Narrative review details Helicobacter pylori immune evasion, epigenetic changes, and oncogenesis in infected hosts, highlighting eradication strategies to prevent gastric cancer.
Helicobacter pylori infects more than 50% of the human population worldwide. Persistence and colonization of this bacterium in the host result in genetic and epigenetic alteration and intra-complicated reactions that enhance innate and adaptive immune responses, which lead to the development of several gastrointestinal illnesses and increase the risk for gastric cancer progression. Even the World Health Organization (WHO) classified a bacterium in the first group of carcinogens; also, it has been associated with multiple extra gastric implications such as autoimmune disease and cardiovascular disease, thereby being considered a highly infectious pathogen and a critical health problem globally. Detection of the infection facilitates prognosis for suitable treatment that enhances eradication of this bacterium to prevent further implication. The aim of this review is to convey several aspects related to the Helicobacter pylori infection, to understand and clarify the epigenetic changes, host immune response, and the pathogenicity of multiple virulence factors involved in the infection, as well as diagnostic options, the fundamental strategy of treatment and the rate of reinfection among variable individuals.
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Alfurjani et al. (2025) studied this question.
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