Plasmacytoid dendritic cell and functional HIV Gag p55-specific T cells before treatment interruption can inform set-point plasma HIV viral load after treatment interruption in chronically suppressed HIV-1+ patients.

The identification of immune correlates of HIV control is important for the design of immunotherapies that could support cure or antiretroviral therapy ( ART) intensification-related strategies. ART interruptions may facilitate this task through exposure of an ART partially reconstituted immune system to endogenous virus. We investigated the relationship between set-point plasma HIV viral load ( VL) during an ART interruption and innate/adaptive parameters before or after interruption. Dendritic cell ( DC), natural killer ( NK) cell and HIV Gag p55-specific T-cell functional responses were measured in paired cryopreserved peripheral blood mononuclear cells obtained at the beginning (on ART) and at set-point of an open-ended interruption from 31 ART-suppressed chronically HIV-1⁺ patients. Spearman correlation and linear regression modeling were used. Frequencies of plasmacytoid DC (p DC), and HIV Gag p55-specific CD3⁺ CD4⁻ perforin⁺ IFN- γ⁺ cells at the beginning of interruption associated negatively with set-point plasma VL. Inclusion of both variables with interaction into a model resulted in the best fit (adjusted R² = 0·6874). Frequencies of p DC or HIV Gag p55-specific CD3⁺ CD4⁻ CSFE^lo CD107a⁺ cells at set-point associated negatively with set-point plasma VL. The dual contribution of p DC and anti- HIV T-cell responses to viral control, supported by our models, suggests that these variables may serve as immune correlates of viral control and could be integrated in cure or ART-intensification strategies. [ABSTRACT FROM AUTHOR]