Genetic Diversity of Helicobacter pylori and its Impact on Disease Outcomes: Host and Environmental Perspectives

Host genetic susceptibility and lifestyle are pivotal factors that determine the incidence and clinical manifestation of persistent infections, including Helicobacter pylori (H. pylori). About 80% of H. pylori infected individuals remains asymptomatic throughout their life time, however, the rest of the infected individuals are associated with multiple clinical manifestations including ulcers, gastric cancer and MALT lymphoma. The International Agency for Research on Cancer (IARC), a specialized cancer research agency of the World Health Organization (WHO), has classified H. pylori as a class I carcinogen to humans. The onset and severity of diseases associated with Helicobacter pylori are dependent on a structured cascade of bacterial infection and the interplay of multiple host physiological processes and variables. Bacterial virulence factors, including the cag-Pathogenicity Island (cagPAI), VacA, and urease, are critical for the bacterium's ability to colonize and damage the gastric epithelium. Additionally, genetic variability among H. pylori strains contributes to differences in disease outcomes and responses to treatment. These factors, in combination, influence the clinical manifestation and progression of H. pylori-associated diseases. Considering both host genetic factors and environmental conditions, including diet, hygiene, and antibiotic use, significantly influences the progression and clinical manifestations of H. pylori infection. This holistic approach may enable the development of more personalized strategies for combating bacterial infections. This review article explores the multifaceted pathogenicity of H. pylori by examining the roles of bacterial virulence factors, genetic variability, and environmental influences. Key words: Helicobacter pylori, CagA, genetic diversity, environmental factors, microRNAs, bacterial virulence and gastric cancer.