ArticleJCI insight2023
Identification and tracking of HTLV-1-infected T cell clones in virus-associated neurologic disease.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Integrated TCRγ Clonality Workflow for Molecular Diagnosis in HTLV-1 Carriers and Adult T-Cell Leukemia/Lymphoma.Diagnostics (Basel, Switzerland) · 2026Article
- Dimethyl fumarate as a promising therapeutic candidate for virus-associated myelopathy.Brain : a journal of neurology · 2026Article
- HTLV-1-Infected CD4Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Unmasking HAM/TSP: understanding HTLV-1-driven neurological disease.Journal of neurovirology · 2026Review
- HTLV-1-Specific CTL Accumulation in CSF Contributes to Neuroinflammation in HTLV-1-Associated Myelopathy.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Therapeutic approaches for HTLV-1-associated adult T-cell leukemia/lymphoma: a comprehensive review.Medical oncology (Northwood, London, England) · 2023Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T lymphotropic virus type 1-assoicated (HTLV-1-associated) myelopathy/tropical spastic paraparesis (HAM/TSP) is a neuroinflammatory disease caused by the persistent proliferation of HTLV-1-infected T cells. Here, we performed a T cell receptor (TCR) repertoire analysis focused on HTLV-1-infected cells to identify and track the infected T cell clones that are preserved in patients with HAM/TSP and migrate to the CNS. TCRβ repertoire analysis revealed higher clonal expansion in HTLV-1-infected cells compared with noninfected cells from patients with HAM/TSP and asymptomatic carriers (ACs). TCR clonality in HTLV-1-infected cells was similar in patients with HAM/TSP and ACs. Longitudinal analysis showed that the TCR repertoire signature in HTLV-1-infected cells remained stable, and highly expanded infected clones were preserved within each patient with HAM/TSP over years. Expanded HTLV-1-infected clones revealed different distributions between cerebrospinal fluid (CSF) and peripheral blood and were enriched in the CSF of patients with HAM/TSP. Cluster analysis showed similarity in TCRβ sequences in HTLV-1-infected cells, suggesting that they proliferate after common antigen stimulation. Our results indicate that exploring TCR repertoires of HTLV-1-infected cells can elucidate individual clonal dynamics and identify potential pathogenic clones expanded in the CNS.
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