Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico

Detalhes bibliográficos
Ano de defesa: 2011
Autor(a) principal: Rafaella Ferreira Avelar Costa
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Minas Gerais
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: https://hdl.handle.net/1843/70241
Resumo: The dupA (“duodenal ulcer promoting gene A”) is constituted by two virB4 genes, jhp0917 and jhp0918, that forms one single gene of 1839 base pairs when there is an insertion of a T or C base after the position 1385 of the jhp0917 3’ region. The gene was described as a putative virulence marker of H. pylori associated exclusively with duodenal peptic ulcer in Asiatic patients. However, the study of this marker in strains isolated from different populations has showed wide variation in its association with diseases. In Brazil, the prevalence of strains considered to be dupA positive by PCR is too high and the presence of the gene has not been associated with the diseases associated with H. pylori infection. The differences observed in the literature may be due to the detection of only part of the gene, when conventional methods are used, since polymorphisms that create premature stop codon have been described. The aim of this study was to investigate, by gene sequencing, the presence of polymorphisms in the entire extension of the dupA gene from H. pylori strains isolated from patients with gastritis (n=26), duodenal ulcer (n=29) and gastric carcinoma (n=20), using the methodology of Primer Walking. From the 75 strains, 41 (54.7%) did not have polymorphisms that create stop codons before the 1839 position and were considered as dupA-intact. On the other hand, 34 (45.3%) strains had one or more polymorphisms that create premature stop codons, splitting the gene in smaller products than the one described as dupA. The presence of the intact dupA was more frequently observed in strains isolated from patients with duodenal ulcer [n=19 (65.5%)] than those from patients with gastritis [n=12 (46.2%)] or gastric carcinoma [n=10 (50%)]. In logistic analysis, adjusting for gender and age, the presence of intact dupA independently associated with duodenal ulcer (p=0.02, OR=5.06, IC 95%=1.22 – 20.96), indicating that the gene is a risk factor for the disease in our population.
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spelling Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástricoMicrobiologiaHelicobacter pyloriPolimorfismo GenéticoHelicobacter pyloridupAPolimorfismosThe dupA (“duodenal ulcer promoting gene A”) is constituted by two virB4 genes, jhp0917 and jhp0918, that forms one single gene of 1839 base pairs when there is an insertion of a T or C base after the position 1385 of the jhp0917 3’ region. The gene was described as a putative virulence marker of H. pylori associated exclusively with duodenal peptic ulcer in Asiatic patients. However, the study of this marker in strains isolated from different populations has showed wide variation in its association with diseases. In Brazil, the prevalence of strains considered to be dupA positive by PCR is too high and the presence of the gene has not been associated with the diseases associated with H. pylori infection. The differences observed in the literature may be due to the detection of only part of the gene, when conventional methods are used, since polymorphisms that create premature stop codon have been described. The aim of this study was to investigate, by gene sequencing, the presence of polymorphisms in the entire extension of the dupA gene from H. pylori strains isolated from patients with gastritis (n=26), duodenal ulcer (n=29) and gastric carcinoma (n=20), using the methodology of Primer Walking. From the 75 strains, 41 (54.7%) did not have polymorphisms that create stop codons before the 1839 position and were considered as dupA-intact. On the other hand, 34 (45.3%) strains had one or more polymorphisms that create premature stop codons, splitting the gene in smaller products than the one described as dupA. The presence of the intact dupA was more frequently observed in strains isolated from patients with duodenal ulcer [n=19 (65.5%)] than those from patients with gastritis [n=12 (46.2%)] or gastric carcinoma [n=10 (50%)]. In logistic analysis, adjusting for gender and age, the presence of intact dupA independently associated with duodenal ulcer (p=0.02, OR=5.06, IC 95%=1.22 – 20.96), indicating that the gene is a risk factor for the disease in our population.CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorUniversidade Federal de Minas Gerais2024-07-11T14:25:27Z2025-09-08T23:07:54Z2024-07-11T14:25:27Z2011-03-30info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisapplication/pdfhttps://hdl.handle.net/1843/70241porRafaella Ferreira Avelar Costainfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMG2025-09-08T23:07:54Zoai:repositorio.ufmg.br:1843/70241Repositório InstitucionalPUBhttps://repositorio.ufmg.br/oairepositorio@ufmg.bropendoar:2025-09-08T23:07:54Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)false
