Journal article
Relationship between CD4 T cell turnover, cellular differentiation and HIV persistence during ART
Charline Bacchus-Souffan, Mark Fitch, Jori Symons, Mohamed Abdel-Mohsen, Daniel B Reeves, Rebecca Hoh, Mars Stone, Joseph Hiatt, Peggy Kim, Abha Chopra, Haelee Ahn, Vanessa A York, Daniel L Cameron, Frederick M Hecht, Jeffrey N Martin, Steven A Yukl, Simon Mallal, Paul U Cameron, Steven G Deeks, Joshua T Schiffer Show all
PLOS PATHOGENS | PUBLIC LIBRARY SCIENCE | Published : 2021
Abstract
The precise role of CD4 T cell turnover in maintaining HIV persistence during antiretroviral therapy (ART) has not yet been well characterized. In resting CD4 T cell subpopulations from 24 HIV-infected ART-suppressed and 6 HIV-uninfected individuals, we directly measured cellular turnover by heavy water labeling, HIV reservoir size by integrated HIV-DNA (intDNA) and cell-associated HIV-RNA (caRNA), and HIV reservoir clonality by proviral integration site sequencing. Compared to HIV-negatives, ART-suppressed individuals had similar fractional replacement rates in all subpopulations, but lower absolute proliferation rates of all subpopulations other than effector memory (TEM) cells, and lower ..
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Grants
Awarded by National Institute of Allergy and Infectious Diseases of the National Institutes of Health
Awarded by amfAR Cure Institute
Awarded by Delaney AIDS Research Enterprise (DARE)
Awarded by "A Collaboration for AIDS Vaccine Discovery" (CAVD) grant from the Bill & Melinda Gates Foundation
Awarded by UCSF Medical Scientist Training Program
Awarded by Center For AIDS Research (CFAR) New Investigator Award
Funding Acknowledgements
Research reported in this publication was supported by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health under the award numbers: R01AI116368 (J. M.M. & P.W.H.), R01DK108349 (S.A.Y.), R01AI132128 (S.A.Y.) and R01DK120387 (S.A.Y.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. This work was also supported by the amfAR Cure Institute (109301-59-RGRL) (S.A.Y.), the Delaney AIDS Research Enterprise (DARE) to Find a Cure (UM1AI126611-01) (J.M.M. & P.W.H.), and the "A Collaboration for AIDS Vaccine Discovery" (CAVD) grant from the Bill & Melinda Gates Foundation (OPP1115400) (P.W.H.). J.H. was funded by the UCSF Medical Scientist Training Program (T32GM007618). D.B.R. is supported by a Center For AIDS Research (CFAR) New Investigator Award (P30 AI027757). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.