Volume 10, Issue s1 pp. 14-20

Pathogenesis of Helicobacter pylori Infection

Céu Figueiredo

Céu Figueiredo

IPATIMUP – Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal;

Faculty of Medicine, University of Porto, Porto, Portugal;

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José Carlos Machado

José Carlos Machado

IPATIMUP – Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal;

Faculty of Medicine, University of Porto, Porto, Portugal;

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Yoshio Yamaoka

Corresponding Author

Yoshio Yamaoka

Department of Medicine/Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USA

Reprint requests to: Yoshio Yamaoka, Department of Medicine/Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center, 2002 Holcombe Blvd. Houston, Texas 77030, USA. E-mail: [email protected]Search for more papers by this author
First published: 14 September 2005
Citations: 41

ABSTRACT

As with many infectious diseases, only a fraction of people infected with Helicobacter pylori develop clinical disease, and host genetics, host immune response, and bacterial virulence factors appear to play critical roles. There has been considerable interest in putative bacterial virulence factors and, while several have been identified, it is not clear whether they act independently or in concert. Disease associations have been proposed for the cag pathogenicity island (PAI), vacA, and genes encoding outer membrane proteins (OMPs). Numerous studies published in the last year have provided new insights into the function of these putative virulence factors in gastroduodenal pathogenesis. This article will review the recent novel findings (from April 2004) for the roles of the putative disease-associated virulence factors as well as their interaction with host.

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