dc.title.none.fl_str_mv Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
title Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
spellingShingle Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
Rafaella Ferreira Avelar Costa
Microbiologia
Helicobacter pylori
Polimorfismo Genético
Helicobacter pylori
dupA
Polimorfismos
title_short Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
title_full Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
title_fullStr Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
title_full_unstemmed Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
title_sort Polimorfismos no gene dupA de Helicobacter pylori e risco de úlcera duodenal e carcinoma gástrico
author Rafaella Ferreira Avelar Costa
author_facet Rafaella Ferreira Avelar Costa
author_role author
dc.contributor.author.fl_str_mv Rafaella Ferreira Avelar Costa
dc.subject.por.fl_str_mv Microbiologia
Helicobacter pylori
Polimorfismo Genético
Helicobacter pylori
dupA
Polimorfismos
topic Microbiologia
Helicobacter pylori
Polimorfismo Genético
Helicobacter pylori
dupA
Polimorfismos
description The dupA (“duodenal ulcer promoting gene A”) is constituted by two virB4 genes, jhp0917 and jhp0918, that forms one single gene of 1839 base pairs when there is an insertion of a T or C base after the position 1385 of the jhp0917 3’ region. The gene was described as a putative virulence marker of H. pylori associated exclusively with duodenal peptic ulcer in Asiatic patients. However, the study of this marker in strains isolated from different populations has showed wide variation in its association with diseases. In Brazil, the prevalence of strains considered to be dupA positive by PCR is too high and the presence of the gene has not been associated with the diseases associated with H. pylori infection. The differences observed in the literature may be due to the detection of only part of the gene, when conventional methods are used, since polymorphisms that create premature stop codon have been described. The aim of this study was to investigate, by gene sequencing, the presence of polymorphisms in the entire extension of the dupA gene from H. pylori strains isolated from patients with gastritis (n=26), duodenal ulcer (n=29) and gastric carcinoma (n=20), using the methodology of Primer Walking. From the 75 strains, 41 (54.7%) did not have polymorphisms that create stop codons before the 1839 position and were considered as dupA-intact. On the other hand, 34 (45.3%) strains had one or more polymorphisms that create premature stop codons, splitting the gene in smaller products than the one described as dupA. The presence of the intact dupA was more frequently observed in strains isolated from patients with duodenal ulcer [n=19 (65.5%)] than those from patients with gastritis [n=12 (46.2%)] or gastric carcinoma [n=10 (50%)]. In logistic analysis, adjusting for gender and age, the presence of intact dupA independently associated with duodenal ulcer (p=0.02, OR=5.06, IC 95%=1.22 – 20.96), indicating that the gene is a risk factor for the disease in our population.
publishDate 2011
dc.date.none.fl_str_mv 2011-03-30
2024-07-11T14:25:27Z
2024-07-11T14:25:27Z
2025-09-08T23:07:54Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/masterThesis
format masterThesis
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://hdl.handle.net/1843/70241
url https://hdl.handle.net/1843/70241
dc.language.iso.fl_str_mv por
language por
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Universidade Federal de Minas Gerais
publisher.none.fl_str_mv Universidade Federal de Minas Gerais
dc.source.none.fl_str_mv reponame:Repositório Institucional da UFMG
instname:Universidade Federal de Minas Gerais (UFMG)
instacron:UFMG
instname_str Universidade Federal de Minas Gerais (UFMG)
instacron_str UFMG
institution UFMG
reponame_str Repositório Institucional da UFMG
collection Repositório Institucional da UFMG
repository.name.fl_str_mv Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)
repository.mail.fl_str_mv repositorio@ufmg.br
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