Previous studies have implicated CagA [encoded by cytotoxin-associated gene A (cagA)] in Helicobacter pylori-associated gastroduodenal pathology and distinct subgenotypes of cagA may circulate in different pathological manifestations of cagA-positive H. pylori infection. To investigate cagA genotype and variants in Chinese H. pylori strains and explore their relationship with gastroduodenal diseases, the cagA status of 82 Chinese H. pylori strains was examined and variation in size of the 39 region of cagA in 71 of these strains was analysed by PCR. cagA was detected in 28 (100 %) of 28 strains from peptic ulcer patients, two (100 %) of two strains from gastric cancer patients, 32 (94 . 1 %) of 34 strains from chronic gastritis patients and 17 (94 . 4 %) of 18 strains from healthy volunteers. PCR products of the cagA 39 variable region were obtained from 71 (92 . 2 %) of 77 Chinese H. pylori strains and could be classified into subgenotypes I, II and III, which gave PCR products of around 825, 900 and 950 bp, respectively. Subgenotype I cagA predominated in Chinese H. pylori strains (67/71), whereas subgenotype II cagA presented in two isolates from patients with chronic gastritis and subgenotype III presented in two isolates from healthy volunteers. Therefore, neither cagA nor its 39 region variants can be used as a sole marker for the presence of particular H. pylori-related gastroduodenal diseases in the Chinese population.
INTRODUCTIONIt is generally accepted that Helicobacter pylori strains that produce CagA, an antigenic outer-membrane protein of variable molecular mass from 128 to 140 kDa, are highly virulent. Several studies have implicated CagA in the development of duodenal ulcer and gastric adenocarcinoma in most western populations (Covacci et al., 1993;Blaser et al., 1995;Torres et al., 1998;Bach et al., 1999;Miehlke et al., 2000;Abasiyanik et al., 2002; Nomura et al., 2002a, b;Oliveira et al., 2003;Wu et al., 2003), whereas the majority of reports from east Asian countries (Miehlke et al., 1996; Pan et al., 1997; Shimoyama et al., 1997;Maeda et al., 1998;Zheng et al., 2000;Groves et al., 2002; Lai et al., 2002), as well as those from Estonia (Andreson et al., 2002) and Argentina (Catalano et al., 2001), showed a very high prevalence of cagA-positive H. pylori, irrespective of clinical manifestation. Furthermore, it was reported that a PCR primer set that amplified cagA from H. pylori isolated in one country failed to detect cagA in isolates from another country (Miehlke et al., 1996; Pan et al., 1997). These discrepancies have led to the hypotheses that there may be several distinct forms of CagA with an uneven geographical distribution, that differences in cagA subgenotypes may provide a marker for differences in virulence among cagA-positive H. pylori strains and that only some forms of CagA are associated with severe gastroduodenal diseases.cagA is noted for its sequence diversity, both within and outside the variable 39 region of the molecule. Repeat sequences in the variable region are the m...