Primary Sjögren's syndrome after infectious mononucleosis.

A healthy young woman developed primary Sjögren's syndrome after protracted infectious mononucleosis. The diagnosis of primary Sjögren's syndrome was supported by histologic evidence of sialadenitis in labial salivary glands, rheumatoid factor, hypergammaglobulinemia, the HLA-B8 phenotype, and a high titer antibody to the anti-La (SS-B) nucleoprotein that co-precipitated the small ribonucleic acids encoded by Epstein-Barr virus, EBER 1 and EBER 2, as well as "host" RNA. There was strong humoral immunity to the Epstein-Barr nuclear and capsid antigens, but weak T-lymphocyte-mediated cytotoxicity to Epstein-Barr-transformed lymphoblasts, anergy to antigens used to elicit delayed-type hypersensitivity, and a low T-helper/T-suppressor cell ratio. The series of events initiated by infectious mononucleosis was attributed to a genetic defect in the immune response. Association of viral RNA with the La nucleoprotein resulted in a break in immunologic tolerance via a T-cell bypass effect with induction of anti-La (SS-B) by polyclonally activated B lymphocytes leading to autoimmune sialadenitis.