To identify the HDAC responsible for counteracting the pro-transcriptional activity of Vpr, we treated HIV-GFP or HIV-GFP-Vpr-infected cells with a selective HDAC1/2i, an HDAC3i, or vorinostat starting two days post-infection and every three days subsequently and assessed the effect on GFP MFI within GFP+ cells after 14 days. The gene discussed is HDAC9; the disease is infection.