Host immune response mediates changes in copy number and virulence potential of .

is the major risk factor for gastric cancer. harboring the type IV secretion system (T4SS) and its effector CagA encoded on the pathogenicity Island (PAI) increases the risk. PMSS1 has a multi- genotype, modulating copy number dynamically from zero to four copies. To examine the effect of the immune response on copy number change, we utilized a mouse model with different immune status. PMSS1 recovered from mice, lacking functional T or B cells, retained more copies. PMSS1 recovered from mice, showing intense inflammation, had fewer copies compared to those recovered from wild-type mice. Moreover, copy number of PMSS1 recovered from wild-type and mice was positively correlated with the capacity to induce IL-8 secretion at four weeks of infection. Since recombination in influences T4SS function, including CagA translocation and IL-8 induction, we constructed a multiple linear regression model to predict -induced IL-8 expression based on copy number and recombination status; induces more IL-8 secretion when the strain has more copies and intact . This study shows that PMSS1 in mice with less intense immune response possess higher copy number than those infected in mice with more intense immune response and thus the multi- genotype, along with recombination, functions as an immune-sensitive regulator of virulence.