IFNG and HIV-1 infection: The enhanced capacity of the PLZF− NK cell subset for IFN-γ production compared with conventional PLZF+ NK cells in HIV-1 infection, and in comparison with HIV-1 negative HCMV-seropositive controls, is reflective of the greater magnitude of PLZF− NK cells, and suggests a more restricted specificity toward CD16 triggering and cytokine production.