Evidence map›Paper›PMID 33400687›Full record

ArticleJCI insight2021

HIV-specific T cell responses reflect substantive in vivo interactions with antigen despite long-term therapy.

Eva M Stevenson, Adam R Ward, Ronald Truong, Allison S Thomas, Szu-Han Huang, Thomas R Dilling, Sandra Terry, John K Bui, Talia M Mota, Ali Danesh and 14 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
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  9. HIV Nef amplifies mechanical heterogeneity to promote immune evasion.bioRxiv : the preprint server for biology · 2025
    Article
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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

24 authors at 7 institutions in 1 country.

Eva M StevensonDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Adam R WardDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Ronald TruongDepartment of Microbiology, Immunology, and Tropical Medicine, School of Medicine & Health Sciences, and.
Allison S ThomasDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA.
Szu-Han HuangDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Thomas R DillingDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Sandra TerryDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
John K BuiDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Talia M MotaDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Ali DaneshDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Guinevere Q LeeDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Andrea GramaticaDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Pragya KhadkaDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Winiffer D Conce AlbertoDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Rajesh T GandhiDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Deborah K McMahonDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Christina M LalamaCenter for Biostatistics in AIDS Research, Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Ronald J BoschCenter for Biostatistics in AIDS Research, Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Bernard MacatangayDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Joshua C CyktorDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Joseph J EronDepartment of Medicine, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
John W MellorsDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
R Brad JonesDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
AIDS Clinical Trials Group A5321 Team
Cornell University · USUniversity of Pittsburgh · USCancer Research And Biostatistics · USBoston University · USMassachusetts General Hospital · USMilken Institute · USUniversity of North Carolina at Chapel Hill · US

Funding

Leadership and Operations Center (LOC), AIDS Clinical Trials Group (ACTG); LOC 1/UM1AI068636 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Joseph J Eron, RAJESH T GANDHI · 2011 to 2026
$1073.1M
Statistical and Data Management Center (SDMC), AIDS Clinical Trials Group (ACTG)UM1AI068634 · NIAID · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Marlene Ann Cooper, Michael David Hughes · 2011 to 2026
$246.6M
Validation, CLIA and Qualification (VQC): Enhancing the RS ratio as a tool for AIDS Clinical Trial Group (ACTG) tuberculosis trialsUM1AI106701 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Grace M Aldrovandi · 2014 to 2026
$116.8M
Disparities in COVID Disease Severity and Outcomes in New York CityUL1TR002384 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI JULIANNE L IMPERATO-MCGINLEY · 2017 to 2026
$86.2M
University of Pittsburgh Clinical Trials UnitUM1AI069494 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SUSAN L KOLETAR, John W Mellors · 2012 to 2026
$38.0M
BELIEVE: Bench to Bed Enhanced Lymphocyte Infusions to Engineer Viral EradicationUM1AI126617 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI JONES, R. BRAD, NIXON, DOUGLAS F · 2016 to 2020
$28.1M
Targeted delivery of cytopathicity enhancing agents, and co-ordination with shock and kill, to reduce HIV reservoirsR01AI147845 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI IRVINE, DARRELL J, JONES, R. BRAD · 2019 to 2023
$4.0M
CTL-Mediated Elimination of Replication Competent vs. Defective HIV Proviruses from Natural Latent Reservoirs: Roles of Antigen Specificity and Functional CharacteristicsR01AI131798 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI JONES, R. BRAD · 2017 to 2021
$2.1M
DETECTION OF HIV TARGETS BY GOLD NANOPARTICLE PROBESR01AI052764 · NIAID · NORTHWESTERN UNIVERSITY · PI WOLINSKY, STEVEN M · 2002 to 2004
$795k
NCATS NIH HHS UL1 TR002384NIAID NIH HHS R01 AI052764NIAID NIH HHS R01 AI131798NIAID NIH HHS R01 AI147845NIAID NIH HHS UM1 AI068634NIAID NIH HHS UM1 AI068636NIAID NIH HHS UM1 AI069494NIAID NIH HHS UM1 AI106701NIAID NIH HHS UM1 AI126617
6 · The paper itself

Abstract

Antiretroviral therapies (ARTs) abrogate HIV replication; however, infection persists as long-lived reservoirs of infected cells with integrated proviruses, which reseed replication if ART is interrupted. A central tenet of our current understanding of this persistence is that infected cells are shielded from immune recognition and elimination through a lack of antigen expression from proviruses. Efforts to cure HIV infection have therefore focused on reactivating latent proviruses to enable immune-mediated clearance, but these have yet to succeed in reducing viral reservoirs. Here, we revisited the question of whether HIV reservoirs are predominately immunologically silent from a new angle: by querying the dynamics of HIV-specific T cell responses over long-term ART for evidence of ongoing recognition of HIV-infected cells. In longitudinal assessments, we show that the rates of change in persisting HIV Nef-specific responses, but not responses to other HIV gene products, were associated with residual frequencies of infected cells. These Nef-specific responses were highly stable over time and disproportionately exhibited a cytotoxic, effector functional profile, indicative of recent in vivo recognition of HIV antigens. These results indicate substantial visibility of the HIV-infected cells to T cells on stable ART, presenting both opportunities and challenges for the development of therapeutic approaches to curing infection.

Indexed as

AdultAgedAnti-HIV AgentsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCohort StudiesFemaleGranzymesHIV-1HIV AntigensHIV InfectionsHost Microbial InteractionsHumansImmune EvasionInterferon-gammaLongitudinal StudiesAnti-HIV AgentsGranzymesGZMB protein, humanHIV AntigensInterferon-gammaAIDS/HIVImmunologyT cells

Identifiers

PMID33400687
PMCPMC7934865
OpenAlexW3120492589

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Registered trials

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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.