HIV-1 promoter is gradually silenced when integrated into BACH2 in Jurkat T-cells

Data from the study "HIV-1 promoter is gradually silenced when integrated into BACH2 in Jurkat T-cells". We developed a novel model using CRISPR/Cas9-mediated, targeted integration of our HIV-1-based, dual-fluorophore vector LTatCL[M], with which we can distinguish between latently and actively infected cells and specifically target any gene of interest. Using the HIV-1 integration hotspot BACH2 as example, we could show that HIV-1 integration into BACH2, but not into the safe-harbor locus AAVS1, leads to HIV-1 latency, which was reversible upon re-activation