The origin of virulence in type I strains of Helicobacter pylori

Abstract

Genetic variation among strains of Helicobacter pylori is high and the population structure non-clonal. The infection historically has been associated with overt clinical outcomes that, for severity, range from chronic active gastritis to peptic ulcer disease and from MALT (mucosa-associated lymphoid tissue) lymphoma to distal gastric adenocarcinoma¹. Assuming that a large fraction of the reshuffled bacterial genes has no relevance for pathology, scientists have tried to reduce the whole to a set of genes associated with virulence. This follows more than a decade of elegant studies on bacterial pathogenesis where pathogens always clustered and separate from non-pathogens and pulses of genetic information segregate with the virulent variants. Helicobacter diversity has been explored by RAPD (random amplification of polymorphic DNA), DNA fingerprinting, multilocus enzyme electrophoresis and by genetic mapping with pulsed-field gel electrophoresis^2–4. All these approaches lead to the conclusion that mutations are frequent and that single genes or operons are scrambled. This is in contrast with the relative genetic stability after repeated passages in vitro and with the observation that, with families with a history of high incidence of H. pylori infections, the strains are highly homogeneous.