title: Presence of the cagA gene in the majority of Helicobacter pylori strains is independent of whether the individual has duodenal ulcer or asymptomatic gastritis.
abstract: BACKGROUND
  Helicobacter pylori infection presents as many different diseases, including asymptomatic gastritis, peptic ulcer disease, and gastric cancer. Although the virulence factor(s) responsible for different H. pylori-related diseases have not been identified, several candidate genes are being investigated for such an association. The polymerase chain reaction (PCR) frequently is used to assess the presence of genetic factors associated with pathogenesis of disease; the cagA gene and its product have been postulated to have a disease-specific relationship to peptic ulcer and gastric cancer because of differential expression in these diseases compared to histological gastritis alone.
  
  
  METHODS
  Genomic DNA was amplified by PCR, using synthetic oligonucleotide primers to the cagA gene to determine the prevalence of the cagA gene in 60 H. pylori isolates obtained from well-documented duodenal ulcer or asymptomatic gastritis patients (30 each). Results were confirmed by hybridization with a 1.4-Kb cagA probe.
  
  
  RESULTS
  The expected PCR product was obtained in 90% of isolates from duodenal ulcer patients, compared to 70% of isolates from individuals with asymptomatic gastritis. The PCR products were polymorphic in size, suggesting cagA gene sequence differences among isolates. Evaluation for the presence of the cagA gene by hybridization with a 1.4-Kb cagA probe showed a homologous product in 29 of 30 strains [96.7%; 95% confidence interval (CI) = 83-100%] from duodenal ulcer patients versus 25 of 30 strains (83.3%; 95% CI = 65-94%) obtained from individuals with asymptomatic gastritis (p = 0.19).
  
  
  CONCLUSIONS
  The high prevalence of the cagA gene in asymptomatic gastritis suggests that it will not prove to be a useful marker to distinguish more virulent or disease-specific H. pylori strains. The genetic heterogeneity among H. pylori strains makes PCR an unwise choice as the single method to determine prevalence of a putative virulence factor. In evaluation of the prevalence of a gene or genetic factor in a population of H. pylori, hybridization with extended probes might be important to ensure that the results are representative of the organism's genotype.
authors.affiliation: Department of Medicine, Veterans Affairs Medical Center, Houston, TX 77030, USA.
authors.forename: M F
authors.initials: MF
authors.lastname: Go
authors.forename: D Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000032:analysis / Q000235:genetics*; D004269:DNA, Bacterial / Q000235:genetics; D004381:Duodenal Ulcer / Q000382:microbiology* / Q000473:pathology; D005260:Female; D005756:Gastritis / Q000382:microbiology* / Q000473:pathology; D005798:Genes, Bacterial; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D014774:Virulence / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004269:DNA, Bacterial; C080866:cagA protein, Helicobacter pylori