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We aimed to develop an H. pylori-infected mousemodel using clinically stored strains in Taiwan and totest whether development of H. pylori infection in an invivo animal model is related to the status of the cagA gene. A total of 100 male BALB/cmice, 6-8 weeks old, including 80 in the experimentalgroup and 20 in the control group, were used. Twoclinically stored H. pylori isolates, a cagA-positive and a cagA-negative strain, were selected toinduce the H. pylori infection in half (N = 40) of themice in the experimental group. Bacterial isolates of0.8 × 109 CFU/ml were orally inoculatedin each mouse of the experimental group for threeconsecutive days. Ten mice in the control group weresacrificed to confirm the initial absence of H. pylori.Eight weeks after inoculation of the experimental group and no inoculation of the remaining 10mice of the control group, each mouse was killed.Gastrectomy was then performed for rapid urease test(CLOtest) and histology. In the control group, none of 20 mice had positive results from the CLOtestor histology. In contrast, excluding eight of 80 micethat died before the eighth week, 90.3% (65/72) of themice challenged with H. pylori showed persistent presence of H. pylori by histology. Theseverity of gastritis at the eighth week was moreevident in H. pylori-infected mice than in control andnoninfected mice (P 0.05). In summary, storedstrains of H. pylori can be applied to induce aninfection model in BALB/c mice. The less virulentcagA-negative strain can induce H. pylori infection inmice as effectively as the cagA-positive strain. Thehigh prevalence of cagA-positive strains in Taiwanesepatients may be related to factors other than only thecagA gene of the bacteria.