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  1. High prevalence of cagA-positive strains in Helicobacter pylori-infected, healthy, young Chinese adults.

    Article - En anglais


    Cytotoxin-associated gene A (cagA) has been implicated as a potential pathogenic marker for Helicobacter pylori-induced severe gastroduodenal diseases.

    Although the prevalence of cagA-positive strains has been reported in patient populations from developed countries, only limited information from developing countries is available.


    Polymerase chain reaction (PCR) in combination with immunoblot analysis was used to determine the prevalence of cagA and its adjacent cagE genes and to evaluate the expression of CagA protein in 55 H. pylori clinical isolates from China.


    The expected PCR products derived from H. pylori cagA and cagE genes were identified in all Chinese H. pylori clinical isolates.

    Similarly, the CagA protein was detected in all 40 isolates tested.


    These results demonstrated that the presence of the cagA gene correlated well with expression of the CagA protein in all surveyed Chinese H. pylori isolates and that infection with cagA-positive H. pylori strains is highly common in China and independent of clinical presentation.

    Mots-clés Pascal : Gastrite, Bactériose, Infection, Helicobacter pylori, Spirillaceae, Spirillales, Bactérie, Incidence, Souche pathogène, Séropositivité, Réaction chaîne polymérase, DNA, Pathogénie, Epidémiologie, Homme, Chine, Asie, Appareil digestif pathologie, Estomac pathologie, Biologie moléculaire, Antigène cagA

    Mots-clés Pascal anglais : Gastritis, Bacteriosis, Infection, Helicobacter pylori, Spirillaceae, Spirillales, Bacteria, Incidence, Pathogen strain, Seropositivity, Polymerase chain reaction, DNA, Pathogenesis, Epidemiology, Human, China, Asia, Digestive diseases, Gastric disease, Molecular biology, Cytotoxin associated antigen

    Logo du centre Notice produite par :
    Inist-CNRS - Institut de l'Information Scientifique et Technique

    Cote : 99-0291515

    Code Inist : 002B30A01A2. Création : 16/11/1999.