Helicobacter pylori is ubiquitous in Africa, with acquisition in childhood
the rule. Despite the prevalence of a virulent strain (in Soweto, most H. p
ylori organisms are cagA- and vacAS(1)-positive) H. pylori-associated patho
logy (duodenal ulcer, gastric ulcer and gastric cancer) has a variable, oft
en low distribution in sub-Saharan Africa that does not parallel H. pylori
prevalence in the population, suggesting a different natural history from t
hat seen in developed countries. Progression to atrophic gastritis in Afric
ans does not appear to differ from that reported in other regions, but as y
et unidentified factors may play a role in inhibiting progression to gastri
c cancer. Studies have suggested that the specific IgG subclass response to
H. pylori is predominately IgG(1) (suggestive of a Th2 response), and the
Th2 response may provide a protective effect against development of gastric
cancer. Host immune mechanisms may be the key to different responses to H.
pylori in the developed and developing worlds.