Single-cell RNA-seq in a model for HIV latency reversal

T cells are the primary target of the virus HIV-1. Upon infection, the expression of the virus may come to a complete shutdown, a phenomenon known as latency. The molecular mechanisms responsible for the latency of HIV-1 are still poorly understood. To shed light on those mechanisms, we used the J-Lat A2 model for latency reversal, that consists of a Jurkat T cell clone containing a mini HIV construct that is transcriptionally silent. We treated J-Lat A2 and Jurkat cells with the latency-reversing drugs SAHA (suberoylanilide hydroxamic acid) and PMA (phorbol 12-myristate 13-acetate), and we performed single-cell RNA-seq to identify transcriptional signatures shared among the cells where HIV is reactivated. Overall design: Jurkat T cells and J-Lat A2 cells were treated by SAHA or PMA, or by the control drug DMSO in two experimental batches. After 24 hours, cells were FACS-sorted down to one cell per well into five 96-well plates (two plates in the first batch, three plates in the second).