In the current study, we indicated the association between virulence genes of H. pylori and the GC. H. pylori infections are frequently asymptomatic and only a few individuals develop GC [31]. It has been indicated that some H. pylori virulence genes may play a significant role in the progress of post-H. pylori infection disorders such as GC.
In the previous studies, cagA and vacA of H. pylori were shown to have a significant association with peptic ulcers and GC [32–36]. Nevertheless, other studies have not established this association, specifying geographic variation [37]. Based on our analysis, the cagA gene was observed in 41.3% of the H. pylori-infected patients. The current reports are in comparison with earlier reports that show the cagA gene was present in about 65% of H. pylori isolates obtained from Asian and Western peoples [37–39]. The cagA-positive isolates of H. pylori have been also reported to be associated with gastric mucosal atrophy and GC [35, 40]. In a meta-analysis study, it was shown that patients infected with cagA-positive H. pylori isolates have an increased risk for GC [32]. Similarly, the subsequent analysis showed that infection by cagA-positive H. pylori isolates can increase the risk of GC [35]. Gohardani et al. showed that the expression of cagA was higher in Iranian patients with peptic ulcers compared to those with non-ulcer dyspepsia [41]. However, in studies conducted in Korea and Japan, there was no significant association between the cagA gene and the severity of gastroduodenal diseases [42, 43]. According to recent studies, the diversity of cagA types may explain such discrepancy [37].
The expression of babA and dupA genes were also significantly associated with GC in the current study.
Gerhard et al., and Hocker et al. revealed that H. pylori strain to carry babA was associated with the highest risk of the ulcer [44, 45]. In our results, however, there was not any association between babA- and dupA-positive H. pylori isolates and the development of GC, even though the expression of babA and dupA genes were also significantly associated with GC.
Our findings were inconsistent with the dupA gene being a marker for intestinal metaplasia and GC. In this survey, there was not any association between the presence of dupA and GC. Hong Lu et al. indicated that dupA was associated with a reduced risk for GC and an increased risk for duodenal ulcers [46]. A study in Brazilian adults also described that the existence of dupA was statistically lower in patients with GC [47]. However, Argent et al., reported that the dupA-positive H. pylori strains were more frequent in GC patients than duodenal ulcers (71% vs. 50%) [48]. The difference between these studies may be related to differences in the descriptions of geographic variations of circulation strains or patient groups.
In the current study, the vacA gene was present in 96.5% of H. pylori isolates, but no significant association between this gene and GC was observed. Likewise, in Asian studies, the existence of vacA was not statistically associated with GC [42, 43].
The iceA1 gene was not associated with GC in this study. However, some reports have proposed a reverse correlation [37, 38]. Two distinct allelic variants of iceA1 exist, in which iceA1 has been suggested to be associated with gastric disease [37].
The oipA gene was existing in 82% of H. pylori isolated in the current which was following the previous studies [49, 50]. Kudo et al. and Yamaoka et al. also identified the oipA gene from 30% and 45.9% of H. pylori isolates, respectively [51, 52]. Similar to our result, Shao et al., declared that no relationship exists between the oipA gene and gastrointestinal diseases [53]. Overall, the association between the oipA gene and GC needs further investigation.
In our study, the expression of some virulence genes of H. pylori was significantly higher in GC patients. Thus, it has been revealed that the eradication of H. pylori in patients with early GC would prevent the progress of new cancer [54].