title: Helicobacter pylori vacA genotypes and cagA gene in a series of 383 H. pylori-positive patients.
abstract: BACKGROUND
  Only 10-15% of all patients infected with Helicobacter pylori develop peptic ulcer disease (PUD) or gastric cancer. Apart from immunological factors in the host, virulence determinants of H. pylori such as the vacuolating cytotoxin (VacA) or the cytotoxin-associated protein A (CagA) might represent a predisposition for the development of PUD.
  
  
  METHODS
  We studied antral biopsies of 383 H. pylori-positive patients with peptic ulcer disease (PUD) or other H. pylori-related diseases for H. pylori vacA genotypes and the presence of the cagA gene by PCR.
  
  
  RESULTS
  VacA genotypes and cagA status could be completely determined in 357 (93.2%) of the patients. In 91 (93.8%) of 97 patients with PUD, the vacA s1 genotype (s1m1, 45; s1m2, 46 patients) was present. The vacA s2m2 genotype was found in only 6 (6.2%) of 97 patients with PUD. In contrast, 180 (75.3%) of 239 patients (s1m1, 89; s1m2, 91 patients) without PUD and without gastric malignancies harbored strains with the vacA s1 genotype. The vacA genotype s2m2 was found in 59 (24.7%) of these patients. The presence of the cagA gene was closely associated with the vacA genotype s1 and found in 124 (88.6%) and in 113 (80.7%) of patients with the s1m1 or s1m2 genotypes, respectively, whereas strains with the genotype s2m2 were almost exclusively cagA negative.
  
  
  CONCLUSIONS
  Most H. pylori strains found in patients with PUD possess the vacA s1 genotype and the cagA gene. Patients with this type of H. pylori strain but without PUD might be at higher risk of developing PUD. In contrast, the risk for PUD might be significantly decreased in those patients who are infected by H. pylori strains with the vacA s2 genotype lacking the cagA gene.
authors.affiliation: Medizinische Klinik IV (Abteilung für Gastroenterologie), Ruprecht-Karls-Universität, Heidelberg. jochen_rudi@med.uni-heidelberg.de
authors.forename: J
authors.initials: J
authors.lastname: Rudi
authors.forename: D
authors.initials: D
authors.lastname: Kuck
authors.forename: A
authors.initials: A
authors.lastname: Rudy
authors.forename: A
authors.initials: A
authors.lastname: Sieg
authors.forename: M
authors.initials: M
authors.lastname: Maiwald
authors.forename: W
authors.initials: W
authors.lastname: Stremmel
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics*; D001427:Bacterial Toxins / Q000235:genetics*; D001483:Base Sequence; D016009:Chi-Square Distribution; D005260:Female; D005798:Genes, Bacterial / Q000235:genetics*; D005838:Genotype; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction / Q000379:methods / Q000706:statistics & numerical data; D014617:Vacuoles / Q000235:genetics; D014774:Virulence / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D001427:Bacterial Toxins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori