Table 2.

Virulence factors of H. pylori and their polymorphisms associated with gastric diseases.

Virulence factor	Function	Key polymorphisms/alleles/variants	Association with gastric diseases	Reference
Urease	Neutralizes gastric acidity by converting urea to basic ammonia. Induce inflammatory damage to gastric epithelium by activating various immune cells	-	Essential for bacterial colonization and further stages of H. pylori pathogenesis.	Mobley, 1996
BabA	Facilitates adhesion of H. pylori to gastric epithelial cells.	BabA-L: No Leb binding activity	Associated with high gastric mucosal damage and gastric cancer	Fujimoto et al., 2007
		BabA-H: Show Leb binding activity	Associated with mild gastric mucosal damage
		BabA-ve: No Leb binding activity
CagA	Virulence protein which alters host cell signaling pathways	ESS-CagA (EPIYA-D) Binds more strongly with SHP2 than WSS type and potentially activates the downstream pathways	Positively associated with aggressive gastric diseases.	Higashi et al., 2002
		K636N mutation	Higher risk of severe pathology	Ulloa-Guerrero et al., 2018
CagL	Type IV secretion system (TFSS) protein that binds with integrinβ1 receptor on host cell.	Y58/E59 polymorphism	Increased risk of gastric cancer.	Yeh et al., 2019
VacA	Pore forming toxin that induces vacuolation, mitochondrial damage and cell death.	vacA s1m	High risk of gastric precancerous lesions	Chang et al., 2018
		vacA c1and d1	Increased risk of gastric cancer	Thi Huyen Trang et al., 2016
DupA	Duodenal ulcer promoting protein	-	Increased risk of duodenal ulcer.	Lu et al., 2005
OipA	Enhance IL-8 secretion and induces inflammation	Functional oipA “on” status	Increased risk of peptic ulcer and gastric cancer	Liu et al., 2013
HPne4160	Non-coding RNA that regulate expression of outer membrane protein (OMP) and CagA	T-repeats present upstream of HPnc4160	Silences HPnc4160 resulting in increased expression of OMP and CagA	Kinoshita-Daitoku et al., 2021