Abstract
Helicobacter pylori infection induces chronic inflammation and is the strongest known risk factor for gastric cancer. The genomes of H pylori are highly diverse and therefore bacterial virulence factors play an important role in determining the outcome of H pylori infection, in combination with host responses that are augmented by environmental and dietary risk factors. It is important to gain further understanding of the pathogenesis of H pylori infection to develop more effective treatments for this common but deadly malignancy. This review focuses on the specific mechanisms used by H pylori to drive gastric carcinogenesis.