Update on the pathogenesis and clinical management of <i>Helicobacter pylori</i> gastric infection and associated diseases

<i>Helicobacter pylori</i> (<i>H. pylori</i>) is a gram-negative, spiral-shaped, microaerophilic bacterium that infects over 43% of the global population, with higher prevalence in regions of low socioeconomic status and poor sanitation. It is transmitted mainly through oral-oral and fecal-oral routes and has evolved multiple mechanisms that allow colonization of the acidic gastric environment, including urease production, chemotaxis, and a variety of adhesins. The bacterium expresses several virulence factors that enhance its pathogenicity, such as cytotoxin-associated antigen A, vacuolating cytotoxin A, and the small regulatory RNA NikS, found to be essential for the fine-tuning of the bacterial virulence. Although many infected individuals remain asymptomatic, <i>H. pylori</i> infection is associated with multiple clinical outcomes, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma, all correlated to the host immune response and chronic inflammation. Diagnosis relies on both invasive and non-invasive methods, and growing antibiotic resistance poses a major challenge to treatment. New therapeutic strategies, such as tailored therapy, potassium-competitive acid blockers, and probiotics are under investigation. Vaccine development remains a key area of research, with several candidates currently in preclinical and clinical evaluation.