LATENT EPSTEIN-BARR-VIRUS INFECTION IS AN UNLIKELY EVENT IN THE PATHOGENESIS OF IMMUNOPROLIFERATIVE SMALL-INTESTINAL DISEASE

Background. The observed seasonal and geographic variations in the inc idence of immunoproliferative small intestinal disease (IPSID) suggest that environmental factors contribute to its pathogenesis. One such e nvironmental factor, the Epstein-Barr virus (EBV), has been associated with other B-cell lymphoproliferative disorders. Methods. IPSID tissu es obtained at the time of initial diagnosis were retrieved from the A merican University of Beirut pathology archives (1972-1983) and examin ed for EBV genetic information by colorimetric in situ hybridization ( ISH) and polymerase chain reaction (PCR). Eight patients were identifi ed, four of whom also had serologic and immunohistochemical evidence o f alpha-heavy chain disease. Thirteen tissue samples from these eight patients were available for study: eight were intestinal and five were nodal. Non-Hodgkin's B-cell lymphoma cases (nine) were randomly selec ted from the same archive to serve as a control for EBV in that geogra phic location. The ISH method used a probe to the ''W'' repetitive reg ion of EBV, with the human placental DNA probe as a control for sample preparation. The PCR method amplified a 110 base pair region in the l ong internal direct repeat with amplification of beta-actin as control for DNA preservation. Both assays used formalin fixed paraffin embedd ed Raji cells as a positive control. Results. Neither ISH nor PCR demo nstrated EBV in any of the eight patients with IPSID. The results for one of seven control blocks with adequate DNA preservation were positi ve when PCR was used but were negative when ISH was used. Conclusions. These findings do not support a role for EBV in the induction of B-ce ll proliferation in IPSID.