Evidence map›Paper›PMID 42053910›Full record

ArticleGeroScience2026

A telomere-lipid-immunity axis linking viral integration to autoimmune disease risk.

May A Beydoun, Minkyo Song, Choa Yun, Hind A Beydoun, Nigus G Asefa, Jordan Weiss, Nicole Noren Hooten, Michele K Evans, Alan B Zonderman

Abstract read
PubMed Publisher
In one paragraph

Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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.

May A BeydounLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA. baydounm@mail.nih.gov.ORCID http://orcid.org/0000-0002-1050-4523
Minkyo SongLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA.
Choa YunLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA.
Hind A BeydounVA National Center On Homelessness Among Veterans, U.S. Department of Veterans Affairs, Washington, DC, 20420, USA.
Nigus G AsefaLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA.
Jordan WeissOptimal Aging Institute, New York University Grossman School of Medicine, New York, NY, USA.
Nicole Noren HootenLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA.
Michele K EvansLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA.
Alan B ZondermanLaboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, MD, 21224, USA.

Funding

NIA NIH HHS AG000513
6 · The paper itself

Abstract

Autoimmune diseases rise steeply with biological aging, reflecting progressive failure of immune regulation. Inherited chromosomally integrated human herpesvirus 6 (iciHHV-6) represents a unique lifelong viral exposure in which the viral genome is embedded within host telomeres, potentially altering leukocyte telomere length (LTL), a core biomarker of immune aging. Circulating metabolites may further modify these viral-telomeric interactions. We analyzed 156,927 UK Biobank participants free of autoimmune disease at baseline. Baseline iciHHV-6 carrier status, LTL, and plasma metabolomic profiles were related to incident autoimmune disease during follow-up. Mediation and interaction models were used to test whether LTL and various metabolomic pathways mediated or modified viral effects. Over follow-up, 7.8% of participants developed autoimmune disease and 1.3% were iciHHV-6 carriers. iciHHV-6 was not directly associated with autoimmune disease despite higher baseline comorbidity. Longer LTL was independently protective overall, especially for rheumatoid arthritis, although it was positively associated with multiple sclerosis. iciHHV-6 carriers had longer LTL, yielding a small but significant indirect protective effect on autoimmune risk. LTL also modified viral effects, with stronger protection among iciHHV-6-positive individuals, suggesting telomere length buffers adverse viral-immune interactions. Metabolomic analyses showed that triglyceride-rich lipoproteins and proinflammatory lipids were associated with shorter LTL and higher autoimmune risk, whereas omega-3 fatty acids, albumin, and HDL phospholipids were protective. Lipidomic pathways mediated a substantial portion of the LTL-autoimmune association and modified viral effects. These findings identify a telomere-lipid-immunity axis linking lifelong viral integration, metabolic aging, and autoimmune susceptibility, highlighting biological aging pathways as targets for autoimmune disease prevention.

Indexed as

Autoimmune diseaseHuman herpesvirus 6MetabolomeTelomeres

Identifiers

PMID42053910

What OpenQuestion holds

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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.