Evidence map›Paper›PMID 27553844›Full record

ArticleRetrovirology2016

New insights into the heterogeneity of Th17 subsets contributing to HIV-1 persistence during antiretroviral therapy.

Vanessa Sue Wacleche, Jean-Philippe Goulet, Annie Gosselin, Patricia Monteiro, Hugo Soudeyns, Rémi Fromentin, Mohammad-Ali Jenabian, Shant Vartanian, Steven G Deeks, Nicolas Chomont and 2 more

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 97 citations in OpenAlex.

  1. Trial
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  11. Metformin Enhances Antibody-Mediated Recognition of HIV-Infected CD4bioRxiv : the preprint server for biology · 2024
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  15. Group AScience immunology · 2023
    Article
  16. Article
  17. Article
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  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 7 institutions in 2 countries.

Vanessa Sue WaclecheDépartement of Microbiologie, Infectiologie Et immunologie, Faculté de Médecine, Université de Montréal, Montreal, QC, Canada.
Jean-Philippe GouletCaprion, Montreal, QC, Canada.
Annie GosselinCentre de recherche du CHUM, 900 rue Saint-Denis, Tour Viger, R09.416, Montreal, QC, H2X 0A9, Canada.
Patricia MonteiroDépartement of Microbiologie, Infectiologie Et immunologie, Faculté de Médecine, Université de Montréal, Montreal, QC, Canada.
Hugo SoudeynsDépartement of Microbiologie, Infectiologie Et immunologie, Faculté de Médecine, Université de Montréal, Montreal, QC, Canada.
Rémi FromentinCentre de recherche du CHUM, 900 rue Saint-Denis, Tour Viger, R09.416, Montreal, QC, H2X 0A9, Canada.
Mohammad-Ali JenabianDépartement des Sciences Biologiques, Université du Québec à Montréal, Montreal, QC, Canada.
Shant VartanianDepartment of Medicine, University of California San Francisco, San Francisco, CA, USA.
Steven G DeeksDepartment of Medicine, University of California San Francisco, San Francisco, CA, USA.
Nicolas ChomontDépartement of Microbiologie, Infectiologie Et immunologie, Faculté de Médecine, Université de Montréal, Montreal, QC, Canada.
Jean-Pierre RoutyChronic Viral Illness Service and Research Institute, McGill University Health Centre, Montreal, QC, Canada.
Petronela AncutaDépartement of Microbiologie, Infectiologie Et immunologie, Faculté de Médecine, Université de Montréal, Montreal, QC, Canada. petronela.ancuta@umontreal.ca.
Centre Hospitalier de l’Université de Montréal · CAUniversité de Montréal · CAUniversity of California, San Francisco · USCaprion (Canada) · CACentre Hospitalier Universitaire Sainte-Justine · CAMcGill University Health Centre · CAUniversité du Québec à Montréal · CA

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
CIHR MOP-114957CIHR MOP-82849NIAID NIH HHS P30 AI027763
6 · The paper itself

Abstract

backgroundTh17 cells are permissive to HIV-1 infection and their depletion from the gut of infected individuals leads to microbial translocation, a major cause for non-AIDS co-morbidities. Most recent evidence supports the contribution of long-lived Th17 cells to HIV persistence during antiretroviral therapy (ART). However, the identity of long-lived Th17 cells remains unknown.

resultsHere, we performed an in-depth transcriptional and functional characterization of four distinct Th17 subsets and investigated their contribution to HIV reservoir persistence during ART. In addition to the previously characterized CCR6(+)CCR4(+) (Th17) and CCR6(+)CXCR3(+) (Th1Th17) subsets, we reveal the existence of two novel CCR6(+) subsets, lacking (double negative, CCR6(+)DN) or co-expressing CXCR3 and CCR4 (double positive, CCR6(+)DP). The four subsets shared multiple Th17-polarization markers, a fraction of cells proliferated in response to C. albicans, and exhibited lineage commitment and plasticity when cultured under Th17 and Th1 conditions, respectively. Of note, fractions of CCR6(+)DN and Th17 demonstrated stable Th17-lineage commitment under Th1-polarization conditions. Among the four subsets, CCR6(+)DN expressed a unique transcriptional signature indicative of early Th17 development (IL-17F, STAT3), lymph-node homing (CCR7, CD62L), follicular help (CXCR5, BCL6, ASCL2), and self-renewal (LEFI, MYC, TERC). Cross sectional and longitudinal studies demonstrated that CCR6(+)DN cells were the most predominant CCR6(+) subset in the blood before and after ART initiation; high frequencies of these cells were similarly observed in inguinal lymph nodes of individuals receiving long-term ART. Importantly, replication competent HIV was isolated from CCR6(+)DN of ART-treated individuals.

conclusionsTogether, these results provide new insights into the functional heterogeneity of Th17-polarized CCR6(+)CD4(+) T-cells and support the major contribution of CCR6(+)DN cells to HIV persistence during ART.

Indexed as

Antiretroviral Therapy, Highly ActiveCross-Sectional StudiesHIV-1HIV InfectionsHumansImmunologic MemoryLongitudinal StudiesReceptors, CCR4Receptors, CCR6Receptors, CXCR3Th17 CellsVirus ReplicationCCR4 protein, humanCCR6 protein, humanCXCR3 protein, humanReceptors, CCR4Receptors, CCR6Receptors, CXCR3ARTCCR4CCR6CXCR3HIV reservoirsHumanTh17

Identifiers

PMID27553844
PMCPMC4995622
OpenAlexW2517479804

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.