A central unanswered question in understanding the impact of Helicobacter pylori on the human host relates to pathogenesis: why does Helicobacter infection cause disease only in a small proportion of the infected population, and why are different diseases associated with Helicobacter in separate geographic locations? Helicobacter is one of the most common chronic bacterial infections of humans, affecting more than 50% of the world’s population, but the majority of those infected remain asymptomatic throughout life. About 20% of infected adults manifest one of many different outcomes, such as duodenal ulcer, gastric ulcer disease, gastric cancers, or lymphoma. Several studies have highlighted inconsistencies between the prevalence rates for Helicobacter and disease. In industrialized countries there is generally a low prevalence of Helicobacter and gastric cancer yet a relatively high prevalence of peptic ulcer disease. On the other hand, some countries with high Helicobacter prevalence rates, have high gastric cancer prevalence rates but low peptic ulcer disease prevalence rates (e.g., Peru), yet other nonindustrialized countries with similar high Helicobacter prevalence rates have a disease distribution similar to that in industrialized countries (e.g., Iran)

This question is particularly intriguing in sub-Saharan Africa, where H. pylori infection is common but several studies have indicated a low incidence of peptic ulceration. Seroepidemiological studies have shown an early age of acquisition in children (50% by 10 years) , and prevalence in asymptomatic individuals is approximately equal to that in dyspeptic individuals.

A possible explanation for this “African enigma” may be that other factors are involved; these could relate to specific bacterial virulence factors, to differences in the host response to Helicobacter antigens, to differences in the environment (e.g., levels of antioxidants in the diet, water contamination, opportunities for hand washing), or to a combination of these, which might alter the processes by which ulceration or cancer develop. Alternatively, the burden of comorbidity or coinfection may modify the outcome of colonization by Helicobacter.

A number of studies have addressed the question of whether H. pylori infection is more or less frequent in people also infected with human immunodeficiency virus (HIV). The results are contradictory, with some studies demonstrating no difference in prevalence compared to a control population, while others show a lower or a higher prevalence. Most studies have investigated either North American, European, or Australian populations. In one study of African children a lower prevalence of H. pylori colonization was noted. In an Italian study the prevalences of both H. pylori colonization and peptic ulcer disease were noted, and these both correlated with CD4 count.

Several potential virulence factors or markers such as cytotoxin-associated protein (CagA), urease, lipopolysaccharide (LPS), or vacuolating cytotoxin (VacA) have been proposed. However, the relative contributions of these factors are still debated. Additionally, host genetics may also be involved in determining the outcome of infection, as it has recently been demonstrated that polymorphism in the interleukin-1 (IL-1) gene may predispose to the development of gastric cancer. Laboratory evidence also suggests that there is an interaction between Helicobacter and viral or parasitic infections which may modify the outcome of either or both infective processes.

The objective of the work described here was to assess the prevalence of H. pylori infection and gastroduodenal pathology in a population in sub-Saharan Africa with high HIV seroprevalence and to relate this to immune status, environmental factors, and bacterial pathogenicity factors.