(A) Twelve weeks after infection, mice were treated with IFNR blocking antibody (αIFNR) or an isotype antibody control (iso) for 8 days. Expression levels of the ISGs MX1, OAS1, and IRF7 in human PBMCs from humanized BLT mice after treatment were measured by real-time RT-PCR (n = 3–5 per group). (B) PD-1, TIM-3, and CD38 expression as measured by flow cytometry (quantitatively by gating of percentages positive and relative MFIs ± SEM) on T cells from uninfected or infected mice that were treated with IFNR blocking antibody or isotype control (n = 3–7 per group). (C) Splenocytes from HIV-1–infected, isotype antibody–treated, or IFNR antibody–treated mice were stimulated with PMA/ionomycin for 6 hours, and IFN-γ and IL-2 production by CD8 cells was measured by flow cytometry (representative of n = 3 per group). (D) Summary of C as measured by relative MFI. (E) Splenocytes from HIV-1–infected, isotype-treated, or IFNR antibody–treated mice were stimulated with an HIV-1 clade B peptide pool (Pol, Gag, Env, and Nef), and production of IFN-γ by CD8 cells was measured by flow cytometry (representative of n = 3 per group). (F) Summary of the total percentage of IFN-γ⁺CD8⁺ cells after HIV peptide pool stimulation. (G) Summary of IFN-γ production by CD8⁺ cells as measured by relative MFI after HIV peptide pool stimulation. (H) Summary of IFN-γ⁺CD8⁺ cell numbers per million lymphocytes. (I) Summary of the relative HLA-DR MFI on CD4 T cells from infected mice treated with isotype or type I IFNR antibody (n = 4–6 per group). The Mann-Whitney test was used to compare 2 groups (*P < 0.05, **P < 0.005), and the Kruskal-Wallis test was used for multiple comparisons (A and B, both P < 0.05). Data represent mean ± SEM. Representative experiments were performed more than 3 times (C and E).