H. pylori genotypes, environmental and epidemiological factors can play a role in its pathogenicity. The genetic diversity and epigenetic modifications of H. pylori give rise to different levels of pathogenicity. Several studies have shown that the incidence and/or severity of gastroduodenal pathologies related to H. pylori may vary between geographic areas, such as studies have shown genotype of H. pylori in Europe differs from South-East Asia but is the same for the North of Iran and Uzbekistan [21, 22]. The predominant H. pylori strain circulating among geographic locations differs concerning the genomic structure [23]. The present study reports common H. pylori genotypes in Jahrom, Iran, and their clinical relevance.
The vacA gene was present in all H. pylori strains and it is a useful marker in predicting disease outcomes [24]. The vacA strain’s structure determines its in vitro cytotoxic activity, with m1 vacA type being more active than m2 type, s1a more active than s1b, and s2 vacA not producing detectable activity [17]. We found an apparent correlation between vacAs1bm1 positive cases and GERD (P = 0.002). Genotype vacA s1/m2 is a dominant H.pylori genotype in Iran, but no relationships were found between these genotypes and clinical outcomes. In this study, we found the vac A gene of H. pylori has 8 different combinations with its subtypes, and their prevalence are; vacAs1am1 (22.1%), vacAs1am2 (27.9%), vacAs1bm1 (2.3%), vacAs1bm2 (1.2%), vacAs1cm1 (1.2%), vacAs1cm2 (1.2%), vacAs2m1 (18.6%) and vacAs2m2 (25.6%). The most common genotype is vac A s1am2 with a prevalence of approximately 28%; however, S1m1 was the most common genotype in some research studies conducted on Afghan, Iranian, Turkish, and Thai patients [25–28]; however, in our research prevalence of s1m1(22.1%) is the third common genotype. A study from Shiraz, southern Iran, reported that vacA-positive strains were more frequently found in PUD patients than in NUD patients [29]. Another study in Tehran reported that the vacA s1 genotype was detected in 79% and 68% of PUD and NUD patients, respectively [30]. However, in our study, we didn't observe any correlation between any vacA subtypes and PUD or NUD.
The cagA toxin can induce severe gastric mucosa inflammation and is related to peptic ulcers and gastric cancer [17]. Based on literature regarding H. pylori genotype in Iran and worldwide, the prevalence of cag A genotype varies in different areas. The prevalence of cag A genotype is high based on studies conducted on Iranian and Iraqi patients [30]. However, in research conducted on Malaysian and Jordanian patients, cag A's prevalence is relatively low [31, 32]. The cagA was present in 60–70% of isolates from the Western population [33]. In our research, cagA was present in 60.5% of isolates. We observed hiatal hernia occurs in patients who were infected with cag A positive strain (P = 0.02). Several European and North American studies have shown that infection with cagA-positive H. pylori strains increases the risk for atrophic gastritis and gastric cancer [33]. However, several studies in Asian populations did not confirm these relationships, indicating important geographic differences, which is consistent with our research finding [34].
The association of the cagA-positive, vacA s1 genotypes with peptic ulcer disease (PUD) and gastric cancer was reported in Western countries, which was not consistent with our research and research in East Asian countries [23]. Patients infected with less virulent genotypes are more likely to have mild gastritis throughout their entire life, whereas patients infected with more virulent genotypes have a higher probability of developing peptic ulcer disease, atrophic gastritis, and eventually gastric carcinoma [34].
Our results showed that the most common allele in our isolates is m2 (55.9%), and s1 (55.9%), then s2 (44.2%). Although in other research on Iranian and Afghan patients [27], the most common allele is s1.
limitation
The limitation to our study was that some patients did not consent to undergo endoscopic investigations, and also, using endoscopy can cause inflammation in the mucosa and can interfere with the results of the H. pylori effect on mucosa.