Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation (ChIP-Seq)

We screened for small molecules that reactivated latent HIV-1 and identified benzotriazoles as latency-reducing agents. Here, we characterize the effects of HODHBt on gene expression in cultured T cells from three donors by polyA RNA-Seq and on STAT5A occupancy of the HIV-1 LTR promoter by ChIP-Seq. These and other results demonstrate that benzotriazoles block SUMOylation of phosphorylated STAT5, prolonging its transcriptional activity. Overall design: 1.2 million HIV-infected primary T cells per treatment with matching 1% inputs