Evolution of Helicobacter pylori: the role of recombination

Helicobacter pylori is one of the most common pathogenic bacteria infecting humans. It is estimated that more than half of the human population is chronically colonized with this bacterium, which invariably causes a chronic inflammatory response of the stomach known as type B gastritis. Type B gastritis is asymptomatic in most patients but leads to ulceration of the stomach or the duodenum in ∼10% of those infected. H. pylori infection is also a risk factor for malignant gastric diseases, including carcinoma and lymphoma of the mucosa-associated lymphoid tissue (MALT). H. pylori has long been known to exhibit considerable genetic diversity. Molecular typing methods, such as restriction patterns of genomic DNA, random amplified polymorphic DNA (RAPD), pulsed-field gel electrophoresis or nucleotide sequencing of single genes, show that almost all H. pylori isolates from unrelated patients are unique and no clonal relationships have been observed 1 Majewski S.I. Goodwin C.S. J. Infect. Dis. 1988; 157: 465-471 Crossref PubMed Scopus (111) Google Scholar , 2 Akopyanz N. et al. Nucleic Acids Res. 1992; 20: 5137-5142 Crossref PubMed Scopus (688) Google Scholar , 3 Kansau I. et al. Res. Microbiol. 1996; 147: 661-669 Crossref PubMed Scopus (122) Google Scholar , 4 Taylor D.E. et al. J. Bacteriol. 1992; 174: 6800-6806 Crossref PubMed Scopus (141) Google Scholar . The origin of this diversity has been attributed to several mechanisms, including an elevated mutation rate, impaired DNA repair mechanisms and frequent recombination (for an extensive review, see 5 Marshall D.G. et al. Microbiology. 1998; 144: 2925-2939 Crossref PubMed Scopus (71) Google Scholar ). Recent molecular genetic, population genetic and genomic studies have quantified the extent of H. pylori diversity and elucidated some of the underlying mechanisms.