In our 5 years of NIH funding, we enrolled a cohort of 486 children from 3 sites (Atlanta, Cleveland, Miami); 184 (38%) were Hp-infected. We made novel observations regarding environmental exposures, pilot validation of a symptom assessment instrument, pediatric Hp strain genotype/disease phenotype relationships, and disease paradigms not previously described in the pediatric population; i.e., atrophic gastritis and intestinal metaplasia associated with Hp infection. Overall hypothesis for competitive renewal: gastroduodenal disease (e.g., duodenal ulcer) in Hp-infected children is associated with specific host factors (i.e., race/ethnicity), environmental exposures, and infection by Hp strains carrying specific virulence genes contained within the cag pathogenicity island. These combined factors drive either a predominant Th2 gastric mucosal response with antral predominant severe mucosal inflammation (i.e., ulcer disease) or a Th1 response resulting in a more chronic, corpus-predominant inflammatory infiltrate (i.e., atrophy).