Our results revealed that the co-infection of H. pylori with EBV not only dramatically enhances the expression of the EBV latent antigen EBNA1 and the key activator ZTA (encoded by BZLF1) for lytic replication, but also leads to a significant change in tissue structure (enhanced phagosome-like vesicle size, with co-localization of both H. pylori and EBV-like particles, and the accumulation of enzyme-like particles) and upregulates the expression of host genes, including VIL1 and Lgr5, which are related to cell proliferation and tissue morphogenesis (Fig. 9). The gene discussed is VIL1; the disease is coinfection.