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Microbiology and Molecular Biology Reviews, September 1999, p. 675-707, Vol. 63, No. 3
1092-2172/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Helicobacter pylori Physiology Predicted from Genomic Comparison of Two Strains

Peter Doig,1,* Boudewijn L. de Jonge,1 Richard A. Alm,1 Eric D. Brown,1,dagger Maria Uria-Nickelsen,1 Brian Noonan,1 Scott D. Mills,1 Peter Tummino,1 Gilles Carmel,2 Braydon C. Guild,2 Donald T. Moir,2 Gerald F. Vovis,2,Dagger and Trevor J. Trust1

AstraZeneca R&D Boston, Cambridge,1 and Genome Therapeutics Corp., Waltham,2 Massachusetts

Helicobacter pylori is a gram-negative bacteria which colonizes the gastric mucosa of humans and is implicated in a wide range of gastroduodenal diseases. This paper reviews the physiology of this bacterium as predicted from the sequenced genomes of two unrelated strains and reconciles these predictions with the literature. In general, the predicted capabilities are in good agreement with reported experimental observations. H. pylori is limited in carbohydrate utilization and will use amino acids, for which it has transporter systems, as sources of carbon. Energy can be generated by fermentation, and the bacterium possesses components necessary for both aerobic and anaerobic respiration. Sulfur metabolism is limited, whereas nitrogen metabolism is extensive. There is active uptake of DNA via transformation and ample restriction-modification activities. The cell contains numerous outer membrane proteins, some of which are porins or involved in iron uptake. Some of these outer membrane proteins and the lipopolysaccharide may be regulated by a slipped-strand repair mechanism which probably results in phase variation and plays a role in colonization. In contrast to a commonly held belief that H. pylori is a very diverse species, few differences were predicted in the physiology of these two unrelated strains, indicating that host and environmental factors probably play a significant role in the outocme of H. pylori-related disease.

* Corresponding author. Mailing address: AstraZeneca R&D Boston, 128 Sidney St., Cambridge, MA 02139. Phone: (617) 234-2534. Fax: (617) 576-3030. E-mail: Peter.Doig{at}arcb.us.astra.com.

dagger Present address: Department of Biochemistry, Health Sciences, McMaster University, Hamilton, Ontario, Canada, L8N 3Z5.

Dagger Present address: Genaissance Pharmaceuticals, New Haven, CT 06511. 

Microbiology and Molecular Biology Reviews, September 1999, p. 675-707, Vol. 63, No. 3
1092-2172/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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