ArticleThe Journal of general virology2010
Transcription factor Spi-B binds unique sequences present in the tandem repeat promoter/enhancer of JC virus and supports viral activity.
Article in The Journal of general virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- MicroRNA biomarkers for JC virus reactivation and progressive multifocal leukoencephalopathy in natalizumab-treated multiple sclerosis patients: a systematic review.Journal of neurovirology · 2026Review
- Revisiting JC virus and progressive multifocal leukoencephalopathy.Journal of neurovirology · 2023Review
- Understanding polyomavirus CNS disease - a perspective from mouse models.The FEBS journal · 2022Review
- Article
- Determining host factors contributing to the reactivation of JC virus in kidney transplant recipients.Virology journal · 2022Article
- Rearrangement in the Hypervariable Region of JC Polyomavirus Genomes Isolated from Patient Samples and Impact on Transcription Factor-Binding Sites and Disease Outcomes.International journal of molecular sciences · 2022Article
- Innovative therapeutic concepts of progressive multifocal leukoencephalopathy.Journal of neurology · 2022Review
- Progressive multifocal leukoencephalopathy and the spectrum of JC virus-related disease.Nature reviews. Neurology · 2021Review
- JCPyV VP1 Mutations in Progressive MultifocalLeukoencephalopathy: Altering Tropismor Mediating Immune Evasion?Viruses · 2020Review
- Review
- Article
- JC Polyomavirus Infection Reveals Delayed Progression of the Infectious Cycle in Normal Human Astrocytes.Journal of virology · 2020Article
- Host-Immune Interactions in JC Virus Reactivation and Development of Progressive Multifocal Leukoencephalopathy (PML).Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- [Progress on pathogenesis of progressive multifocal leukoence-phalopathy].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
- Understanding Progressive Multifocal Leukoencephalopathy Risk in Multiple Sclerosis Patients Treated with Immunomodulatory Therapies: A Bird's Eye View.Frontiers in immunology · 2018Review
- ViroFind: A novel target-enrichment deep-sequencing platform reveals a complex JC virus population in the brain of PML patients.PloS one · 2018Article
- Replication of JC Virus DNA in the G144 Oligodendrocyte Cell Line Is Dependent Upon Akt.Journal of virology · 2017Article
- Host cell virus entry mechanisms enhance anti-JCV-antibody switch in natalizumab-treated multiple sclerosis patients.Journal of neurovirology · 2016Observational
- Progressive Multifocal Leukoencephalopathy in HIV-Uninfected Individuals.Current infectious disease reports · 2016Review
- Natalizumab-induced POU2AF1/Spi-B upregulation: A possible route for PML development.Neurology(R) neuroimmunology & neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Progressive multifocal leukoencephalopathy (PML) is an often fatal demyelinating disease caused by lytic infection of oligodendrocytes with JC virus (JCV). The development of PML in non-immunosuppressed individuals is a growing concern with reports of mortality in patients treated with mAb therapies. JCV can persist in the kidneys, lymphoid tissue and bone marrow. JCV gene expression is restricted by non-coding viral regulatory region sequence variation and cellular transcription factors. Because JCV latency has been associated with cells undergoing haematopoietic development, transcription factors previously reported as lymphoid specific may regulate JCV gene expression. This study demonstrates that one such transcription factor, Spi-B, binds to sequences present in the JCV promoter/enhancer and may affect early virus gene expression in cells obtained from human brain tissue. We identified four potential Spi-B-binding sites present in the promoter/enhancer elements of JCV sequences from PML variants and the non-pathogenic archetype. Spi-B sites present in the promoter/enhancers of PML variants alone bound protein expressed in JCV susceptible brain and lymphoid-derived cell lines by electromobility shift assays. Expression of exogenous Spi-B in semi- and non-permissive cells increased early viral gene expression. Strikingly, mutation of the Spi-B core in a binding site unique to the Mad-4 variant was sufficient to abrogate viral activity in progenitor-derived astrocytes. These results suggest that Spi-B could regulate JCV gene expression in susceptible cells, and may play an important role in JCV activity in the immune and nervous systems.
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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 Socratic graph.