Skip to main content
  • Meeting abstract
  • Published:

Epstein–Barr virus load is higher in rheumatoid arthritis patients than in normal controls


For 20 years the Epstein–Barr virus (EBV) has been suspected to contribute to the pathogenesis of rheumatoid arthritis (RA). RA is strongly associated with shared epitope positive HLA-DR alleles. EBV load has been extensively studied in RA patients, using semiquan-titative PCR. Inconsistent results reflect the lack of sensitivity and accuracy of this technique. We quantified EBV in peripheral blood mononuclear cells by real time PCR, to determine whether EBV load is higher in RA patients than in controls and to test whether HLA-DR alleles or treatment influences EBV load.


Eighty-four patients fulfilling the 1987 ACR criteria for RA and 22 patients with rheumatic conditions other than RA were studied. Sixty-nine healthy controls were chosen from bone marrow donors at the Marseille blood transfusion center. HLA-DR genotyping of patients and controls was performed by PCR-SSP. Real-time PCR was performed using a Roche LightCycler. A 214-bp fragment from the highly conserved long internal repeat IR1 was amplified. Two specific hybridization probes were used to recognize adjacent internal sequences within the target. EBV-positive Burkitt's lymphoma cell line was used as an external standard.

Results and conclusion

EBV load is expressed in EBV genome copy number per 500 ng of human genomic DNA (1.5 × 105 cells). We found that patients with RA have a higher EBV load (median 8.84) than non-RA patients (median 1.56) and healthy controls (median 0.6). EBV load is not obviously influenced by disease-modifying antirheumatic drugs nor by HLA-DR and is stable over time.

Author information

Authors and Affiliations


Rights and permissions

Reprints and permissions

About this article

Cite this article

Pieri-Balandraud, N., Baptiste Meynard, J., Auger, I. et al. Epstein–Barr virus load is higher in rheumatoid arthritis patients than in normal controls. Arthritis Res Ther 5 (Suppl 1), 83 (2003).

Download citation

  • Received:

  • Published:

  • DOI: