PURPOSE: It is hypothesized that Epstein-Barr virus (EBV) has already infected the noncarcinomatous gastric mucosa before carcinogenesis of EBV-associated gastric carcinoma. However, the frequency and distribution of EBV infection in the gastric mucosa of chronic atrophic gastritis (CAG) are still unclear. To clarify these points, we evaluated the EBV DNA load in gastric mucosa with CAG. METHODS: We tested samples from 35 CAG cases. Paired biopsy specimens from five sites of the stomach were obtained according to the Updated Sydney System. One of each pair of specimens was subjected to areal-time quantitative polymerase chain reaction (Q-PCR) assay to detect EBV. Q-PCR was performed using the LightCycler System (Roche, Mannheim, Germany). The other was subjected to hematoxylin and eosin (H&E) and Giemsa staining. The histological degree of CAG was graded according to the Updated Sydney System. To evaluate the surface distribution of gastric mucosal atrophic changes of CAG, we modified the endoscopic classification of Kimura and Takemoto. RESULT: EBV DNA was detected in 65.7% (23 of 35 cases) of the gastric biopsy specimens of the cases examined. EBV DNA was detected most frequently (92.3%; 12 of 13 cases) in the cases with endoscopically moderate CAG (p < 0.01). There was a significant association between EBV detection and the presence of inflammatory cell infiltration and atrophy in the stomach with endoscopically moderate CAG. CONCLUSION: EBV mainly infects the gastric mucosa of patients with moderate CAG.
PURPOSE: It is hypothesized that Epstein-Barr virus (EBV) has already infected the noncarcinomatous gastric mucosa before carcinogenesis of EBV-associated gastric carcinoma. However, the frequency and distribution of EBV infection in the gastric mucosa of chronic atrophic gastritis (CAG) are still unclear. To clarify these points, we evaluated the EBV DNA load in gastric mucosa with CAG. METHODS: We tested samples from 35 CAG cases. Paired biopsy specimens from five sites of the stomach were obtained according to the Updated Sydney System. One of each pair of specimens was subjected to areal-time quantitative polymerase chain reaction (Q-PCR) assay to detect EBV. Q-PCR was performed using the LightCycler System (Roche, Mannheim, Germany). The other was subjected to hematoxylin and eosin (H&E) and Giemsa staining. The histological degree of CAG was graded according to the Updated Sydney System. To evaluate the surface distribution of gastric mucosal atrophic changes of CAG, we modified the endoscopic classification of Kimura and Takemoto. RESULT: EBV DNA was detected in 65.7% (23 of 35 cases) of the gastric biopsy specimens of the cases examined. EBV DNA was detected most frequently (92.3%; 12 of 13 cases) in the cases with endoscopically moderate CAG (p < 0.01). There was a significant association between EBV detection and the presence of inflammatory cell infiltration and atrophy in the stomach with endoscopically moderate CAG. CONCLUSION:EBV mainly infects the gastric mucosa of patients with moderate CAG.
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