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Epstein–Barr virus infection in non‐carcinomatous gastric epithelium
Author(s) -
Yanai Hideo,
Takada Kenzo,
Shimizu Norio,
Mizugaki Yuzo,
Tada Masahiro,
Okita Kiwamu
Publication year - 1997
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199711)183:3<293::aid-path937>3.0.co;2-c
Subject(s) - in situ hybridization , atrophic gastritis , chronic gastritis , intestinal metaplasia , biology , pathology , virus , epstein–barr virus , southern blot , stomach , immunohistochemistry , gastritis , virology , medicine , immunology , dna , messenger rna , gene , biochemistry , genetics
Gastric tissue specimens from 20 patients with chronic atrophic gastritis, one of whom also had an early gastric carcinoma, were studied for evidence of Epstein–Barr virus (EBV) infection by Southern blot analysis, DNA and RNA in situ hybridization, and immunohistochemistry for the presence of the EBV‐determined nuclear antigen 1 (EBNA‐1) and the latent membrane protein 1 (LMP‐1). EBV DNA was detected in two cases with chronic atrophic gastritis and in the case with early gastric carcinoma by Southern blot hybridization. DNA in situ hybridization showed EBV genomes in the epithelial cells of two other cases with chronic atrophic gastritis and in non‐carcinomatous and carcinomatous epithelial cells of the early gastric carcinoma case. EBNA‐1 was detected in all cases. LMP‐1 was detected in areas of intestinal metaplasia in eight patients with chronic atrophic gastritis. EBV‐encoded small RNA 1 (EBER‐1) expression was limited to carcinoma cells. These results show that gastric epithelium is frequently infected with EBV and suggest that prolonged EBV persistence may contribute to the development of gastric carcinoma. © 1997 John Wiley & Sons, Ltd.