Aim. The aim of this study was to identify the presence of H. pylori in biopsy specimens from symptomatic patients by PCR. In addition, the rate of cagA, vacA, iceA1, and iceA2 virulence genes was determined. Materials and Methods. One hundred antral gastric biopsy specimens were collected during endoscopy from patients suffering from gastroduodenal symptoms. The samples were collected by the gastroenterologists in their own clinics in Ramallah, Palestine. DNA was extracted from the biopsies and subsequently used for PCR identification of H. pylori and the virulence genes using specific primers. Results. The rate of positive H. pylori in the collected biopsies was 44%. The rates of the virulence genes in this sample: cagA, vacA, iceA1, and iceA2 were 65.9%, 40.9%, 63.6%, and 84.1%, respectively. Conclusion. The iceA2 gene was the most frequent in this study. Much research is necessary to determine the presence of an association of this gene with gastric pathology. Variation in the rates of the iceA gene in different countries is a strong indication of its geographical distribution. This study would provide important information regarding the prevalence of virulence genes (vacA, cagA, iceA1, and iceA2) in H. pylori strains in the sample tested in this country. 1. Introduction Helicobacter pylori is a microaerophilic, spiral shaped Gram-negative bacterium that colonizes the human stomach. It has been linked to chronic active gastritis, peptic ulcers disease, gastric cancer, and mucosa-associated lymphoid tissue lymphoma [1, 2]. H. pylori has been classified as a definite class I carcinogen by the World Health Organization [3]. Although the prevalence of H. pylori infection may exceed 70% in some developing countries [4, 5], only a small percentage of the population develop severe disease. This can be attributed to the involvement of specific factors that contribute to the pathogenicity of this organism. The cytotoxin-associated gene (cagA), a marker for cag pathogenicity island, is associated with severe clinical diseases as seen in peptic ulcer disease and gastric adenocarcinoma [1]. The vacuolating cytotoxin (vacA) gene encodes for the vacuolating cytotoxin, the pore forming toxin which causes progressive vacuolation and injury to gastric epithelium [6, 7]. The induced by contact with epithelium (iceA) A gene has been considered as the marker for peptic ulcer disease. The aims of this study were to identify H. pylori directly from biopsy specimen collected from symptomatic patients using primers to amplify the ureA and glmM (ureC) genes and to determine
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