f gastro-duodenal diseases, such as chronic active gastritis, peptic ulcer disease, gastric cancer, and gastric mucosa associated lymphoid tissue (MALT) lymphoma1. It is estimated that about half of the world's population is infected with H. pylori. But despite the high prevalence of infections only a minority of infected individuals will develop gastric carcinoma or MALT lymphoma. Therefore, it is essential to identify factors that might determine the possible sequelae of the H. pylori infection, such as host and environmental factors and bacterial virulence genes.
The specific H. pylori virulence genes found to be associated with possible disease outcome are the various alleles of the vacA gene, the presence of the cagA gene as a marker for a pathogenicity island, and the allelic variants of the iceA gene. The vacA gene is present in all H. pylori strains and encodes for the vacuolating cytotoxin, VacA which causes vacuolar degeneration of gastric epithelial cells. The vacA gene, although present in all strains, differs in its allelic variants in the signal region and the mid-region of the gene. The sequence variations in the signal region are distinguished into vacA s1 and vacA s2 subtypes, and the mid-region can be distinguished into m1 or m2 subtypes2. The allelic variants of the vacA gene that were detected by nested PCR were vacAs1/m1, vacAs1/m2 and vacAs2/m2. These vacA gene variants are associated with different cytotoxin activities. The cagA gene is a marker for the presence of the cag pathogenicity island, which is a 40 kb locus containing 31 genes associated with the induction of interleukin 8 secretion by gastric epithelial cells3. The allelic variants of the iceA gene are distinguished into iceA1 or iceA2 and only one of which being found in all H. pylori strains. The iceA gene seems to be induced by contact with epithelium
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