each additional risk-associated genotype. Further studies are needed to clarify the specific roles of glutathione transferases omega in innate immune response and vitamin C homeostasis once the SARS-CoV-2 infection is initiated in the host cell.
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spelling pubmed-89557362022-03-26 GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19 Djukic, Tatjana Stevanovic, Goran Coric, Vesna Bukumiric, Zoran Pljesa-Ercegovac, Marija Matic, Marija Jerotic, Djurdja Todorovic, Nevena Asanin, Milika Ercegovac, Marko Ranin, Jovan Milosevic, Ivana Savic-Radojevic, Ana Simic, Tatjana J Pers Med Article Based on the close relationship between dysregulation of redox homeostasis and immune response in SARS-CoV-2 infection, we proposed a possible modifying role of ACE2 and glutathione transferase omega (GSTO) polymorphisms in the individual propensity towards the development of clinical manifestations in COVID-19. The distribution of polymorphisms in ACE2 (rs4646116), GSTO1 (rs4925) and GSTO2 (rs156697) were assessed in 255 COVID-19 patients and 236 matched healthy individuals, emphasizing their individual and haplotype effects on disease development and severity. Polymorphisms were determined by the appropriate qPCR method. The data obtained showed that individuals carrying variant GSTO1*AA and variant GSTO2*GG genotypes exhibit higher odds of COVID-19 development, contrary to ones carrying referent alleles (p = 0.044, p = 0.002, respectively). These findings are confirmed by haplotype analysis. Carriers of H2 haplotype, comprising GSTO1*A and GSTO2*G variant alleles were at 2-fold increased risk of COVID-19 development (p = 0.002). Although ACE2 (rs4646116) polymorphism did not exhibit a statistically significant effect on COVID-19 risk (p = 0.100), the risk of COVID-19 development gradually increased with the presence of each additional risk-associated genotype. Further studies are needed to clarify the specific roles of glutathione transferases omega in innate immune response and vitamin C homeostasis once the SARS-CoV-2 infection is initiated in the host cell. MDPI 2022-03-14 /pmc/articles/PMC8955736/ /pubmed/35330457 http://dx.doi.org/10.3390/jpm12030458 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Djukic, Tatjana
Stevanovic, Goran
Coric, Vesna
Bukumiric, Zoran
Pljesa-Ercegovac, Marija
Matic, Marija
Jerotic, Djurdja
Todorovic, Nevena
Asanin, Milika
Ercegovac, Marko
Ranin, Jovan
Milosevic, Ivana
Savic-Radojevic, Ana
Simic, Tatjana
GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19
title GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19
title_full GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19
title_fullStr GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19
title_full_unstemmed GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19
title_short GSTO1, GSTO2 and ACE2 Polymorphisms Modify Susceptibility to Developing COVID-19
title_sort gsto1, gsto2 and ace2 polymorphisms modify susceptibility to developing covid-19
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955736/
https://www.ncbi.nlm.nih.gov/pubmed/35330457
http://dx.doi.org/10.3390/jpm12030458
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