Journal article

CD4 T Cells Expressing PD-1, TIGIT and LAG-3 Contribute to HIV Persistence during ART

R Fromentin, W Bakeman, MB Lawani, G Khoury, W Hartogensis, S DaFonseca, M Killian, L Epling, R Hoh, E Sinclair, FM Hecht, P Bacchetti, SG Deeks, SR Lewin, RP Sékaly, N Chomont

Plos Pathogens | PUBLIC LIBRARY SCIENCE | Published : 2016

Abstract

HIV persists in a small pool of latently infected cells despite antiretroviral therapy (ART). Identifying cellular markers expressed at the surface of these cells may lead to novel therapeutic strategies to reduce the size of the HIV reservoir. We hypothesized that CD4+ T cells expressing immune checkpoint molecules would be enriched in HIV-infected cells in individuals receiving suppressive ART. Expression levels of 7 immune checkpoint molecules (PD-1, CTLA-4, LAG-3, TIGIT, TIM-3, CD160 and 2B4) as well as 4 markers of HIV persistence (integrated and total HIV DNA, 2-LTR circles and cell-associated unspliced HIV RNA) were measured in PBMCs from 48 virally suppressed individuals. Using negat..

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University of Melbourne Researchers

Grants

Awarded by National Institute of Allergy and Infectious Diseases


Funding Acknowledgements

This work was supported by the Delaney AIDS Research Enterprise (DARE) to Find a Cure 1U19AI096109, NIH grant 1R21AI113096 (NC, SRL, SD, RPS), NIH grant R01 AI110334, the UCSF-GIVI Center for AIDS Research grant P30AI027763 and by the Foundation for AIDS Research (amfAR Research Consortium on HIV Eradication (108687-54-RGRL and 108928-56-RGRL). RF is supported by an amfAR fellowship (108264-51-RFRL). SRL is supported by a practitioner fellowship from the National Health and Medical Research Council (NHMRC) of Australia. GK is a recipient of an NHMRC Dora Lush biomedical post-graduate scholarship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.