Evidence map›Paper›PMID 38855141›Full record

ArticleFrontiers in bioinformatics2024

Decreased but persistent epigenetic age acceleration is associated with changes in T-cell subsets after initiation of highly active antiretroviral therapy in persons living with HIV.

Mary E Sehl, Elizabeth Crabb Breen, Roger Shih, Fengxue Li, Joshua Zhang, Peter Langfelder, Steve Horvath, Jay H Bream, Priya Duggal, Jeremy Martinson and 4 more

Abstract read
In one paragraph

Article in Frontiers in bioinformatics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Epigenetic age acceleration and mortality among persons with poorly controlled HIV.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
    Article
  4. Review
  5. Review
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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

14 authors.

Mary E SehlDivision of Hematology-Oncology, Department of Medicine, David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles, CA, United States.
Elizabeth Crabb BreenDepartment of Psychiatry and Biobehavioral Sciences, Cousins Center for Psychoneuroimmunology, David Geffen School of Medicine at UCLA, University of California, Los Angeles, Los Angeles, CA, United States.
Roger ShihDivision of Hematology-Oncology, Department of Medicine, David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles, CA, United States.
Fengxue LiDepartment of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, Los Angeles, CA, United States.
Joshua ZhangDepartment of Human Genetics, David Geffen School of Medicine at UCLA, University of California, Los Angeles, Los Angeles, CA, United States.
Peter LangfelderCenter for Neurobehavioral Genetics, Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, United States.
Steve HorvathDepartment of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, Los Angeles, CA, United States.
Jay H BreamDepartment of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Immunology Training Program, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Priya DuggalDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States.
Jeremy MartinsonDepartment of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States.
Steven M WolinskyDepartment of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, United States.
Otoniel Martinez-MazaDepartments of Obstetrics and Gynecology and Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine at UCLA, University of California, Los Angeles, CA, United States.
Christina M RamirezDepartment of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, Los Angeles, CA, United States.
Beth D JamiesonDivision of Hematology-Oncology, Department of Medicine, David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles, CA, United States.

Funding

UCLA Rapid, Relevant, Rigorous Implementation Science HubP30MH058107 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Sung-Jae Lee · 1997 to 2026
$53.5M
University of Pittsburgh MWCCS Clinical Research SiteU01HL146208 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Bernard Jonas C Macatangay, CHARLES R RINALDO · 2019 to 2026
$32.2M
Northwestern CORE Clinical Research Site: Trans-omics for HIV/AIDS ResearchU01HL146240 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Frank J Palella, Valentina Stosor · 2019 to 2026
$31.5M
NHLBI NIH HHS U01 HL146208NHLBI NIH HHS U01 HL146240NIMH NIH HHS P30 MH058107
6 · The paper itself

Abstract

Introduction: Persons living with HIV (PLWH) experience the early onset of age-related illnesses, even in the setting of successful human immunodeficiency virus (HIV) suppression with highly active antiretroviral therapy (HAART). HIV infection is associated with accelerated epigenetic aging as measured using DNA methylation (DNAm)-based estimates of biological age and of telomere length (TL). Methods: DNAm levels (Infinium MethylationEPIC BeadChip) from peripheral blood mononuclear cells from 200 PLWH and 199 HIV-seronegative (SN) participants matched on chronologic age, hepatitis C virus, and time intervals were used to calculate epigenetic age acceleration, expressed as age-adjusted acceleration residuals from 4 epigenetic clocks [Horvath's pan-tissue age acceleration residual (AAR), extrinsic epigenetic age acceleration (EEAA), phenotypic epigenetic age acceleration (PEAA), and grim epigenetic age acceleration (GEAA)] plus age-adjusted DNAm-based TL (aaDNAmTL). Epigenetic age acceleration was compared for PLWH and SN participants at two visits: up to 1.5 years prior and 2-3 years after HAART (or equivalent visits). Flow cytometry was performed in PLWH and SN participants at both visits to evaluate T-cell subsets. Results: Epigenetic age acceleration in PLWH decreased after the initiation of HAART but remained greater post-HAART than that in age-matched SN participants, with differences in medians of 6.6, 9.1, and 7.7 years for AAR, EEAA, and PEAA, respectively, and 0.39 units of aaDNAmTL shortening (all Discussion: In this large longitudinal study, we demonstrated that, although the magnitude of the difference decreases with HAART is associated with the cumulative viral load, PLWH are persistently epigenetically older than age-matched SN participants even after the successful initiation of HAART, and these changes are associated with changes in T-cell subsets.

Indexed as

agingantiretroviral therapyDNA methylationepigenetic clockhuman immunodeficiency virus

Identifiers

PMID38855141
PMCPMC11157435

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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.