The pathogenesis of H. pylori infection. Virulence factors such as CagA, genes within the cag PAI, VacA, BabA and SabA are involved in numerous host cell effects. H. pylori adherence to gastric epithelial cells is mediated by BabA and SabA binding Lewis^b, and Lewis^x/a respectively, thus facilitating H. pylori colonization and the efficient delivery of virulence factors to host cells. Following the attachment of H. pylori to gastric epithelial cell, the CagA protein is delivered into gastric epithelial cells through the H. pylori type 4 secretion system (T4SS). There, CagA may be tyrosine phosphorylated at EPIYA sites initially by SRC and in more sustained fashioned by ABL kinases. CagA can interact with intracellular proteins and deregulate distinct signaling pathways through both tyrosine phosphorylation-dependent or independent mechanisms. The pathobiological effects including cell elongation (producing cell scattering and the “hummingbird” phenotype), disruption of intercellular junctions, loss of cell polarity, the promotion of inflammation and dysregulation of proliferation and apoptosis. The effects of VacA on host cells include induction of cytoplasmic vacuolation, mitochondrial damage, cytochrome c release, apoptosis and immune evasion. Many of these events may contribute to gastric carcinoma development.