ArticleThe American journal of pathology2004
Differential distribution of the JC virus receptor-type sialic acid in normal human tissues.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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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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.
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Who cites it
27 citing papers in PubMed, 67 citations in OpenAlex.
- Review
- JC Virus Agnogene Regulates Histone-Modifying Enzymes via PML-NBs: Transcriptomics in VLP-Expressing Cells.Viruses · 2025Article
- Human B cells and dendritic cells are susceptible and permissive to enterovirus D68 infection.mSphere · 2024Article
- Polyomavirus Wakes Up and Chooses Neurovirulence.Viruses · 2023Review
- The oncogenic roles of JC polyomavirus in cancer.Frontiers in oncology · 2022Review
- The pathogenesis and virulence of enterovirus-D68 infection.Virulence · 2021Review
- The Oncogenic Roles of JC Virus T Antigen in Breast Carcinogenesis.Frontiers in molecular biosciences · 2021Article
- Possible Oncogenic Viruses Associated with Lung Cancer.OncoTargets and therapy · 2020Review
- Viral Factors Important for Efficient Replication of Influenza A Viruses in Cells of the Central Nervous System.Journal of virology · 2019Article
- Human Polyomavirus JCPyV and Its Role in Progressive Multifocal Leukoencephalopathy and Oncogenesis.Frontiers in oncology · 2019Review
- Nasal Infection of Enterovirus D68 Leading to Lower Respiratory Tract Pathogenesis in Ferrets (Mustela putorius furo).Viruses · 2017Article
- Specific and quantitative detection of Human polyomaviruses BKPyV and JCPyV in the healthy Pakistani population.Virology journal · 2017Article
- Article
- JC polyomavirus attachment, entry, and trafficking: unlocking the keys to a fatal infection.Journal of neurovirology · 2015Review
- The oncogenic role of JC virus T antigen in lens tumors without cell specificity of alternative splicing of its intron.Oncotarget · 2015Article
- Article
- Structure-function analysis of the human JC polyomavirus establishes the LSTc pentasaccharide as a functional receptor motif.Cell host & microbe · 2010Article
- Progressive multifocal leukoencephalopathy and promyelocytic leukemia nuclear bodies: a review of clinical, neuropathological, and virological aspects of JC virus-induced demyelinating disease.Acta neuropathologica · 2010Review
- Adaptive mutations in the JC virus protein capsid are associated with progressive multifocal leukoencephalopathy (PML).PLoS genetics · 2009Article
- Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans.The American journal of pathology · 2008Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
JC virus (JCV), a member of the polyomavirus family, causes a demyelinating disease of the central nervous system (CNS) in humans known as progressive multifocal leukoencephalopathy. Although glial cells are the principal target of JCV productive infection in progressive multifocal leukoencephalopathy patients, little is known regarding the site of JCV persistence and the mechanisms by which the virus spreads to the CNS to cause disease. Previous work has demonstrated the presence of replicating JCV DNA in B lymphocytes from peripheral blood, tonsil, and spleen and it has been hypothesized that lymphocytes may be one site of JCV persistence. Detection of viral gene products in renal tubules and excretion of JC virions in the urine suggests JCV persistence in the kidney. A respiratory route of viral transmission has also been hypothesized implicating the lung as another possible site of persistent JCV infection. Earlier studies from our laboratory have shown that terminal alpha 2,6-linked sialic acid is a critical component of the JCV receptor. In this report we examined the tissue distribution of this JCV receptor-type sialic acid in a panel of normal human tissues. Our results demonstrate that in normal brain JCV receptor-type sialic acids are expressed on oligodendrocytes and astrocytes, but not on cortical neurons. The receptor-type sialic acid is also more highly expressed on B lymphocytes than on T lymphocytes in normal human spleen and tonsil. In addition, both the kidney and lung express abundant levels of alpha 2-6-linked sialic acids. Our data show a striking correlation between the expression of the JCV receptor-type sialic acid on cells and their susceptibility to infection by the virus. These findings also support the hypothesis of JCV persistence in lymphoid tissue and B-cell-facilitated viral dissemination to the CNS.
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