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Helicobacter pylori is perhaps the most prevalent and successful human pathogen worldwide. Since it was initially suggested in 1983 by Marshall and Warren to be implicated in gastritis and peptic ulcer disease, H. pylori has also been implicated in gastric carcinoma and was classified as a class I carcinogen. Over half of the world's population is colonised with this gram-negative bacterium with most infections being acquired early in life and may persist for the life of the individual. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. While infected individuals mount an inflammatory response that becomes chronic, along with a detectable adaptive immune response, these responses are ineffective in clearing the infection. H. pylori has unique features that allow it to reside within the harsh conditions of the gastric environment, and also to evade the host immune response. Therefore, disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonise a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonisation of the gastric mucosa and subsequently seem to modulate the host's immune system. In this review, the various virulence factors expressed by this bacterium and how they interact with the host epithelium to influence pathogenesis are discussed.

iosr journal of pharmacy

Helicobacter Pylori- Factors of Virulence and Persistence: The Ability to Colonise the Human Stomach for Extended Periods Despite Host Immune and Inflammatory Responses.