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A Novel Histone Deacetylase Inhibitor, AR-42, Reactivates HIV-1 from Chronically and Latently Infected CD4+ T-cells.
- Source :
-
Retrovirology: Research & Treatment . 2015, Issue 7, p1-5. 5p. 3 Graphs. - Publication Year :
- 2015
-
Abstract
- Human immunodeficiency virus type 1 (HIV-1) latency is a major barrier to a cure of AIDS. Latently infected cells harbor an integrated HIV-1 genome but are not actively producing HIV-1. Histone deacetylase (HDAC) inhibitors, such as vorinostat (SAHA), have been shown to reactivate latent HIV-1. AR-42, a modified HDAC inhibitor, has demonstrated efficacy against malignant melanoma, meningioma, and acute myeloid leukemia and is currently used in clinical trials for non-Hodgkin's lymphoma and multiple myeloma. In this study, we evaluated the ability of AR-42 to reactivate HIV-1 in the two established CD4+ T-cell line models of HIV-1 latency. In HIV-1 chronically infected ACH-2 cells, AR-42-induced histone acetylation was more potent and robust than that of vorinostat. Although AR-42 and vorinostat were equipotent in their ability to reactivate HIV-1, AR-42-induced maximal HIV-1 reactivation was twofold greater than vorinostat in ACH-2 and J-Lat (clone 9.2) cells. These data provide rationale for assessing the efficacy of AR-42-mediated HIV-1 reactivation within primary CD4+ T-cells. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 11781238
- Issue :
- 7
- Database :
- Academic Search Index
- Journal :
- Retrovirology: Research & Treatment
- Publication Type :
- Academic Journal
- Accession number :
- 111311431
- Full Text :
- https://doi.org/10.4137/RRT.S31632