This leads to chronic inflammation, which also contributes to development of cancer.Association with <i>H. pylori</i> increases the risk of gastric carcinoma, and coexistence with EBV enhances proliferation of infected cells.Further, <i>H. pylori</i>-EBV coinfection causes chronic inflammation in pediatric patients.We have established an <i>H. pylori</i>-EBV coinfection model system using human gastric epithelial cells.We showed that <i>H. pylori</i> infection can increase the oncogenic phenotype of EBV-infected cells and that the cytotoxin-associated gene (CagA) protein encoded by <i>H. pylori</i> stimulated EBV-mediated cell proliferation in this coinfection model system.
Amerindian CagA proteins induced less production of IL-8 and cancer-associated Mucin 2 than did those of prototype Western or East Asian strains and behaved as dominant negative inhibitors of action of prototype CagA during mixed infection of Mongolian gerbils.
Numerous coinfections with different H. pylori strains in PU or CG patients indicate diversity of the infected H. pylori origins. s and m regions of vacA gene from different H. pylori isolates show high nucleotide sequence similarities. cagA gene positive rate, different vacA gene subtypes and coinfection with different H. pylori strains are not closely associated with severity of the diseases.
The cagA gene of H. pylori was used to test for mixed infection because it is present in only some strains, and its presence has been associated with ulcers.