Fig. 6

Effect of FACT-mediated chromatin remodeling chemical promotion on early steps of HIV-1 LAI virus and derived lentiviral vectors. HeLa P4 and HEK293T cells were treated with CBLC137 curaxin 6 h before cell infection with LAI wild type virus or transduction with lentiviral vectors. The structure of the CBLC137 drug is shown in (a) as well as its effect on FACT. CDLC137 binds to nucleosomal DNA and forms structures with high FACT affinity leading to the trapping of the complex into dissociated nucleosomes, preventing its histone chaperone activity and enhancing the histone dissociation [32, 33]. This induces a global increase in chromatin accessibility that was evaluated by FAIRE (data obtained in HEK293T cells are reported in b). The effect on LAI virus replication was evaluated by quantifying the LTR-dependent β-galactodisase expression (c) and viral DNA populations at 0–48 h post-transduction (see 24 and 48 h time points in d and full time course analysis in Additional file 6: Figure S6). Early steps of lentiviral vector replication were evaluated by quantifying GFP-positive HEK293T cells (e) and viral DNA populations at 0–48 h post-transduction (see 24 and 48 h time points in f and full time course analysis in Additional file 6: Figure S6). Quantification of the viral DNA populations were done after optimal 0.1 µM curaxins treatment. All values are shown as the mean ± standard deviation (error bars) of at least three independent sets of experiments. The p-values were calculated by Student’s t-test and are shown as *p < 0.05 and **p < 0.005 to represent the probability of obtaining significant differences compared with untreated conditions