CD4 and HIV-1 infection: As such, the detailed spatiotemporal characterization of the mechanisms encompassing Vpr-mediated G2 arrest, as well as their functional interconnection with essential steps of viral replication, will undoubtedly serve as the necessary precedent to attain a more exhaustive understanding of Vpr’s role in mediating viral pathogenicity, taking special consideration of the particularities various CD4+ T cell subsets exhibit during the course of HIV-1 infection.