Published online 16 July 2009
Haematologica, Vol 94, Issue 11, 1618-1622 doi:10.3324/haematol.2009.008607
Copyright © 2009 by Ferrata Storti Foundation
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Infectious Disorders

Reactivation of DNA viruses in association with histone deacetylase inhibitor therapy: a case series report

David Ritchie1, Richard L. Piekarz2, Piers Blombery1, Laszlo J. Karai3, Stefania Pittaluga3, Elaine S. Jaffe3, Mark Raffeld3, John E. Janik4, H. Miles Prince1, Susan E. Bates2

1 Department of Haematology and Medical Oncology, Peter MacCallum Cancer Centre and University of Melbourne, Melbourne, Victoria, Australia
2 Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
3 Laboratory of Pathology, Hematopathology Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD
4 Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Correspondence: David S Ritchie, Department of Haematology and Medical Oncology, Peter MacCallum Cancer Centre and University of Melbourne, Melbourne, Victoria 3002, Australia. E-mail:david.ritchie{at}petermac.org

Histone deacetylase inhibitors are a class of anti-neoplastic agents that induce growth arrest, differentiation, and/or apoptotic cell death of transformed cells in vitro and in vivo. A phase II study exploring the efficacy of romidepsin, an histone deacetylase inhibitor, in patients with cutaneous or peripheral T-cell lymphomas was initiated at the National Cancer Institute. To date, over 120 patients with T-cell lymphoma have been treated on a multi-institutional phase II trial of romidepsin. Reactivation of latent DNA viruses including EBV, HBV, and VZV is well described as a consequence of the immune suppression associated with systemic chemotherapy. The incidence of viral reactivation in patients treated with histone deacetylase inhibitors is not yet known. We report the observation of EBV-associated illnesses in 2 patients and the reactivation of HBV in an additional patient treated with romidepsin. These cases may represent reactivation of DNA viruses due to histone deacetylase inhibitor induced immunosuppression, or direct promotion of viral replication via histone deacetylase inhibitor induced chromatin remodeling, or, alternatively, may be related to the underlying disease process. These observations suggest that vigilance for DNA virus reactivation is needed to quantify the risk in patients treated with histone deacetylase inhibitors.

Key words: DNA virus, histone deacetylase inhibitor, therapy.