Epstein-Barr virus, arthritis, and the development of lymphoma in arthritis patients

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Purpose of review

Rheumatoid arthritis is a complex multisystem disorder. The manifestations of joint disease are usually clinically apparent, but the effects of the concomitant abnormalities of immune function are more subtle. It has been suggested that patients with rheumatoid arthritis have an impaired capacity to control infection with Epstein-Barr virus. Epstein-Barr virus has oncogenic potential and is implicated in the development of some lymphomas. This review analyses the relation between Epstein-Barr virus, rheumatoid arthritis, and the risk of lymphoma and considers the effect of immunosuppression on this triad.

Recent findings

Recent publications provide evidence for an altered Epstein-Barr virus—host balance in patients with rheumatoid arthritis, who have a relatively high Epstein-Barr virus load. Large epidemiologic studies confirm that lymphoma is more likely to develop in patients with rheumatoid arthritis than in the general population. The overall risk of development of lymphoma has not risen with the increased use of methotrexate or biologic agents. Histologic analysis reveals that most lymphomas in rheumatoid arthritis patients are diffuse large B cell lymphomas, a form of non-Hodgkin lymphoma. Epstein-Barr virus is detected in a proportion of these.


Overall, patients with rheumatoid arthritis have approximately a twofold increased risk of experiencing lymphoma. Some, but not all, of this increased risk reflects an increase in Epstein-virus–associated lymphomas. This in turn may be influenced by the elevated Epstein-Barr virus load found in rheumatoid arthritis patients and may reflect subtle impairment of antiviral immunity in this group of patients.

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