Fig. 7

Protective shRNAs recruit AGO1 and HDAC1 during HIV-1 reactivation with TNF. Parental and transduced J-Lat 9.2 cell lines were stimulated for 48 h with 5 ng/mL of TNF, and ChIP assays performed on sorted live GFP- and GFP + populations. Significance of immunoprecipitation levels of a AGO1 and b HDAC1 during HIV-1 latency (left panels) and HIV-1 reactivation (middle panels), was analysed by performing “in-between” cell lines multiple comparisons against Parental (dark-grey bar). Multiple comparisons “in- within” cell lines where also performed to examine significant changes from latency to reactivation for each cell line (right panels). Data are presented as the % Input normalised to Parental from two independent ChIP assays (Mean ± SD)(n = 4)(* = p values from 0.05 to 0.01, ** = p values from 0.009 to 0.001, *** = p values from 0.0009 to 0.0001 and **** = p values < 0.0001). c Upper panel: Schematic of latency disruption during HIV-1 reactivation with TNF. Lower panel: Schematic of latency maintenance by TGS-inducing si/shRNAs during treatment with TNF. ShA/143 is not explicitly illustrated because PromA/143 cell line simultaneously co-expresses each, PromA and 143, from independent lentiviral cassettes