Epstein-Barr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment
– Source: Rheumatology (Oxford), Oct 2010
By Mattias Magnusson, et al.
[Note: To read the free full text of this article, which may be significant for CFS trials employing rituximab therapy, go to
Objectives: Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients.
Methods: Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion.
Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months.
Before RTX treatment:
• EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus.
• Parvovirus was further detected in eight patients (parvo-positive group).
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• Twelve patients were negative for the analysed viruses.
• EBV was cleared, whereas parvovirus was unaffected.
• Eighteen patients were responders, of which 12 were EBV positive.
• The decrease in the 28-joint disease activity score was significantly higher in EBV-positive group compared with parvo-positive group (P=0.002) and virus-negative patients (P=0.04).
• Most of EBV-negative patients that responded to RTX (75%) required retreatment within the following 11 months
• Compared with only 8% of responding EBV-positive patients.
A decrease of RF, Ig-producing cells and CD19(+) B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups.
EBV and parvovirus genomes are frequently found in bone marrow of RA patients.
The presence of EBV genome was associated with a better clinical response to RTX.
Thus, presence of EBV genome may predict clinical response to RTX.
Source: Rheumatology, Oct 2010; 49(10):1911-9. Magnusson M, Brisslert M, Zendjanchi K, Lindh M, Bokarewa MI. Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, Göteborg, Sweden. [Email: email@example.com]