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Sir, The recent determination of the complete Helicobacter pylori genome sequence (Tomb et al ., 1997, Nature 388 : 539–547) and functional studies on the CAG pathogenicity island (Censini et al ., 1997, Proc Natl Acad Sci USA 93 : 14648–14653; Covacci et al ., 1997, Trends Microbiol 5 : 205–208) are major contributions to our understanding of this important pathogen. Current investigations focus on the CAG genes coding for a cytotoxin‐associated antigen (CagA, ORF 547) and potential virulence factors such as homologues of Agrobacterium VirB4 (ORF 544), VirB7 (lipoprotein CagT, ORF 532), VirB9 (ORF 528), VirB10 (ORF 527), VirB11 (ORF 525) and VirD4 (ORF 524) proteins. Three additional virb4 gene copies (ORFs 017, 441 and 459) as well as a gene encoding a vacuolating toxin (VacA, ORF 887) are located outside the CAG region. CagA, VacA and a few other proteins were found to be secreted and to enhance the inflammatory response in the gastric mucosa. The presence of vir genes and several GC‐rich islands further suggests the existence of an adapted DNA‐transfer apparatus for delivering virulence genes across bacterial boundaries. Evidence for conjugation‐like DNA‐transfer mechanisms between Helicobacter pylori strains has already been demonstrated in vitro (Kuipers
Molecular Microbiology – Wiley
Published: Nov 1, 1998
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