Evidence for HIV-1 cure after CCR5Δ32/Δ32 allogeneic haemopoietic stem-cell transplantation 30 months post analytical treatment interruption: a case report.


Journal

The lancet. HIV
ISSN: 2352-3018
Titre abrégé: Lancet HIV
Pays: Netherlands
ID NLM: 101645355

Informations de publication

Date de publication:
05 2020
Historique:
received: 03 02 2020
revised: 17 02 2020
accepted: 19 02 2020
pubmed: 15 3 2020
medline: 1 9 2020
entrez: 15 3 2020
Statut: ppublish

Résumé

The London patient (participant 36 in the IciStem cohort) underwent allogeneic stem-cell transplantation with cells that did not express CCR5 (CCR5Δ32/Δ32); remission was reported at 18 months after analytical treatment interruption (ATI). Here, we present longer term data for this patient (up to 30 months after ATI), including sampling from diverse HIV-1 reservoir sites. We used ultrasensitive viral load assays of plasma, semen, and cerebrospinal fluid (CSF) samples to detect HIV-1 RNA. In gut biopsy samples and lymph-node tissue, cell-copy number and total HIV-1 DNA levels were quantified in multiple replicates, using droplet digital PCR (ddPCR) and quantitative real-time PCR. We also analysed the presence of intact proviral DNA using multiplex ddPCR targeting the packaging signal (ψ) and envelope (env). We did intracellular cytokine staining to measure HIV-1-specific T-cell responses. We used low-sensitive and low-avidity antibody assays to measure the humoral response to HIV-1. We predicted the probability of rebound using a mathematical model and inference approach. HIV-1 viral load in plasma remained undetectable in the London patient up to 30 months (last tested on March 4, 2020), using an assay with a detection limit of 1 copy per mL. The patient's CD4 count was 430 cells per μL (23·5% of total T cells) at 28 months. A very low-level positive signal for HIV-1 DNA was recorded in peripheral CD4 memory cells at 28 months. The viral load in semen was undetectable in both plasma (lower limit of detection [LLD] <12 copies per mL) and cells (LLD 10 copies per 10 The London patient has been in HIV-1 remission for 30 months with no detectable replication-competent virus in blood, CSF, intestinal tissue, or lymphoid tissue. Donor chimerism has been maintained at 99% in peripheral T cells. We propose that these findings represent HIV-1 cure. Wellcome Trust and amfAR (American Foundation for AIDS Research).

Sections du résumé

BACKGROUND
The London patient (participant 36 in the IciStem cohort) underwent allogeneic stem-cell transplantation with cells that did not express CCR5 (CCR5Δ32/Δ32); remission was reported at 18 months after analytical treatment interruption (ATI). Here, we present longer term data for this patient (up to 30 months after ATI), including sampling from diverse HIV-1 reservoir sites.
METHODS
We used ultrasensitive viral load assays of plasma, semen, and cerebrospinal fluid (CSF) samples to detect HIV-1 RNA. In gut biopsy samples and lymph-node tissue, cell-copy number and total HIV-1 DNA levels were quantified in multiple replicates, using droplet digital PCR (ddPCR) and quantitative real-time PCR. We also analysed the presence of intact proviral DNA using multiplex ddPCR targeting the packaging signal (ψ) and envelope (env). We did intracellular cytokine staining to measure HIV-1-specific T-cell responses. We used low-sensitive and low-avidity antibody assays to measure the humoral response to HIV-1. We predicted the probability of rebound using a mathematical model and inference approach.
FINDINGS
HIV-1 viral load in plasma remained undetectable in the London patient up to 30 months (last tested on March 4, 2020), using an assay with a detection limit of 1 copy per mL. The patient's CD4 count was 430 cells per μL (23·5% of total T cells) at 28 months. A very low-level positive signal for HIV-1 DNA was recorded in peripheral CD4 memory cells at 28 months. The viral load in semen was undetectable in both plasma (lower limit of detection [LLD] <12 copies per mL) and cells (LLD 10 copies per 10
INTERPRETATION
The London patient has been in HIV-1 remission for 30 months with no detectable replication-competent virus in blood, CSF, intestinal tissue, or lymphoid tissue. Donor chimerism has been maintained at 99% in peripheral T cells. We propose that these findings represent HIV-1 cure.
FUNDING
Wellcome Trust and amfAR (American Foundation for AIDS Research).

Identifiants

pubmed: 32169158
pii: S2352-3018(20)30069-2
doi: 10.1016/S2352-3018(20)30069-2
pmc: PMC7606918
pii:
doi:

Substances chimiques

CCR5 protein, human 0
Receptors, CCR5 0

Types de publication

Case Reports Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e340-e347

Subventions

Organisme : Medical Research Council
ID : MRM008614/2
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/R008698/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/L006588/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : WT108082AIA
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N001265/1
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.

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Auteurs

Ravindra Kumar Gupta (RK)

Department of Medicine, University of Cambridge, Cambridge, UK; Africa Health Research Institute, Durban, South Africa. Electronic address: rkg20@cam.ac.uk.

Dimitra Peppa (D)

Nuffield Department of Medicine, University of Oxford, Oxford, UK; Population, Policy and Practice, UCL Great Ormond Street Institute of Child Health, London, UK.

Alison L Hill (AL)

Department for Organismic and Evolutionary Biology, Harvard University, Cambridge, MA, USA.

Cristina Gálvez (C)

IrsiCaixa AIDS Research Institute, Badalona, Spain; Autonomous University of Barcelona, Cerdanyola del Vallès, Spain.

Maria Salgado (M)

IrsiCaixa AIDS Research Institute, Badalona, Spain.

Matthew Pace (M)

Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Laura E McCoy (LE)

Division of Infection and Immunity, University College London (UCL), London, UK.

Sarah A Griffith (SA)

Division of Infection and Immunity, University College London (UCL), London, UK.

John Thornhill (J)

Imperial College London, London, UK.

Aljawharah Alrubayyi (A)

Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Laura E P Huyveneers (LEP)

Department of Medical Microbiology, University Medical Center, Utrecht, Netherlands.

Eleni Nastouli (E)

Division of Infection and Immunity, University College London (UCL), London, UK; Department of Virology, UCL Hospitals, London, UK; Population, Policy and Practice, UCL Great Ormond Street Institute of Child Health, London, UK.

Paul Grant (P)

Department of Virology, UCL Hospitals, London, UK.

Simon G Edwards (SG)

Mortimer Market Centre, Department of HIV, Central and North West London NHS Trust, London, UK.

Andrew J Innes (AJ)

Imperial College London, London, UK; Imperial College NHS Healthcare Trust, Hammersmith Hospital, London, UK.

John Frater (J)

Nuffield Department of Medicine, University of Oxford, Oxford, UK; Oxford National Institute for Health Research Biomedical Research Centre, Oxford, UK.

Monique Nijhuis (M)

Department of Medical Microbiology, University Medical Center, Utrecht, Netherlands.

Anne Marie J Wensing (AMJ)

Department of Medical Microbiology, University Medical Center, Utrecht, Netherlands.

Javier Martinez-Picado (J)

IrsiCaixa AIDS Research Institute, Badalona, Spain; University of Vic - Central University of Catalonia, Vic, Spain; Catalan Institution for Research and Advanced Studies, Barcelona, Spain.

Eduardo Olavarria (E)

Imperial College London, London, UK; Mortimer Market Centre, Department of HIV, Central and North West London NHS Trust, London, UK.

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Classifications MeSH