Co-infection of <i>Helicobacter pylori</i> with Epstein-Barr virus in gastric organoids enhances cell proliferation and morphogenesis

<i>Helicobacter pylori</i> (<i>H. pylori</i>) infection is a major contributor to chronic inflammation and the development of gastric cancer. Furthermore, Epstein-Barr virus (EBV) has been shown to play a role in the oncogenic process of gastric cancer by promoting chronic inflammation and increasing tissue damage. However, the mechanism by which co-infection contributes to gastric carcinogenesis remains unclear. In this study, we used patient-derived gastric organoids as a model to establish EBV-<i>H. pylori</i> co-infection using microinjection technology and found that co-infection causes significant structural changes and promotes cell proliferation. This model will not only contribute to a better understanding of the pathogenesis of gastric cancer but will also be important for drug efficacy evaluation and the development of new therapeutic approaches.