Figure 3. Proposed generation of host-specific H. pylori Lewis antigen expression diversity. The original inoculum contains a mixed population of H. pylori cells, with the predominant cells having an 9-cytosine homopolymeric in-frame tract in futC, permitting the conversion of Lewis^x into Lewis^y. The mixed population also includes a small proportion of cells that each have a 10-cytosine futC tract, leading to a frame shift, and an inactive -(1,2) fucosyltransferase. The H. pylori inoculum was introduced into the stomachs of monkeys that predominantly expressed gastric epithelial Le^a and Le^x significantly greater then Le^b and Le^y (left stomach), or vice versa (right stomach). Over the ensuing 40 wk, cells with the 9-cytosine inframe futC that catalyzed Lewis^y production were selected in the monkeys that had the Le^b/Le^y predominant stomach, whereas in the Le^a/Le^x stomach, there was selection for the 10-cytosine out-of-frame futC, in which no Lewis^y was produced. In this model, the stoichiometry of the slipped-strand mispairing affects the speed at which phenotypic conversion can occur, but it is the homogeneity of the host environment and the differential fitness of the competing cellular forms that determine the ultimate location of the population equilibrium between the two molecular forms.