The relationship between H. pylori infection and gastric cancer is an important research topic at home and abroad at present. It has been tentatively identified that HP is one of the initiating factors for gastric carcinogenesis. The main evidence of its relationship with gastric cancer comes from epidemiological surveys, and the HP infection rate and serum antibody level in areas with high incidence of gastric cancer are higher than those in low incidence areas. Foreign studies have more conclusively indicated that the risk of gastric cancer in patients with HP infection is six times higher than that in those without HP infection. Therefore, Forman and Genta et al. proposed the model of “chronic gastritis-atrophic gastritis-intestinal metaplasia-gastric cancer”, in which the gastric mucosa of HP-positive patients mainly shows chronic active inflammatory changes such as lymphocytic infiltration and lymphoid follicle formation, neutrophil infiltration, and epithelial erosion, which may be accompanied by decreased secretion of gastric mucosa epithelium and atrophy of gastric glands. It may be accompanied by decreased secretion of gastric mucosal epithelium and atrophy of gastric glands. In recent years, there have been more reports on the detection of CagA and CacA in different disease tissues (or strains) using PCR, and it was consistently found that the virulence of HP bacteria colonized in the stomach of patients with gastric cancer, precancerous state and ulcer disease was higher than that of those with gastritis alone. Yan Xiaojun et al. found that the rates of oncogene ras and oncogene P53 and P16 mutations were higher in HP-positive gastric cancer and precancerous tissue than in negative ones. The results of Houjie Liang et al. confirmed that HP infection, accelerated the proliferation of gastric mucosal cells, making them at a higher risk of cancer, while HP infection increased the degree of DNA damage in gastric mucosal cells, providing strong evidence for the relationship between HP infection and gastric cancer from the molecular level. Many clinical studies have found that HP infection can promote the development of gastric precancerous states such as atypical hyperplasia and atrophic gastritis, supporting a positive correlation between the two. In this study, we observed HP infection at various stages in the model of “chronic gastritis-atrophic gastritis-intestinal hyperplasia-gastric cancer”, and concluded that HP is more important in chronic active gastritis, atrophic gastritis, atrophic gastritis with intestinal hyperplasia, atypical hyperplasia and gastric adenocarcinoma. The high prevalence of HP infection in chronic active gastritis, atrophic gastritis, atrophic gastritis with enterocolitis, atypical hyperplasia and gastric adenocarcinoma was 81%, 75%, 78%, 69% and 79%, respectively, which was consistent with the results of domestic and international studies. The significance test of multiple rates confirmed that the HP infection rates were different in different diseases with significant differences. It was also found that the HP infection rate in the process of chronic gastritis-atrophic gastritis-intestinal metaplasia-gastric cancer was 48%, 75%, 78%, and 79%, respectively, showing a gradual increase.