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.
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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Telomere length dynamics in adults living with HIV: A systematic review.BMC infectious diseases · 2026Pooled it
- Unsuppressed Viremia and Lower CD4 Count Associated With Faster Telomere Attrition in African Children With Perinatal Human Immunodeficiency Virus on Long-term Antiretroviral Therapy.The Journal of infectious diseases · 2026Trial
- Epigenetic age acceleration and mortality among persons with poorly controlled HIV.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026Article
- Epigenetic aging is a hallmark of HIV pathogenesis and phenotypic outcomes.Current HIV/AIDS reports · 2026Review
- HIV associated epigenetic trends and chronic diseases: insights into the hidden burden of chronic infection.Clinical epigenetics · 2026Review
- Exercise as a preventive and therapeutic strategy for non-communicable diseases in people living with HIV: evidence, mechanisms and clinical implications.BMJ open sport & exercise medicine · 2026Review
- Perspective: clinical relevance of epigenetic aging and HIV.Epigenomics · 2025Review
- Effects of highly active antiretroviral therapy initiation on epigenomic DNA methylation in persons living with HIV.Frontiers in bioinformatics · 2024Article
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14 authors.
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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.
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