[Possible etiological relations between Sjogren's syndrome and Epstein-Barr virus]

Tissue biopsies from patients with Sjogren's syndrome (SS) and controls were detected by a monoclonal antibody (McAb) of gene engineering against Epstein-Barr virus (EBV) encoded early antigen (EA p138) and a 32p-labelled EBV DNA probe, and also B95-8 and K4 cells as antigens to detect reacting antibodies to EBV in patients' sera. As a result, cytoplasmic fluorescence staining of epithelial cells with the McAb as described above was noted in 15/33 labial and 7/7 renal biopsies from primary SS. The same McAb did not react with biopsies from secondary SS, non-SS connective tissue diseases, benign tumors and normal persons, nor with the other tissues detected from primary SS. By using McAbs against the EBV EA p54 and nuclear antigen (EBNA-1) and by using immunoblotting method, it was found that the reacting antigens in labial biopsies of primary SS had both a M. W. of 54,000 and a M. W. of 65,000, similar to the EA-D and EBNA-1 antigens found in lymphoblastoid cells lytically infected with EBV. Seven out of 21 labial and one out of two renal samples from primary SS patients contained EBV DNA detectable by dot blot hybridization with EBV Bam W probe. Serum levels of both antiviral capsid antigen antibodies and antinuclear antibodies were elevated in patients with primary SS. Our results demonstrated an elevated content of EBV in labial gland and kidney of patients with primary SS, where EBV has been of a lytic fate leading to active replication. It is concluded that EBV may play an important role in the pathogenesis of primary SS.