Yale University

PDC 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(+) Subjects.

TitlePDC 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(+) Subjects.
Publication TypeJournal Article
Year of Publication2015
AuthorsPapasavvas, Emmanouil, Andrea Foulkes, Xiangfan Yin, Jocelin Joseph, Brian Ross, Livio Azzoni, Jay R. Kostman, Karam Mounzer, Jane Shull, and Luis J. Montaner
JournalImmunology
Date Published2015 Feb 12
ISSN1365-2567
AbstractThe 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 via 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 prior or after interruption. Dendritic cell (DC), natural killer (NK) cell and HIV Gag p55-specific T cell functional responses were measured in paired cryo-preserved peripheral blood mononuclear cells (PBMC) obtained at the beginning (on ART) and at set-point of an open-ended interruption from 31 ART-suppressed chronically HIV-1(+) subjects. Spearman correlation and linear regression modeling were used. Frequencies of plasmacytoid DC (PDC), 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 R(2) =0.6874). Frequencies of PDC 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 PDC 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. This article is protected by copyright. All rights reserved.
DOI10.1111/imm.12452
Alternate JournalImmunology

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