Helicobacter pylori Oncogenicity: Mechanism, Prevention, and Risk Factors

Table 1

Major virulence factors of H. pylori and their biochemical effects in pathogenesis.

Virulence factor	Potential biochemical effect	References
Colonizing factors
Urease	Neutralizes stomach acid and urease-medicated activation of neutrophils and platelets causes gastric inflammation	[35]
Flagella	Enables the bacterium to move toward gastric epithelium cells and leads to colonization and persistent infection	[36]
Chemotaxis mechanism	Enables biofilm formation to induce oncogenic process and development of antibiotic resistance	[37]
Cell-surface proteins (adhesins)
BabA	Mediates attachment to the gastric epithelial cells and induces DNA double-strand breaks	[38]
SabA	Mediates bacterial attachment and colonization	[39]
OipA	Damages gastric mucosal membrane and causes cellular apoptosis	[40, 41]
Pathogenicity factors
CagA	Enhances cellular proliferation and IL-8 expression	[42, 43]
VacA	Induces cytoplasmic vacuole formation and causes cellular apoptosis	[44]
HtrA	Helps in delivery of CagA	[45]