TY - JOUR T1 - CagA, the<em>cag</em> pathogenicity island and<em>Helicobacter pylori</em>virulence JF - Gut JO - Gut SP - 307 LP - 308 DO - 10.1136/gut.44.3.307 VL - 44 IS - 3 AU - J C ATHERTON Y1 - 1999/03/01 UR - http://gut.bmj.com/content/44/3/307.abstract N2 - See article on page 336 Most people with stomachs colonised byHelicobacter pylori do not develop peptic ulceration, gastric adenocarcinoma or gastric lymphoma in their lifetime. Development of disease is likely to be determined by a combination of factors: the virulence of the infectingH pylori strain, the susceptibility of the host and environmental co-factors. The best studied of these disease determinants is strain virulence, and the two most studied virulence markers are expression of vacuolating cytotoxin activity and production of a non-toxigenic protein of unknown function called CagA.1 Colonisation with CagA+ strains ofH pylori is easy to detect as CagA provokes a strong systemic antibody response in the human host. In Europe and the USA, more than 60% of those colonised by H pylori have antibodies to CagA: these people have more intense gastric inflammation than those colonised by CagA−H pylori alone and are more likely to develop peptic ulcers and distal gastric adenocarcinoma.1However, most people colonised by CagA+ strains do not develop these conditions and it may be more useful to regard CagA− strains as having reduced pathogenicity than to regard CagA+ strains as pathogenic. In Japan, where Maeda et al’s study (see page 336) was conducted, not only is H pylori colonisation more prevalent than in the West, but also colonisation by CagA− strains is rare.2 … ER -