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Nat Commun. 2015 Oct 9;6:8495. doi: 10.1038/ncomms9495.

Immunological biomarkers predict HIV-1 viral rebound after treatment interruption.

Author information

1
Nuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, John Radcliffe Hospital, Oxford OX1 3SY, UK.
2
Institute for Emerging Infections, The Oxford Martin School, Oxford OX1 3BD, UK.
3
Division of Medicine, Wright Fleming Institute, Imperial College, London W2 1PG, UK.
4
Caldecot Centre, King's College Hospital NHS Foundation Trust, London SE5 9RS, UK.
5
Oxford National Institute of Health Research Biomedical Research Centre, Oxford OX3 7LE, UK.
6
St Vincent's Centre for Applied Medical Research and The Kirby Institute, UNSW Australia, Sydney, New South Wales 2052, Australia.
7
Department of HIV and Sexual Health, Brighton and Sussex University Hospitals, Brighton BN2 5BE, UK.
8
Division of Infection and Immunity, University College London, London WC1E 6BT, UK.
9
Projeto Praça Onze, Hospital Escola São Francisco de Assis, Universidade Federal do Rio de Janeiro, Rio de Janeiro RJ 21941-901, Brazil.
10
Department of Infectious Diseases, Ospedale San Raffaele, Milan 20132, Italy.
11
MRC Clinical Trials Unit at UCL Institute of Clinical Trials &Methodology, London WC2B 6NH, UK.

Abstract

Treatment of HIV-1 infection with antiretroviral therapy (ART) in the weeks following transmission may induce a state of 'post-treatment control' (PTC) in some patients, in whom viraemia remains undetectable when ART is stopped. Explaining PTC could help our understanding of the processes that maintain viral persistence. Here we show that immunological biomarkers can predict time to viral rebound after stopping ART by analysing data from a randomized study of primary HIV-1 infection incorporating a treatment interruption (TI) after 48 weeks of ART (the SPARTAC trial). T-cell exhaustion markers PD-1, Tim-3 and Lag-3 measured prior to ART strongly predict time to the return of viraemia. These data indicate that T-cell exhaustion markers may identify those latently infected cells with a higher proclivity to viral transcription. Our results may open new avenues for understanding the mechanisms underlying PTC, and eventually HIV-1 eradication.

PMID:
26449164
PMCID:
PMC4633715
DOI:
10.1038/ncomms9495
[Indexed for MEDLINE]
Free PMC Article

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