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, Thai Hoa Nguyen1
, Thi Mai Ngan Nguyen2
and Thi Minh Thi Ha2,3
Introduction. The cagA and vacA genes encode the CagA and VacA proteins, which are the two main toxins of Helicobacter pylori. Regardless of whether the illness is benign or malignant, the majority of Asian H. pylori strains are cagA (+) and vacA s1 (vacA signal region 1 allele); hence, these genotypes cannot account for the severity of gastroduodenal disease.
Gap statement. The babA2 gene encodes the important adhesin BabA of H. pylori, which is crucial for persistent colonization and facilitates the translocation of CagA into host gastric epithelial cells. The synergic interaction of toxins, including CagA, VacA and BabA, could significantly contribute to the pathogenesis of H. pylori. The investigation of cagA, vacA and babA2 genes in clinical H. pylori isolates in Asian nations, particularly Vietnam, is insufficient.
Aim. To investigate the cagA, vacA and babA2 genotypes to further understand their synergistic interaction in the development of gastroduodenal disease in Vietnamese populations.
Methodology. A cross-sectional study was conducted on 169 H. pylori strains isolated from patients with gastroduodenal disease. The PCR assays were performed to determine the cagA, vacA and babA2 genotypes on DNA extracted from cultured H. pylori isolates.
Results. The research showed that the percentage of the cagA(+), babA2(+), vacA s1m1 and vacA s1m2 was 87.6%, 73.4%, 52.1% and 44.4%, respectively. The frequencies of cagA(+)/babA2(+)/vacAs1m1 and cagA(+)/babA2(+)/vacAs1m2 combinations were 44.4% and 28.4 %, respectively. The cagA(+)/babA2(+)/vacAs1m2 combination was associated with peptic ulcer disease [adjusted odds ratio (aOR)=5.53, 95 % confidence interval (CI) 1.09–28.16, P=0.039] in male patients and chronic gastritis with precancerous lesions (aOR=5.31, 95 % CI 1.23–22.89, P=0.025) in female patients.
Conclusion. The cagA(+)/babA2(+)/vacAs1m1 and cagA(+)/babA2(+)/vacAs1m2 combinations were found to be quite prevalent among Vietnamese H. pylori strains. The synergistic effect of cagA(+), babA2(+) and vacA s1m2 in increasing the odds of both peptic ulcer disease and gastric precancerous lesions has been observed.
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