ArticleFrontiers in immunology2024
IL-10 predicts incident neuroinflammatory disease and proviral load dynamics in a large Brazilian cohort of people living with human T-lymphotropic virus type 1.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular biomarkers associated with ATLL and HAM progression in HTLV-1 infection: a systematic review.Revista do Instituto de Medicina Tropical de Sao Paulo · 2026Pooled it
- Integrated in vitro and multi-cohort cross-omics analysis of HTLV-1-associated lung pathology reveals a RelA-dependent mechanism for monocyte recruitment and differentiation.Molecular medicine (Cambridge, Mass.) · 2026Article
- In Vitro Model of the Human Blood-Brain Barrier to Explore HTLV-1 Immunopathogenesis.Current issues in molecular biology · 2025Article
- Multi-cohort cross-omics analysis reveals disease mechanisms and therapeutic targets in HTLV-1-associated myelopathy, a neglected retroviral neuroinflammatory disorder.Research square · 2025Article
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17 authors.
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Abstract
Human T-Lymphotropic Virus type-1 (HTLV-1) is a unique retrovirus associated with both leukemogenesis and a specific neuroinflammatory condition known as HTLV-1-Associated Myelopathy (HAM). Currently, most proposed HAM biomarkers require invasive CSF sampling, which is not suitable for large cohorts or repeated prospective screening. To identify non-invasive biomarkers for incident HAM in a large Brazilian cohort of PLwHTLV-1 (n=615 with 6,673 person-years of clinical follow-up), we selected all plasma samples available at the time of entry in the cohort (between 1997-2019), in which up to 43 cytokines/chemokines and immune mediators were measured. Thus, we selected 110 People Living with HTLV-1 (PLwHTLV-1), of which 68 were neurologically asymptomatic (AS) at baseline and 42 HAM patients. Nine incident HAM cases were identified among 68 AS during follow-up. Using multivariate logistic regression, we found that lower IL-10, IL-4 and female sex were independent predictors of clinical progression to definite HAM (AUROC 0.91), and outperformed previously suggested biomarkers age, sex and proviral load (AUROC 0.77). Moreover, baseline IL-10 significantly predicted proviral load dynamics at follow-up in all PLwHTLV-1. In an exploratory analysis, we identified additional plasma biomarkers which were able to discriminate iHAM from either AS (IL6Rα, IL-27) or HAM (IL-29/IFN-λ1, Osteopontin, and TNFR2). In conclusion, female sex and low anti-inflammatory IL-10 and IL-4 are independent risk factors for incident HAM in PLwHTLV-1,while proviral load is not, in agreement with IL-10 being upstream of proviral load dynamics. Additional candidate biomarkers IL-29/IL-6R/TNFR2 represent plausible therapeutic targets for future clinical trials in HAM patients.
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