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Infliximab does not activate replication of lymphotropic herpesviruses in patients with refractory rheumatoid arthritis

Infliximab does not activate replication of lymphotropic herpesviruses in patients with... Objective. The reactivation of human lymphotropic herpesviruses can be related to the intensity of immunosuppression. We analysed the risk of reactivation of lymphotropic herpesviruses in patients with refractory rheumatoid arthritis treated with an anti-tumour necrosis factor-α (TNF-α) agent (infliximab).Methods. Fifteen patients were treated with infliximab (3 mg/kg) at weeks 0, 2 and 6. Samples of both plasma and peripheral blood mononuclear cells (PBMC) were obtained before treatment (week 0) and before each infusion at weeks 2 and 6. Samples were analysed using a multiplex qualitative polymerase chain reaction (PCR) for lymphotropic herpesviruses. Quantification of cytomegalovirus (CMV) viral load (copies/ml) was performed using quantitative PCR. Reactivation was defined as the presence of viral DNA in plasma. Latent infection was defined as the presence of viral DNA in PBMC samples but not in plasma.Results. On baseline, latent CMV infection was detected in eight patients (53.3%), human herpesviruses-6 (HHV-6) in two (13.3%), Epstein–Barr virus (EBV) in seven (46.6%), CMV + HHV-6 in one (6.6%), CMV + EBV in two (13.3%) and HHV-6 + EBV in one (6.6%). Viral reactivation related to infliximab treatment was not observed. There was only one patient who had HHV-6 reactivation, but this was already detected in the baseline sample.Conclusions. Infliximab treatment does not induce replication of human lymphotropic herpesviruses in patients with rheumatoid arthritis. Thus, herpesviruses prophylaxis would not be indicated in these patients. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Rheumatology Oxford University Press

Infliximab does not activate replication of lymphotropic herpesviruses in patients with refractory rheumatoid arthritis

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References (14)

Publisher
Oxford University Press
Copyright
© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
ISSN
1462-0324
eISSN
1462-0332
DOI
10.1093/rheumatology/keh696
pmid
15927999
Publisher site
See Article on Publisher Site

Abstract

Objective. The reactivation of human lymphotropic herpesviruses can be related to the intensity of immunosuppression. We analysed the risk of reactivation of lymphotropic herpesviruses in patients with refractory rheumatoid arthritis treated with an anti-tumour necrosis factor-α (TNF-α) agent (infliximab).Methods. Fifteen patients were treated with infliximab (3 mg/kg) at weeks 0, 2 and 6. Samples of both plasma and peripheral blood mononuclear cells (PBMC) were obtained before treatment (week 0) and before each infusion at weeks 2 and 6. Samples were analysed using a multiplex qualitative polymerase chain reaction (PCR) for lymphotropic herpesviruses. Quantification of cytomegalovirus (CMV) viral load (copies/ml) was performed using quantitative PCR. Reactivation was defined as the presence of viral DNA in plasma. Latent infection was defined as the presence of viral DNA in PBMC samples but not in plasma.Results. On baseline, latent CMV infection was detected in eight patients (53.3%), human herpesviruses-6 (HHV-6) in two (13.3%), Epstein–Barr virus (EBV) in seven (46.6%), CMV + HHV-6 in one (6.6%), CMV + EBV in two (13.3%) and HHV-6 + EBV in one (6.6%). Viral reactivation related to infliximab treatment was not observed. There was only one patient who had HHV-6 reactivation, but this was already detected in the baseline sample.Conclusions. Infliximab treatment does not induce replication of human lymphotropic herpesviruses in patients with rheumatoid arthritis. Thus, herpesviruses prophylaxis would not be indicated in these patients.

Journal

Rheumatology – Oxford University Press

Published: Oct 1, 2005

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