Evidence mapPaperPMID 40986533Full record

SynthesisPloS one2025

Infection and telomere length: A systematic review.

Louis Tunnicliffe, Rutendo Muzambi, Jonathan W Bartlett, Laura D Howe, Khalid A Basit, Kwabena Asare, Georgia Gore-Langton, Kathryn E Mansfield, Veryan Codd, Charlotte Warren-Gash

Abstract readSystematic Review
In one paragraph

Synthesis in PloS one, 2025. 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

10 authors.

Louis TunnicliffeFaculty of Epidemiology & Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.ORCID https://orcid.org/0000-0001-8537-2855
Rutendo MuzambiDepartment of Epidemiology & Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.
Jonathan W BartlettFaculty of Epidemiology & Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.
Laura D HoweMRC Integrative Epidemiology Unit, Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Khalid A BasitFaculty of Epidemiology & Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.
Kwabena AsareFaculty of Epidemiology & Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.ORCID https://orcid.org/0000-0002-5074-2315
Georgia Gore-LangtonFaculty of Epidemiology & Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.
Kathryn E MansfieldSchool of Health and Care Sciences, University of Lincoln, Leicester, United Kingdom.
Veryan CoddDepartment of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Charlotte Warren-GashFaculty of Epidemiology & Population Health, London School of Hygiene & Tropical Medicine, London, United Kingdom.

Funding

Wellcome Trust 225868
6 · The paper itself

Abstract

backgroundInfections may increase the risk of age-related diseases such as dementia. Accelerated immunological ageing, measurable by telomere length (TL), may be a potential mechanism. However, the relationship between different infections and TL or telomere attrition remains unclear. This systematic review synthesises existing evidence on whether infections contribute to TL or telomere attrition and highlights research gaps to inform future studies.

objectiveTo summarise the literature on associations between infections and telomere length or attrition.

methodsWe conducted comprehensive searches across six databases (MEDLINE, EMBASE, Web of Science, Scopus, Global Health, Cochrane Library) from inception to 22 May 2025, using concepts of infections, TL, and study type. Two researchers independently screened studies, extracted data, and assessed risk of bias (ROB) using the ROBINS-E tool. Meta-analysis was unfeasible due to heterogeneity, so a narrative synthesis was conducted. Studies were grouped by infection type, telomere measurement assay, cell type, and statistical approach. A GRADE assessment was performed to evaluate evidence quality.

resultsOur searches identified 10,349 studies, of which 73 met eligibility criteria. Most (59) were cross-sectional and most were published after 2000, with the earliest from 1996. Most studies were from the USA (17). HIV was the most frequently studied infection (35 studies), with 79% (excluding overlapping samples) reporting an association between HIV and reduced TL or increased telomere attrition. Findings for other infections, including herpesviruses and Human Papillomavirus were more variable. Variation in infection type, measurement assay, cell type, and statistical approach made cross-study comparisons challenging. Most studies had a high ROB, mainly due to unmeasured confounding. The GRADE assessment rated evidence quality as very low.

conclusionsOur review highlights a potential link between HIV and TL and telomere attrition. More robust longitudinal studies with standardised measurements and better confounder control are needed, particularly for non-HIV infections. PROSPERO (ID:CRD42023444854).

Indexed as

InfectionsTelomereTelomere HomeostasisTelomere ShorteningAgingHIV InfectionsHumans

Identifiers

PMID40986533
PMCPMC12456831

What Socratic holds

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Read underepoch 390

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 Socratic graph.