Latent Epstein-Barr virus infection is an unlikely event in the pathogenesis of immunoproliferative small intestinal disease.

Abstract

The observed seasonal and geographic variations in the incidence of immunoproliferative small intestinal disease (IPSID) suggest that environmental factors contribute to its pathogenesis. One such environmental factor, the Epstein-Barr virus (EBV), has been associated with other B-cell lymphoproliferative disorders. IPSID tissues obtained at the time of initial diagnosis were retrieved from the American University of Beirut pathology archives (1972-1983) and examined for EBV genetic information by colorimetric in situ hybridization (ISH) and polymerase chain reaction (PCR). Eight patients were identified, four of whom also had serologic and immunohistochemical evidence of 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 selected from the same archive to serve as a control for EBV in that geographic location. The ISH method used a probe to the "W" repetitive region 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 long internal direct repeat with amplification of beta-actin as control for DNA preservation. Both assays used formalin fixed paraffin embedded Raji cells as a positive control. Neither ISH nor PCR demonstrated EBV in any of the eight patients with IPSID: The results for one of seven control blocks with adequate DNA preservation were positive when PCR was used but were negative when ISH was used. These findings do not support a role for EBV in the induction of B-cell proliferation in IPSID: