We aimed to develop an H. pylori-infected mouse model using clinically stored strains in Taiwan and to test whether development of H. pylori infection in an in vivo animal model is related to the status of the cagA gene. A total of 100 male BALB/c mice, 6-8 weeks old, including 80 in the experimental group and 20 in the control group, were used. Two clinically stored H. pylori isolates, a cagA-positive and a cagA-negative strain, were selected to induce the H. pylori infection in half (N = 40) of the mice in the experimental group. Bacterial isolates of 0.8 x 10(9) CFU/ml were orally inoculated in each mouse of the experimental group for three consecutive days. Ten mice in the control group were sacrificed to confirm the initial absence of H. pylori. Eight weeks after inoculation of the experimental group and no inoculation of the remaining 10 mice 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 CLOtest or histology. In contrast, excluding eight of 80 mice that died before the eighth week, 90.3% (65/72) of the mice challenged with H. pylori showed persistent presence of H. pylori by histology. The severity of gastritis at the eighth week was more evident in H. pylori-infected mice than in control and noninfected mice (P < 0.05). Although gastritis was more severe in mice inoculated with the cagA-positive strain than with the cagA-negative strain, the rates of H. pylori infection in mice were not different between cagA-positive and -negative strains (91.4% vs 89.2%, P > 0.05). In summary, stored strains of H. pylori can be applied to induce an infection model in BALB/c mice. The less virulent cagA-negative strain can induce H. pylori infection in mice as effectively as the cagA-positive strain. The high prevalence of cagA-positive strains in Taiwanese patients may be related to factors other than only the cagA gene of the bacteria.