Helicobacter pyloriand gastroduodenal pathology: new threats of the old friend

The human gastric pathogenHelicobacter pyloricauses chronic gastritis, peptic ulcer disease, gastric
carcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma. It infects over 50% of the
worlds' population, however, only a small subset of infected people experienceH. pylori-associated
illnesses. Associations with disease-specific factors remain enigmatic years after the genome
sequences were deciphered. Infection with strains ofHelicobacter pylorithat carry the cytotoxinassociated
antigen A (cagA) gene is associated with gastric carcinoma. Recent studies revealed
mechanisms through which the cagA protein triggers oncopathogenic activities. Other candidate
genes such as some members of the so-called plasticity region cluster are also implicated to be
associated with carcinoma of stomach. Study of the evolution of polymorphisms and sequence
variation inH. pyloripopulations on a global basis has provided a window into the history of human
population migration and co-evolution of this pathogen with its host. Possible symbiotic
relationships were debated since the discovery of this pathogen. The debate has been further
intensified as some studies have posed the possibility thatH. pyloriinfection may be beneficial in
some humans. This assumption is based on increased incidence of gastro-oesophageal reflux
disease (GERD), Barrett's oesophagus and adenocarcinoma of the oesophagus followingH. pylorieradication in some countries. The contribution of comparative genomics to our understanding of
the genome organisation and diversity ofH. pyloriand its pathophysiological importance to human
healthcare is exemplified in this review.