HIV-1 Vpr induces G2 cell cycle arrest in dividing cells (e.g., CD4+ T-cells), enhances the infection of terminally differentiated (non-dividing) myeloid lineage cells (e.g., macrophages), transactivates the HIV-1 Long Terminal Repeat (LTR) to promote viral gene expression, activates the DNA damage response, initiates depletion of several DNA repair proteins, modulates host cell signaling pathways and the host immune response, contributes to nuclear import of viral DNA, and induces apoptosis (reviewed in [16,17,18,19,20,21,22] and discussed in subsequent sections). This evidence concerns the gene CD4 and infection.