This review article is followup of a previous review (Carroll IM, Khan AA and Ahmed N. Infect Genet Evol. 2004, 4:81-90) from us/our collaborators and therefore, should be taken as an update. We missed citing the reference inadvertently, which is now being incorporated as an erratum along with some minor changes that we missed by oversight at the time of final submission. This version indeed entails a fair use of the previous topics, with an intention to bring a derivative update which is publicly accessible, with some value addition. As H. pylori infection is a topic of wider public interest we reproduced much of the previous discussion with an intention to benefit wider audience, especially the patients and the students and those living in developing countries who can not purchase a non-open access article.
The corrected abstract of the article may please be read as follows:
Abstract:
The human gastric pathogen Helicobacter pylori is linked to chronic gastritis, peptic ulcer disease, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma. It infects over 50% of the worlds' population, however, only a small subset of infected people experience the diseases mentioned above. Associations of the virulence factors to the outcome of infection remain enigmatic years after the genome sequences were deciphered. Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA) gene is associated with gastric carcinoma. Recent studies revealed mechanisms through which the cagA protein triggers oncopathogenic activities. Other candidate genes such as some members of the so-called plasticity region cluster are also implicated to be associated with carcinoma of stomach. Study of the evolution of polymorphisms and sequence variation in H. pylori populations on a global basis has provided a window into the history of human population migration and co-evolution of this pathogen with its host. Possible symbiotic relationships were debated since the discovery of this pathogen. However, this debate has been further intensified as some studies reveal that H. pylori infection may be beneficial in some humans in some particular geographical/clinical settings. This assumption is based on increased incidence of gastro-oesophageal reflux disease (GERD), Barrett's oesophagus and adenocarcinoma of the oesophagus following H. pylori eradication in some countries. The contribution of comparative genomics to our understanding of the genome plasticity and diversity of H. pylori and its pathophysiological importance to human healthcare is discussed. This review is written with a fair interest to reproduce through open access channel a follow up and update of our previous detailed discussions on the subject (Carroll IM, Khan AA and Ahmed N. Infect Genet Evol. 2004, 4:81-90).
Author's corrections and clarifications
4 February 2008
This review article is followup of a previous review (Carroll IM, Khan AA and Ahmed N. Infect Genet Evol. 2004, 4:81-90) from us/our collaborators and therefore, should be taken as an update. We missed citing the reference inadvertently, which is now being incorporated as an erratum along with some minor changes that we missed by oversight at the time of final submission. This version indeed entails a fair use of the previous topics, with an intention to bring a derivative update which is publicly accessible, with some value addition. As H. pylori infection is a topic of wider public interest we reproduced much of the previous discussion with an intention to benefit wider audience, especially the patients and the students and those living in developing countries who can not purchase a non-open access article.
The corrected abstract of the article may please be read as follows:
Abstract:
The human gastric pathogen Helicobacter pylori is linked to chronic gastritis, peptic ulcer disease, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma. It infects over 50% of the worlds' population, however, only a small subset of infected people experience the diseases mentioned above. Associations of the virulence factors to the outcome of infection remain enigmatic years after the genome sequences were deciphered. Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA) gene is associated with gastric carcinoma. Recent studies revealed mechanisms through which the cagA protein triggers oncopathogenic activities. Other candidate genes such as some members of the so-called plasticity region cluster are also implicated to be associated with carcinoma of stomach. Study of the evolution of polymorphisms and sequence variation in H. pylori populations on a global basis has provided a window into the history of human population migration and co-evolution of this pathogen with its host. Possible symbiotic relationships were debated since the discovery of this pathogen. However, this debate has been further intensified as some studies reveal that H. pylori infection may be beneficial in some humans in some particular geographical/clinical settings. This assumption is based on increased incidence of gastro-oesophageal reflux disease (GERD), Barrett's oesophagus and adenocarcinoma of the oesophagus following H. pylori eradication in some countries. The contribution of comparative genomics to our understanding of the genome plasticity and diversity of H. pylori and its pathophysiological importance to human healthcare is discussed. This review is written with a fair interest to reproduce through open access channel a follow up and update of our previous detailed discussions on the subject (Carroll IM, Khan AA and Ahmed N. Infect Genet Evol. 2004, 4:81-90).
We apologise for any confusion.
Niyaz Ahmed, Leonardo Sechi
Competing interests
None declared.