ArticleProceedings of the National Academy of Sciences of the United States of America1999
HLA alleles determine human T-lymphotropic virus-I (HTLV-I) proviral load and the risk of HTLV-I-associated myelopathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
160 citing papers in PubMed, 1 synthesis or guideline pooled it, 423 citations in OpenAlex.
- The role of human leukocyte antigen in HTLV-1 infection and progression to ATLL and HAM/TSP: a systematic review and meta-analysis.Virology journal · 2025Pooled it
- HTLV-1 specific CD8+ T cell function augmented by blockade of 2B4/CD48 interaction in HTLV-1 infection.PloS one · 2014Trial
- Systems biology approaches reveal a specific interferon-inducible signature in HTLV-1 associated myelopathy.PLoS pathogens · 2012Trial
- Multiple Sclerosis and Viruses: « Liaisons Dangereuses ».Reviews in medical virology · 2026Review
- Unmasking HAM/TSP: understanding HTLV-1-driven neurological disease.Journal of neurovirology · 2026Review
- Epidemiology and Clinical Outcomes of HTLV-1: A Comprehensive Narrative Review of Endemic and Nonendemic Regions.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Review
- Untangling the causes of geographical disparities in the clinical outcome of HTLV-1 infection: a critical perspective on the contribution of viral genetic diversity.Journal of virology · 2025Review
- Current State of Therapeutics for HTLV-1.Viruses · 2024Review
- Progression of HTLV-1 Associated Myelopathy/Tropical Spastic Paraparesis after Pregnancy: A Case Series and Review of the Literature.Pathogens (Basel, Switzerland) · 2024Review
- HLA-A*24 Increases the Risk of HTLV-1-Associated Myelopathy despite Reducing HTLV-1 Proviral Load.International journal of molecular sciences · 2024Article
- Complete Rescue of HTLV-1Pathogens (Basel, Switzerland) · 2024Article
- An HTLV-1 envelope mRNA vaccine is immunogenic and protective in New Zealand rabbits.Journal of virology · 2024Article
- HTLV-1 induces an inflammatory CD4+CD8+ T cell population in HTLV-1-associated myelopathy.JCI insight · 2024Article
- Pentraxin 3, a serum biomarker in human T-cell lymphotropic virus type-1-associated myelopathy patients and asymptomatic carriers.Medical microbiology and immunology · 2023Article
- The transcriptome of HTLV-1-infected primary cells following reactivation reveals changes to host gene expression central to the proviral life cycle.PLoS pathogens · 2023Article
- Th17/IL-17 Axis in HTLV-1-Associated Myelopathy Tropical Spastic Paraparesis and Multiple Sclerosis: Novel Insights into the Immunity During HAMTSP.Molecular neurobiology · 2023Review
- Innate receptors modulating adaptive T cell responses: KIR-HLA interactions and T cell-mediated control of chronic viral infections.Immunogenetics · 2023Review
- Article
- Putative role of HLA polymorphism among a Brazilian HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) population.Scientific reports · 2023Article
- Article
100 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
The risk of disease associated with persistent virus infections such as HIV-I, hepatitis B and C, and human T-lymphotropic virus-I (HTLV-I) is strongly determined by the virus load. However, it is not known whether a persistent class I HLA-restricted antiviral cytotoxic T lymphocyte (CTL) response reduces viral load and is therefore beneficial or causes tissue damage and contributes to disease pathogenesis. HTLV-I-associated myelopathy (HAM/TSP) patients have a high virus load compared with asymptomatic HTLV-I carriers. We hypothesized that HLA alleles control HTLV-I provirus load and thus influence susceptibility to HAM/TSP. Here we show that, after infection with HTLV-I, the class I allele HLA-A*02 halves the odds of HAM/TSP (P < 0.0001), preventing 28% of potential cases of HAM/TSP. Furthermore, HLA-A*02(+) healthy HTLV-I carriers have a proviral load one-third that (P = 0.014) of HLA-A*02(-) HTLV-I carriers. An association of HLA-DRB1*0101 with disease susceptibility also was identified, which doubled the odds of HAM/TSP in the absence of the protective effect of HLA-A*02. These data have implications for other persistent virus infections in which virus load is associated with prognosis and imply that an efficient antiviral CTL response can reduce virus load and so prevent disease in persistent virus infections.
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Registered trials
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.