![]() pylori isolates recovered from antral biopsies of Iranian patients with stomach symptoms. In this study, we employed PCR-RFLP to investigate the genetic diversity of cagA as a virulence gene among H. However, the accuracy of the data provided by the PCR-RFLP method should be verified by a gold standard method when differentiating clinical isolates of H. ![]() pylori genes, especially those that encode proteins in relation to bacterial pathogenicity, such as cagA and vacA, and urease structural and accessory proteins ( 14- 18). PCR-RFLP analysis is another molecular method that has been used to investigate H. However, the sensitivity and specificity of this method were not compared with nucleic acid sequencing as a gold standard method. In this study, specific probes were used for the differentiation of H. pylori in gastric biopsy specimens has been introduced ( 13). Recently, a novel peptide nucleic acid probe for the specific detection of H. However, reproducibility is the main problem with this method. In comparison to PFGE, RAPD-PCR exhibits reasonable speed, cost, and efficiency. pylori genetic diversity and transmission ( 12). RAPD-PCR, on the other hand, has been reported to be a valuable method for the study of H. However, the PFGE method is time-consuming and requires a unique apparatus to handle a large number of clinical specimens. pylori genotyping has been described ( 11). By using restriction enzyme EcoRI and the PFGE method, a 97% improvement in H. pylori genotyping, such as pulsed-field gel electrophoresis (PFGE), PCR-based randomly amplified polymorphic DNA (RAPD) fingerprinting, and hybridization with specific probes ( 8- 10). Various methods have been employed for H. pylori possesses a remarkable degree of genetic diversity, closely related to its epidemiological and pathological characteristics and dynamics of transmission. Many investigators have demonstrated that H. The cagA gene encodes proteins that increase the virulence potencies of strains, such as by increasing host-cell cytokine production and altering protein tyrosine phosphorylation ( 6, 7). The cagA gene is a virulence gene located in the cag pathogenicity island of the bacterial genome, and is frequently associated with more severe clinical outcomes ( 3- 5). While the vacA gene is present in all strains of H. pylori, including urease, vacuolating cytotoxin (a product of the vacA gene), and the immunogenic protein CagA, encoded by the cytotoxin-associated gene A ( cagA). Many virulence factors are involved in the pathogenicity of H. Helicobacter pylori, the most common pathogenic bacterium in the human stomach, is a microaerophilic, Gram-negative organism involved in peptic ulcer disease and gastric cancer ( 1). Polymerase Chain Reaction Restriction Fragment Length Polymorphism 1. However, the data showed that cagA genotype III may play a role in duodenitis and duodenal ulcers in patients infected with H. Genotype I, which was predominant among the isolates, was significantly associated with gastritis. pylori cagA genotypes were detected in antral biopsies. Using the PCR-RFLP method, three distinctive H.
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