Susceptibility to Helicobacter pylori infection may manifest itself as
an increased prevalence of H. pylori infection, as reinfection after
eradication, or as different clinical outcomes (gastritis, peptic ulce
r disease, primary gastric B-cell lymphoma, or gastric cancer). These
outcomes are likely to be a result of interaction between environmenta
l and genetic factors. Genetic factors include both host genetic predi
sposition to infection as well as genetic differences in H. pylori str
ains. Twin studies indicate that the correlation coefficient for the r
elative importance of genetic effects (heritability) on acquisition of
H. pylori infection is approximately 0.66. The remaining variance is
accounted for by shared rearing environmental factors (20%), and non-s
hared environmental factors (23%), which contribute to the differences
and not the similarities seen between family members. Molecular epide
miological studies of both the whole bacterial genome and of amplified
regions between specific repetitive DNA sequences also suggest that t
here are disease-specific strains of H. pylori. There are, therefore,
many different facets of susceptibility to H. pylori infection.