Strategies used by helicobacter pylori to establish persistent infection

Table 1 Major virulence factors involved in the persistence of Helicobacter pylori

Virulence factors	Roles in persistent infection
OipA	Induces pro-inflammatory cytokines
	In combination with CagA, causes disruption of cell tight junctions
VacA	Increases IL8 expression and causes inflammation
	Contributes to long-term colonization
	Cell proliferation and elongation
	Increases the level of MAPK signaling
CagA	Stimulates the NF-κB pathway
	Induces apoptosis
	Induces pro-inflammatory cytokines
	Disrupts cell tight junctions
	Increases mucosal inflammation
BabA	Leads to effective cell adherence
	Mediates in the effective interaction between H. pylori and epithelial cells
DupA	Induces pro-inflammatory cytokines
	Induces apoptosis
GGT	Contributes to long-term gastric colonization
	Induces immune response tolerance
SabA	Mediates the effective interaction between H. pylori and epithelial cells

MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-κB; H. pylori: Helicobacter pylori.