CD69 and HIV-1 infection: Co-culture of resting target T cells with donor T cells infected with HIV-1 accessory protein mutants showed that deletion of Vpr (HIV-1 ΔVpr) prevented induction of the TRM-like phenotype following HIV-1 infection, evidenced by no CD69 upregulation and no increase in the CD69+/CXCR6+/CD49a+ triple-positive TRM-like memory population (Figures 3A, 3B, 3D, S5A–S5E, and S6).