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World J Gastroenterol. Sep 7, 2019; 25(33): 4870-4884
Published online Sep 7, 2019. doi: 10.3748/wjg.v25.i33.4870
Helicobacter pylori virulence genes
Anja Šterbenc, Erika Jarc, Mario Poljak, Matjaž Homan
Anja Šterbenc, Erika Jarc, Mario Poljak, Institute of Microbiology and Immunology, Faculty of Medicine, University of Ljubljana, Ljubljana 1000, Slovenia
Matjaž Homan, Department of Gastroenterology, Hepatology and Nutrition, University Children’s Hospital, Faculty of Medicine, University of Ljubljana, Ljubljana 1000, Slovenia
Author contributions: All authors contributed equally to this paper, with conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.
Conflict-of-interest statement: No potential conflicts of interest. No financial support.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Matjaž Homan, MD, PhD, Assistant Professor, Department of Gastroenterology, Hepatology and Nutrition, University Children’s Hospital, Faculty of Medicine, University of Ljubljana, Bohoričeva 20, Ljubljana 1000, Slovenia. matjaz.homan@guest.arnes.si
Telephone: +386-1-5229276 Fax: +386-1-5229350
Received: May 18, 2019
Peer-review started: May 20, 2019
First decision: July 21, 2019
Revised: July 29, 2019
Accepted: August 7, 2019
Article in press: August 7, 2019
Published online: September 7, 2019
Processing time: 112 Days and 12 Hours
Abstract

Helicobacter pylori (H. pylori) is one of the most important human pathogens, infecting approximately half of the global population. Despite its high prevalence, only a subset of H. pylori infected individuals develop serious gastroduodenal pathology. The pathogenesis of H. pylori infection and disease outcome is thus thought to be mediated by an intricate interplay between host, environmental and bacterial virulence factors. H. pylori has adapted to the harsh milieu of the human stomach through possession of various virulence genes that enable survival of the bacteria in the acidic environment, movement towards the gastric epithelium, and attachment to gastric epithelial cells. These virulence factors enable successful colonization of the gastric mucosa and sustain persistent H. pylori infection, causing chronic inflammation and tissue damage, which may eventually lead to the development of peptic ulcers and gastric cancer. Numerous studies have focused on the prevalence and role of putative H. pylori virulence genes in disease pathogenesis. While several virulence factors with various functions have been identified, disease associations appear to be less evident, especially among different study populations. This review presents key findings on the most important H. pylori virulence genes, including several bacterial adhesins and toxins, in children and adults, and focuses on their prevalence, clinical significance and potential relationships.

Keywords: Helicobacter pylori; Virulence genes; Disease association; Children; Adults; Outer membrane proteins; Bacterial toxins

Core tip: The assessment of pathogenicity of a plethora of Helicobacter pylori (H. pylori) virulence genes appears to be relatively difficult. In specific, H. pylori isolates show a high degree of geographic variability, with certain H. pylori genotypes being associated with a more severe clinical outcome in some regions, while presenting as virtually harmless variants in other studied populations. To date, cagA and certain allelic variants of vacA have been most consistently associated with severe gastroduodenal disease in both children and adults, whereas the role of outer membrane proteins, such as babA2, sabA, homB and oipA, is somewhat more ambiguous.