Ivy Bastos Ramis
Júlia Silveira Vianna
Lande Vieira da Silva Junior
Andrea Von Groll
Pedro Eduardo Almeida da Silva 
Centro de Desenvolvimento Tecnológico, Universidade Federal de Pelotas, Pelotas, RS
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rio Grande, RS
We read with great interest the comments made by Drs. Nawfal R. Hussein and Rawand Al-Qadi regarding our results presented in the article entitled “cagE as a biomarker of the pathogenicity of Helicobacter pylori.” We agree that H. pylori infection should be viewed as multifaceted process, where the environment, host, and microorganism play specific roles in determining asymptomatic infection, colonization, or gastric disease.
In the above-mentioned study, we showed that cagE, a member of the cag pathogenicity island, is one more biomarker that should be considered to best understand the relationship between the microorganism and the host.
Although others authors1–3 had found similar results, we think that geographic factors (environment and host) have important roles in determining what biomarkers are more significant in each location.
1. Chomvarin C, Namwat W, Chaicumpar K, Mairiang P, Sangchan A, Sripa B, et al. Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA and babA2 genotypes in Thai dyspeptic patients. Int J Infect Dis 2008 12:30-36. [ Links ]
2. Podzorski RP, Podzorski DS, Wuerth A, Tolia V. Analysis of the vacA, cagA, cagE, iceA, and babA2 genes in Helicobacter pylori from sixty-one pediatric patients from the Midwestern United States. Diagn Microbiol Infect Dis 2003; 46:83-88. [ Links ]
3. Quiroga AJ, Cittelly DM, Bravo MM. BabA2, oipA and cagE Helicobacter pylori genotypes in Colombian patients with gastroduodenal diseases. Biomedica 2005; 25:325-334. [ Links ]