EPSTEIN-BARR-VIRUS AND THE LACRIMAL GLAND PATHOLOGY OF SJOGRENS-SYNDROME

The lacrimal gland (LG) immunopathology Of Sjokren's syndrome (SS) con sists of a proliferation of B and CD4 lymphocytes surrounding epitheli al structures (Pepose JS, et al: Ophthalmology 1990, 97:1599-1605). Ba sed on the detection of EBV genomes in a greater percentage of SS than normal LG biopsies, we previously postulated that Epstein-Barr virus (EBV) is a risk factor for LG lymphoproliferation in SS (Pflugfelder S C, et al: Ophthalmology 1990, 97.976-984). The purpose of this study w as to determine the cellular site(s) of infection, virus type, and ant igen expression of EBV infecting normal and SS LGs. EBV DNA was detect ed by in situ hybridization in intraductal epithelia in 13-33% of lobu les in 21 % of normal LGs and in cells in areas of B lymphoproliferati on as well as the majority of epithelia in 86% of SS LGs. EBV genomic sequences were amplified from 36% of normal and 88% of SS LG biopsies by polymerase chain reaction. Only type 1 EBV sequences were amplified in SS LGs; in contrast EBV nuclear antigen 2-deleted but not type 1 s equences were amplified in normal LGs. Immunohistochemistry with EBV-s pecific monoclonal antibodies was performed on normal and SS LGs. No E BV antigens were detected in normal LGs. In contrast, latent antigens (latent membrane protein, EBV nuclear antigen 2) were detected in lymp hocytes in areas of B lymphoproliferation, and early and late lytic cy cle antigens were observed in epithelia in SS LGs. These studies sugge st that EBV may play a role in the LG B lymphoproliferation and epithe lial pathologic changes observed in SS.