Fig. 1

Effect of panobinostat on histone acetylation, HIV RNA, and viral outgrowth from patient cells. a Human PBMCs (n = 3) were incubated with panobinostat or DMSO control for 6 h, and histone H3 acetylation was measured by flow cytometry. b Resting CD4⁺ T cells were isolated from leukapheresis product obtained from three HIV-infected patients on suppressive antiretroviral therapy (outlined in Table 1), then pulsed with panobinostat (20 nM) or untreated. HIV RNA levels were measured from 10 to 12 individual wells (1 × 10⁶ cells each) by quantitative real-time PCR. c Resting CD4⁺ T cells were isolated from leukapheresis product obtained from seven HIV-infected patients on suppressive antiretroviral therapy (outlined in Table 1), then incubated with panobinostat (20 nM) or untreated. Viral outgrowth was measured by QVOA. Mean and SEM plotted with comparison by unpaired t test in a; Mann–Whitney test in b; Wilcoxon matched-pairs signed rank test in c: ns p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Blue bars/symbols denote control; pink and red bars/symbols denote panobinostat-treated