Journal article
Ex vivo response to histone deacetylase (HDAC) inhibitors of the HIV long terminal repeat (LTR) derived from HIV-infected patients on antiretroviral therapy
HK Lu, LR Gray, F Wightman, P Ellenberg, G Khoury, WJ Cheng, TM Mota, S Wesselingh, PR Gorry, PU Cameron, MJ Churchill, SR Lewin
Plos One | PUBLIC LIBRARY SCIENCE | Published : 2014
Open access
Abstract
Histone deacetylase inhibitors (HDACi) can induce human immunodeficiency virus (HIV) transcription from the HIV long terminal repeat (LTR). However, ex vivo and in vivo responses to HDACi are variable and the activity of HDACi in cells other than T-cells have not been well characterised. Here, we developed a novel assay to determine the activity of HDACi on patient-derived HIV LTRs in different cell types. HIV LTRs from integrated virus were amplified using triple-nested Alu-PCR from total memory CD4+ T-cells (CD45RO+) isolated from HIV-infected patients prior to and following suppressive antiretroviral therapy. NL4-3 or patient-derived HIV LTRs were cloned into the chromatin forming episoma..
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Awarded by National Science Foundation
Funding Acknowledgements
This work was supported by an Australian National Health and Medical Research Council (NHMRC) project grant 1009533 and 1051093; the National Institutes of Health, USA (NIMH100594) and the Division of AIDS, National Institute of Allergy and Infectious Disease, US National Institutes of Health (Delaney AIDS Research Enterprise, DARE; U19AI096109). S. R. L. is an NHMRC senior practitioner fellow. P. R. G is supported by an Australian Research Council Future Fellowship (FT2). L. R. G was supported by a NHMRC Early Career Fellowship (GNT0606967). G. K. is a recipient of an NHMRC Dora Lush biomedical post-graduate scholarship (579719). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.