ArticleJournal of clinical microbiology2004
The cag pathogenicity island of Helicobacter pylori is disrupted in the majority of patient isolates from different human populations.
Article in Journal of clinical microbiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 90 citations in OpenAlex.
- Review
- Long-term assessment of Helicobacter pylori cagA EPIYA motif changes and pathology outcomes in gastric biopsies of dyspeptic patients: 10-year follow-up.BMC gastroenterology · 2024Article
- Molecular pathogenesis, targeted therapies, and future perspectives for gastric cancer.Seminars in cancer biology · 2022Review
- Pre-Treatment with Grape Seed Extract Reduces Inflammatory Response and Oxidative Stress Induced byAntioxidants (Basel, Switzerland) · 2021Article
- Review
- Inference from the analysis of genetic structure of Helicobacter pylori strains isolates from two paediatric patients with recurrent infection.BMC microbiology · 2019Article
- DifferentialPathogens (Basel, Switzerland) · 2019Article
- Review
- Comparison of lipopolysaccharides composition of two different strains of Helicobacter pylori.BMC microbiology · 2017Article
- Determination ofMedical journal of the Islamic Republic of Iran · 2017Article
- Genetic variants ofGut pathogens · 2017Article
- Mixed Infections ofGastroenterology research and practice · 2016Article
- Diversification of theFrontiers in microbiology · 2016Article
- What exists beyond cagA and vacA? Helicobacter pylori genes in gastric diseases.World journal of gastroenterology · 2015Review
- Why do we still have Helicobacter Pylori in our Stomachs.The Malaysian journal of medical sciences : MJMS · 2015Article
- Friend and foe: factors influencing the movement of the bacterium Helicobacter pylori along the parasitism-mutualism continuum.Evolutionary applications · 2015Review
- Investigation of the association between clinical outcome and the cag pathogenicity-island and other virulence genes of Helicobacter pylori isolates from patients with dyspepsia in Eastern Turkey.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2013Article
- CagA EPIYA polymorphisms in Colombian Helicobacter pylori strains and their influence on disease-associated cellular responses.World journal of gastrointestinal oncology · 2013Article
- Ethnicity association of Helicobacter pylori virulence genotype and metronidazole susceptibility.World journal of gastroenterology · 2013Article
- Association of IS605 and cag-PAI of Helicobacter pylori Isolated from Patients with Gastrointestinal Diseases in Taiwan.Gastroenterology research and practice · 2013Article
Corrections and comments
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Authors and funding
15 authors at 10 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cag pathogenicity island (cag-PAI) is one of the major virulence determinants of Helicobacter pylori. The chromosomal integrity of this island or the lack thereof is speculated to play an important role in the progress of the gastroduodenal pathology caused by H. pylori. We determined the integrity of the cag-PAI by using specific flanking and internally anchored PCR primers to know the biogeographical distribution of strains carrying fully integral cag-PAI with proinflammatory behavior in vivo. Genotypes based on eight selected loci were studied in 335 isolates obtained from eight different geographic regions. The cag-PAI appeared to be disrupted in the majority of patient isolates throughout the world. Conservation of cag-PAI was highest in Japanese isolates (57.1%). However, only 18.6% of the Peruvian and 12% of the Indian isolates carried an intact cag-PAI. The integrity of cag-PAI in European and African strains was minimal. All 10 strains from Costa Rica had rearrangements. Overall, a majority of the strains of East Asian ancestry were found to have intact cag-PAI compared to strains of other descent. We also found that the cagE and cagT genes were less often rearranged (18%) than the cagA gene (27%). We attempted to relate cag-PAI rearrangement patterns to disease outcome. Deletion frequencies of cagA, cagE, and cagT genes were higher in benign cases than in isolates from severe ulcers and gastric cancer. Conversely, the cagA promoter and the left end of the cag-PAI were frequently rearranged or deleted in isolates linked to severe pathology. Analysis of the cag-PAI genotypes with a different biogeoclimatic history will contribute to our understanding of the pathogen-host interaction in health and disease.
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