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See article on page 499 Helicobacter pylori colonisation in the stomach is associated with increased risk for the development of peptic ulcer disease and non-cardia gastric adenocarcinoma.1 However, the incidences of these diseases vary in different parts of the world, and these rates have been changing over the past century. It now is clear that the mere presence of H pylori is insufficient to account for this variation. Alternative hypotheses to explain differing outcomes include variation in bacterial strains, in host related factors, or in the particular interactions governing the long term equilibrium between H pylori strain populations and the colonised host.2 In this issue, Kidd et al (see page 499) explore whether H pylori strain differences are related to illness occurrence in South African patients undergoing endoscopy. Why was such a study undertaken? Despite overall conservation of most genes, H pylori are a highly diverse bacterial species.3Their population structure indicates that they are freely recombining,4 which tends to eliminate clonal or allelic variation. Yet, in accordance with previous work, Kidd et al …
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Martin J. Blaser (1999) studied this question.
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