ArticleJournal of neuropathology and experimental neurology2009
Frequent infection of cerebellar granule cell neurons by polyomavirus JC in progressive multifocal leukoencephalopathy.
Article in Journal of neuropathology and experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Overview of MRI findings in progressive multifocal leukoencephalopathy.Japanese journal of radiology · 2025Review
- Cortical lesions are common in a longitudinal progressive multifocal leukoencephalopathy cohort.Brain communications · 2025Article
- Recent advances in discovery and functional analysis of the small proteins and microRNA expressed by polyomaviruses.Virology · 2025Review
- Insights into the genetic characteristics, clustering patterns, and phylogeographic dynamics of the JC polyomavirus, 1993 to 2023.Virus research · 2024Article
- Progressive Multifocal Leukoencephalopathy: Pathogenesis, Diagnostic Tools, and Potential Biomarkers of Response to Therapy.Neurology · 2023Review
- Newly diagnosed AIDS patient with cerebellar JC virus.IDCases · 2023Article
- Human neurotropic polyomavirus, JC virus, agnoprotein targets mitochondrion and modulates its functions.Virology · 2021Article
- Progressive multifocal leukoencephalopathy and the spectrum of JC virus-related disease.Nature reviews. Neurology · 2021Review
- Progressive multifocal leukoencephalopathy in a patient with systemic sclerosis treated with methotrexate: A case report and literature review.Journal of scleroderma and related disorders · 2020Article
- Review
- The Role of the JC Virus in Central Nervous System Tumorigenesis.International journal of molecular sciences · 2020Review
- JC virus infection of meningeal and choroid plexus cells in patients with progressive multifocal leukoencephalopathy.Journal of neurovirology · 2019Article
- Development of demyelinating lesions in progressive multifocal leukoencephalopathy (PML): Comparison of magnetic resonance images and neuropathology of post-mortem brain.Neuropathology : official journal of the Japanese Society of Neuropathology · 2019Article
- Expression of novel proteins by polyomaviruses and recent advances in the structural and functional features of agnoprotein of JC virus, BK virus, and simian virus 40.Journal of cellular physiology · 2019Review
- JC Polyomavirus Attachment and Entry: Potential Sites for PML Therapeutics.Current clinical microbiology reports · 2017Article
- Case report: progressive multifocal encephalopathy (PML) causing an isolated cerebellar syndrome.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016Article
- JC Virus Infects Neurons and Glial Cells in the Hippocampus.Journal of neuropathology and experimental neurology · 2016Article
- Concomitant granule cell neuronopathy in patients with natalizumab-associated PML.Journal of neurology · 2016Article
- JC polyomavirus attachment, entry, and trafficking: unlocking the keys to a fatal infection.Journal of neurovirology · 2015Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Progressive multifocal leukoencephalopathy (PML) occurs most often in immunosuppressed individuals. The lesions of PML result from astrocyte and oligodendrocyte infection by the polyomavirus JC (JCV); JCV has also been shown to infect and destroy cerebellar granule cell neurons (GCNs) in 2 human immunodeficiency virus (HIV)-positive patients. To determine the prevalence and pattern of JCV infection in GCNs, we immunostained formalin-fixed paraffin-embedded cerebellar samples from 40 HIV-positive and 3 HIV-negative PML patients for JCV, and glial and neuronal markers. The JCV infection was detected in 30 patients (70%); 28 (93%) of them had JCV-infected cells in the GC layer; JCV-infected GCNs were demonstrated in 15 (79%) of 19 tested cases. The JCV regulatory T antigen was expressed more frequently and abundantly in GCNs than JCV VP1 capsid protein. None of 37 HIV-negative controls but 1 (3%) of 35 HIV-positive subjects without PML had distinct foci of JCV-infected GCNs. Thus, JCV infection of GCNs is frequent in PML patients and may occur in the absence of cerebellar white matter demyelinating lesions. The predominance of Tantigen over VP1 expression in GCNs suggests that they may be the site of early or latent central nervous system JCV infection. These results indicate that infection of GCNs is an important, previously overlooked, aspect of JCV pathogenesis in immunosuppressed individuals.
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