Summary Background Helicobacter pylori is the main microorganism causing gastrointestinal diseases, such as chronic gastritis, peptic ulcer, MALT lymphoma, among others. The presence of the s1/m1 genotype of the vacA gene and EPIYA phosphorylation motifs of the cagA gene have been linked to the production of prolonged gastric inflammation. This study determines the presence of these virulence genotypes and their relationship with atrophic gastritis. Methods We included 231 patients with a history of dyspepsia undergoing upper gastrointestinal endoscopy. Samples of gastric tissue were taken to establish, through molecular techniques, the presence of H. pylori by amplifying the ureA and flaA2 housekeeping genes; in addition, the alleles of signal (s) and of the middle region (m) present in the vacA gene were amplified; and by sequencing the repeating patterns of the tyrosine phosphorylation motifs within the Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs of the cagA gene were also amplified. A chi-square test was performed in order to establish the relationship between the virulence genes and the degrees of gastric injury. Results A total of (91/231) samples were positive for H. pylori, of which (57/91) amplified the cagA gene and (66/91) the vacA gene. 81.8% (54/66) of the positive samples for the vacA gene showed the combination of the s1/m1 alleles, associated mostly with atrophic gastritis (AG). The most frequent EPIYA motifs were ABC and ABCC, with 54.4% (31/57) and 40.4% (23/57) respectively. A relation of the genes with AG and its injury severity with a p>0.05 value was observed. The cagA +/vacA s1/m1+/EPIYA ABC pattern is found in most samples. A p=0.02 relationship was found between the presence of the vacA gene and the cagA gene. Conclusions The results show a higher proportion of gastric atrophy in patients infected with H. pylori. The sum of the pathogenicity factors such as the cagA+/vacA s1/m1+/EPIYA ABCC genotype increases the virulence potential of the microorganism, suggesting that the coexistence of these genes could result in an increase in the severity of the progression of inflammation that leads to precancerous lesions.
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