Trial reportPLoS pathogens2012
Systems biology approaches reveal a specific interferon-inducible signature in HTLV-1 associated myelopathy.
Trial report in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled 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.
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
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- An insight to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) pathogenesis; evidence from high-throughput data integration and meta-analysis.Retrovirology · 2019Pooled 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
- Interferon dynamics in deltaretroviruses: why HTLV-1 evades, but BLV responds.Molecular biology reports · 2026Review
- Article
- IgG Idiotype Diversity Shapes Cytokine Profiles and Autoantibody Targets in HTLV-1 Clinical Outcomes.International journal of molecular sciences · 2025Article
- Efgartigimod Combined With Steroid Treatment for HAM/TSP: A Case Report.Annals of clinical and translational neurology · 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
- HTLV-1-infected cells drive the differentiation of monocytes into macrophages in vitro.BMC immunology · 2025Article
- Peculiar transcriptional reprogramming with functional impairment of dendritic cells upon exposure to transformed HTLV-1-infected cells.PLoS pathogens · 2024Article
- Gene biomarkers and classifiers for various subtypes of HTLV-1-caused ATLL cancer identified by a combination of differential gene co‑expression and support vector machine algorithms.Medical microbiology and immunology · 2023Article
- The role of viruses in cancer development versus cancer therapy: An oncological perspective.Cancer medicine · 2023Review
- Potential miRNA-gene interactions determining progression of various ATLL cancer subtypes after infection by HTLV-1 oncovirus.BMC medical genomics · 2023Article
- HBZ upregulates myoferlin expression to facilitate HTLV-1 infection.PLoS pathogens · 2023Article
- Differential modulation of IL-4, IL-10, IL-17, and IFN-γ production mediated by IgG from Human T-lymphotropic virus-1 (HTLV-1) infected patients on healthy peripheral T (CD4+, CD8+, and γδ) and B cells.Frontiers in medicine · 2023Article
- Systemic cytokines and GlycA discriminate disease status and predict corticosteroid response in HTLV-1-associated neuroinflammation.Journal of neuroinflammation · 2022Article
- Article
- Exploration of mRNAs and miRNA classifiers for various ATLL cancer subtypes using machine learning.BMC cancer · 2022Article
- Monitoring of HTLV-1-associated diseases by proviral load quantification using multiplex real-time PCR.Journal of neurovirology · 2022Article
- Article
- Identification of dysregulated pathways underlying HTLV-1-associated myelopathy/tropical spastic paraparesis through co-expression network analysis.Journal of neurovirology · 2021Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that persists lifelong in the host. In ∼4% of infected people, HTLV-1 causes a chronic disabling neuroinflammatory disease known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The pathogenesis of HAM/TSP is unknown and treatment remains ineffective. We used gene expression microarrays followed by flow cytometric and functional assays to investigate global changes in blood transcriptional profiles of HTLV-1-infected and seronegative individuals. We found that perturbations of the p53 signaling pathway were a hallmark of HTLV-1 infection. In contrast, a subset of interferon (IFN)-stimulated genes was over-expressed in patients with HAM/TSP but not in asymptomatic HTLV-1 carriers or patients with the clinically similar disease multiple sclerosis. The IFN-inducible signature was present in all circulating leukocytes and its intensity correlated with the clinical severity of HAM/TSP. Leukocytes from patients with HAM/TSP were primed to respond strongly to stimulation with exogenous IFN. However, while type I IFN suppressed expression of the HTLV-1 structural protein Gag it failed to suppress the highly immunogenic viral transcriptional transactivator Tax. We conclude that over-expression of a subset of IFN-stimulated genes in chronic HTLV-1 infection does not constitute an efficient host response but instead contributes to the development of HAM/TSP.
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What OpenQuestion holds
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.