Data repository for: "AP-1/c-Fos supports SIV and HIV-1 latency in CD4 T-cells infected in vivo"

<p><strong>Abstract</strong></p> <p><br></p> <p>Persistent HIV-1 reservoirs of infected CD4 T-cells are a major barrier to HIV-1 cure, though the mechanisms by which they are established and maintained <em>in vivo </em>remain poorly characterized. To study host properties that govern productive cellular infection, we analyzed viral mRNA+ (vRNA) CD4 T-cells of untreated SIV-infected macaques by single-cell transcriptomics. Transcriptionally active infected cells, defined by spliced vRNA, were highly enriched for vRNA: 10.3% and 7.5% of all mRNA in two animals. These cells expressed diminished <em>FOS, </em>a component of the Activator protein 1 (AP-1) transcription factor, relative to vRNA-low and -negative cells. Conversely, <em>FOS </em>and <em>JUN</em>, another AP-1 component, were upregulated in HIV-infected cells compared to uninfected cells from people with HIV-1 on suppressive therapy. c-Fos inhibition augmented reactivatable HIV-1 infection in latently infected primary CD4 T cells <em>in vitro</em>. These findings implicate AP-1 in latency establishment and maintenance. Therapeutic strategies targeting AP-1 may limit HIV-1 reservoirs.</p> <p><br></p> <p>This repository contains Seurat objects with the scRNA-seq data from the two rhesus macaques in the paper.</p>