Virulence Attributes of Helicobacter Pylori Isolates & Their Association with Gastroduodenal Disease (Report‪)‬

Helicobacter pylori has been identified as a major cause of peptic ulcer disease (PUD) and a risk factor for gastric cancer (GC) and mucosa-associated lymphoid tissue (MALT) lymphoma (1,2). On a global scale, GC is the second commonest cancer in the world. There is substantial international variation in GC incidence with the highest rates reported from China, Japan and other Eastern Asian countries. Epidemiological studies have proved that H. pylori infection is considered as a risk factor for GC, and WHO International Agency for Research on Cancer has classified this bacterium as a definite carcinogen (2). While the majority of the H. pylori infected individuals develop no significant clinical disease, some develop two kinds of divergent clinical diseases, PUD and GC3. The reasons for this may be related to differences in genetic susceptibility of the host, environmental factors, and genetic diversity of H. pylori (4). In this context, the relevance of specific H. pylori virulence associated genes has been extensively studied. The cytotoxin associated gene A (cagA) was the first to be identified; about 60-70 per cent of H. pylori strains in the West were found to be cagA+ and these strains were associated with duodenal ulcer (DU) and GC (5,6). However, more than 90 per cent of H. pylori strains in Asia are cagA+ irrespective of DU and GC (7,8). The cagA gene can be classified into type A, B, C and D based on its 3'- terminal repetitive sequences (8), however, the association of these subtypes with clinical disease remains unclear. The vacuolating toxin (vacA) was subsequently discovered and its allelic variants were identified in the signal region (sla, sib, sic or s2) and mid region (m1 or m2) (9). Specifically, vacA si/ml strains have higher cytotoxic activity than si/ m2 strains, whereas s2/m2 strains have no cytotoxic activity (9). Specific vacA genotypes are associated with level of toxin production and clinical diseases like PUD and GC in different part of the world (9-10). Studies have also provided evidence that bacterial adherence factors may also contribute to the pathogenicity of H. pylori. The blood group antigen binding adhesin (babA) has been shown to mediate adherence of H. pylori to human blood group antigens on gastric epithelial cells (11). However, the role of babA2 gene in the development of GC and PUD remains undefined. It is well established that differential cagA and vacA genetic characteristics exist in H. pylori strains isolated from different geographical regions. Therefore, using molecular techniques to study the association of H. pylori genotypes or strains with gastroduodenal diseases has become an important study area. The current study was done with an objective to identify the frequency cagA, cagA3/ region subtypes, babA2 and vacA genotypes of H. pylori isolates and their association with gastroduodenal diseases. Material & Methods