The H. pylori cagA gene, vacA gene and iceA gene are considered to be important virurence factors that have been implicated in the development of gastric adenocarcinoma. It was reported that the presence of IS605 elements may be responsible for rearrangements and lead to partial or total deletions of the cag pathogenicity island (PAI) and the virulence of cag PAI may be changed. However, different results regarding the association between these virulence factors and clinical disease have been reported from different geographic regions. This study evaluated the relationship between H. pylori virulence factors such as cagA, vacA, iceA, IS605 and gastric adenocarcinoma.

H. pylori isolates were obtained from 54 infected patients (24 cases of gastric adenocarcinoma, 30 cases of control). H. pylori isolates were identified by PCR with ureC gene and 16S rRNA. PCR was performed to examine cagA, vacA, iceA and IS605 genotypes.

Significant difference was found in the negative rates of cagA between gastric adenocarcinoma group and control (62.5% vs. 33.3% P=0.033). No significant difference was found in the prevalence of iceA, vacA between gastric adenocar cinoma and control. The genotype of cagA⁺ vacA s1-m1 iceA1 was predominant in H. pylori isolates irrespective of the clinical outcome. IS605 in PAI was not found in gastric adenocarcinoma gruop and control. The positive rates of IS605 in genome were 33.3% in gastric adenocarcinoma group and 36.7% in control (P>0.05). In gastric carcinoma, the positive rate of cagA⁺/IS605⁻ was lower than in control (12.5% vs. 40.0%, P=0.025) and the positive rate of cagA⁻/IS605⁻ was higher than in control (54.2% vs. 23.3%, P=0.02).

H. pylori virulence factors had not related significantly with gastric adenocarcinoma. Further study is needed to examine the specificity of H. pylori strains.