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Latent HIV in primary T lymphocytes is unresponsive to histone deacetylase inhibitors

Gautam K Sahu2 and Miles W Cloyd1*

Author Affiliations

1 Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Blvd, Galveston, TX-77555, USA

2 Biotherapeutics Development Laboratory, Roger Williams Medical Center, 825 Chalkstone Avenue, NC-143, Providence, RI 02908, USA

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Virology Journal 2011, 8:400  doi:10.1186/1743-422X-8-400

Published: 12 August 2011


Recently, there is considerable interest in the field of anti-HIV therapy to identify and develop chromatin-modifying histone deacetylase (HDAC) inhibitors that can effectively reactivate latent HIV in patients. The hope is that this would help eliminate cells harboring latent HIV and achieve an eventual cure of the virus. However, how effectively these drugs can stimulate latent HIVs in quiescent primary CD4 T cells, despite their relevant potencies demonstrated in cell line models of HIV latency, is not clear. Here, we show that the HDAC inhibitors valproic acid (VPA) and trichostatin A (TSA) are unable to reactivate HIV in latently infected primary CD4 T cells generated in the H80 co-culture system. This raises a concern that the drugs inhibiting HDAC function alone might not be sufficient for stimulating latent HIV in resting CD4 T cells in patients and not achieve any anticipated reduction in the pool of latent reservoirs.