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Anti-dsDNA antibodies associated with acute EBV infection in Sjögren's syndrome
  1. Laboratory Medicine, Immunology
  2. University Hospitals Leuven
  3. Herestraat 49
  4. 3000 Leuven, Belgium
  1. Dr Bossuyt

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The role of viral infection in the pathogenesis of autoimmune diseases is not clear. Some authors have suggested a role for herpes viruses and retroviruses in the pathogenesis of systemic rheumatic diseases,1-4 whereas others have produced evidence against this idea.5-7 In this report we present a case in which an association was found between Epstein-Barr virus (EBV) infection and anti-DNA antibodies in a patient with Sjögren's syndrome.

A 28 year old woman was diagnosed with Sjögren's syndrome. The clinical presentation included diffuse myalgias, tiredness, and intermittent respiratory complaints. Electrophoresis showed polyclonal hypergammaglobulinaemia. Antinuclear antibody testing by indirect immunofluorescence on HEp-2 cells (Immunoconcepts, Sacramento, CA) showed a fine speckled nuclear pattern. The antibodies were identified as anti-Ro/SS-A antibodies by counterimmunoelectrophoresis.8 No anti-double stranded DNA (anti-dsDNA) antibodies were present (Crithidia luciliae assay; Immunoconcepts). Four years after the diagnosis of Sjögren's syndrome, the patient had an acute EBV infection with persistent tiredness, icterus, and hepatosplenomegaly. The EBV infection was documented by positive heterophile antibodies and the presence of IgM (titre 1/32) and IgG (titre 1/256) antibodies to EBV viral capsid antigen. The antibodies to early antigens were negative (<1/8). The patient did not have IgM rheumatoid factor, which excluded the possibility of a false positive IgM-viral capsid antigen test induced by the presence of rheumatoid factor. Neither antiviral capsid antigen antibodies nor anti-early antigen antibodies had been found one year before the patient presented with the EBV infection. TheCrithidia luciliae test was negative two months before the EBV infection. Three months and eight months after the acute infection, respectively, the Farr assay (Ortho Clinical Diagnostics, Amersham, UK) and the Crithidia luciliae assay disclosed anti-dsDNA antibodies. The patients showed no progressive disease and did not develop signs of systemic lupus erythematosus.

The association between EBV and anti-dsDNA antibodies in the case presented here indicates a possible role of the virus in the generation of anti-dsDNA antibodies. The formation of anti-dsDNA autoantibodies may result from the activation of specific B lymphocyte clones or from an imbalance in the regulation of the immune system due to EBV infection. This is consistent with the finding that EBV transformed B cells can produce IgG antibodies with specificity for dsDNA,9 ,10 and with the suggestion that EBV infection may be a causative factor in lupus.11



  • This work was presented at the 52nd AACC annual meeting, San Francisco, CA in June 2000 and has been published in abstract form in Clin Chem 2000;46(suppl 6):A44.