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“Conflicting results have been reported regarding the ability of valproic acid (VPA) to reduce the size of HIV reservoirs in patients receiving suppressive highly active antiretroviral therapy (HAART). In a randomized multicentre, cross-over study, we assessed whether adding VPA to stable HAART could potentially reduce the size of the latent viral reservoir in CD4 T cells of chronically infected patients. A total of 56 virologically suppressed patients were randomly assigned

either to receive VPA plus HAART for 16 weeks followed by HAART alone for 32 weeks (arm 1; n = 27) GSI-IX solubility dmso or to receive HAART alone for 16 weeks and then VPA plus HAART for 32 weeks (arm 2; n = 29). VPA was administered at a dose of 500 mg twice a day (bid) and was adjusted to the therapeutic range. A quantitative culture assay was used to assess HIV reservoirs in CD4 T cells at baseline and at weeks 16 and 48. No significant reductions in the frequency of CD4 T cells harbouring replication-competent HIV after 16 and 32 weeks of VPA therapy were observed. In arm 1, median (range) values of IU per Erythromycin log10 billion (IUPB) cells were 2.55 (range 1.20–4.20), 1.80 (range 1.0–4.70) and 2.70 (range 1.0–3.90; P = 0.87) for baseline, week 16 and week 48, respectively. In arm 2, median values

of IUPB were 2.55 (range 1.20–4.65), 1.64 (range 1.0–3.94) and 2.51 (range 1.0–4.48; P = 0.50) for baseline, week 16 and week 48, respectively. Our study demonstrates that adding VPA to stable HAART does not reduce the latent HIV reservoir in virally suppressed patients. Despite its ability to sustain durable inhibition of viral replication, highly active antiretroviral therapy (HAART) does not eliminate HIV-1 infection even after years of therapy [1]. The persistence of replication-competent virus in resting memory CD4 T cells has emerged as a major obstacle to eradication of HIV-1 [2, 3]. Mechanisms that allow HIV-1 to establish and maintain latency are still poorly understood, but recent evidence suggests that the modulation of chromatin architecture within the viral promoter plays a key role in this process [4, 5].