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Information Journal Paper

Title

HELICOBACTER PYLORIVIRULENCE GENES AND MICROEVOLUTION IN HOST AND THE CLINICAL OUTCOME: REVIEW ARTICLE

Pages

  575-587

Abstract

 Helicobacter pylori (H. pylori) is the causative agent in development of gastroduodenal diseases, such as chronic atrophic gastritis, PEPTIC ULCERs, mucosa associated lymphoid tissue (MALT) lymphoma, and gastric cancer. H. pylori has been associated with inflammation in cardia, showing the fact that infection with this bacterium could also be a risk factor for gastric cardia cancer. Gastric cancer is the fourth most common cancer worldwide. This is the second leading cause of cancer-related deaths, and approximately 700, 000 people succumb each year to gastric adenocarcinoma. It has been estimated that 69% of the IRANian population currently harbor H. pylori infection. The prevalence of duodenal ulcer and gastric cancer is high in IRANian populations. However, this has been largely influenced by geographic and/or ethnic origin. Epidemiology studies have shown that host, environmental, and bacterial factors determine the outcome of H. pylori infection. The bacterium contains allelic diversity and high genetic variability into core- and virulence-genes and that this diversity is geographically and ethnically structured. The genetic diversity within H. pylori is greater than within most other bacteria, and its diversity is more than 50-fold higher than that of human DNA. The maintenance of high diversification makes this bacterium to cope with particular challenges in individual hosts. It has been reported that the recombination contributed to the creation of new genes and gene family. Furthermore, the microevolution incag A and vac A genes is a common event, leading to a change in the virulence phenotype. These factors contribute to the bacterial survival in acidic conditions in stomach and protect it from host immune system, causing tissue damage and clinical disease. In this review article, we discussed the correlation between H. pylori virulence factors and clinical outcomes, microevolution of H. pylori VIRULENCE GENES in a single host, microevolution of H. pylori during primary infection and progression of atrophic gastritis to adenocarcinoma, and H. pylori infection status in IRAN. Finally, we put forward the hypothesis that if the pattern of nucleotide sequence evolution shifts from recombination (r) to mutation (m) and the r/m ratio is reduced, bacterial pathogenicity may be reduced while maintaining the bacterial life. However, this hypothesis should be further studied with future experiments.

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    APA: Copy

    BAKHTI, SEYEDEH ZAHRA, LATIFI NAVID, SAEID, & ZAHRI, SABER. (2014). HELICOBACTER PYLORIVIRULENCE GENES AND MICROEVOLUTION IN HOST AND THE CLINICAL OUTCOME: REVIEW ARTICLE. TEHRAN UNIVERSITY MEDICAL JOURNAL (TUMJ), 72(9), 575-587. SID. https://sid.ir/paper/39530/en

    Vancouver: Copy

    BAKHTI SEYEDEH ZAHRA, LATIFI NAVID SAEID, ZAHRI SABER. HELICOBACTER PYLORIVIRULENCE GENES AND MICROEVOLUTION IN HOST AND THE CLINICAL OUTCOME: REVIEW ARTICLE. TEHRAN UNIVERSITY MEDICAL JOURNAL (TUMJ)[Internet]. 2014;72(9):575-587. Available from: https://sid.ir/paper/39530/en

    IEEE: Copy

    SEYEDEH ZAHRA BAKHTI, SAEID LATIFI NAVID, and SABER ZAHRI, “HELICOBACTER PYLORIVIRULENCE GENES AND MICROEVOLUTION IN HOST AND THE CLINICAL OUTCOME: REVIEW ARTICLE,” TEHRAN UNIVERSITY MEDICAL JOURNAL (TUMJ), vol. 72, no. 9, pp. 575–587, 2014, [Online]. Available: https://sid.ir/paper/39530/en

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