Evidence map›Paper›PMID 38548722›Full record

ArticleNature communications2024

Autophagy-enhancing ATG16L1 polymorphism is associated with improved clinical outcome and T-cell immunity in chronic HIV-1 infection.

Renée R C E Schreurs, Athanasios Koulis, Thijs Booiman, Brigitte Boeser-Nunnink, Alexandra P M Cloherty, Anusca G Rader, Kharishma S Patel, Neeltje A Kootstra, Carla M S Ribeiro

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Review
  8. Article
  9. Article
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

9 authors at 2 institutions in 1 country.

Renée R C E SchreursAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.
Athanasios KoulisAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.
Thijs BooimanAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0002-0433-8047
Brigitte Boeser-NunninkAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.
Alexandra P M ClohertyAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.
Anusca G RaderAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0002-4889-3691
Kharishma S PatelAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.
Neeltje A KootstraAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0001-9429-7754
Carla M S RibeiroAmsterdam UMC location University of Amsterdam, Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands. c.m.ribeiro@amsterdamumc.nl.ORCID http://orcid.org/0000-0002-5682-4143
Amsterdam University Medical Centers · NLNetherlands Center for Occupational Diseases · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic HIV-1 infection is characterized by T-cell dysregulation that is partly restored by antiretroviral therapy. Autophagy is a critical regulator of T-cell function. Here, we demonstrate a protective role for autophagy in HIV-1 disease pathogenesis. Targeted analysis of genetic variation in core autophagy gene ATG16L1 reveals the previously unidentified rs6861 polymorphism, which correlates functionally with enhanced autophagy and clinically with improved survival of untreated HIV-1-infected individuals. T-cells carrying ATG16L1 rs6861(TT) genotype display improved antiviral immunity, evidenced by increased proliferation, revamped immune responsiveness, and suppressed exhaustion/immunosenescence features. In-depth flow-cytometric and transcriptional profiling reveal T-helper-cell-signatures unique to rs6861(TT) individuals with enriched regulation of pro-inflammatory networks and skewing towards immunoregulatory phenotype. Therapeutic enhancement of autophagy recapitulates the rs6861(TT)-associated T-cell traits in non-carriers. These data underscore the in vivo relevance of autophagy for longer-lasting T-cell-mediated HIV-1 control, with implications towards development of host-directed antivirals targeting autophagy to restore immune function in chronic HIV-1 infection.

Indexed as

HIV-1HIV InfectionsAutophagyAutophagy-Related ProteinsHumansPolymorphism, GeneticATG16L1 protein, humanAutophagy-Related Proteins

Identifiers

PMID38548722
PMCPMC10979031
OpenAlexW4393261812

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.