ArticleThe Journal of general virology2009
SMAD proteins of oligodendroglial cells regulate transcription of JC virus early and late genes coordinately with the Tat protein of human immunodeficiency virus type 1.
Article in The Journal of general virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Single-Cell Multi-Modal Differential Analysis of the Human Neo-Cortex in HIV Infection Reveals Similarities with Hallmarks of Alzheimer's Disease.Research square · 2025Article
- Transcriptomic Analysis Reveals Key Pathways Influenced by HIV-2 Vpx.International journal of molecular sciences · 2025Article
- HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.Frontiers in immunology · 2025Review
- HIV encephalopathy is contributed by macrophages and microglia.Science China. Life sciences · 2024Article
- Carbohydrates: Binding Sites and Potential Drug Targets for Neural-Affecting Pathogens.Advances in neurobiology · 2023Article
- Irrespective of Plaque Activity, Multiple Sclerosis Brain Periplaques Exhibit Alterations of Myelin Genes and a TGF-Beta Signature.International journal of molecular sciences · 2022Article
- Determining host factors contributing to the reactivation of JC virus in kidney transplant recipients.Virology journal · 2022Article
- The oncogenic roles of JC polyomavirus in cancer.Frontiers in oncology · 2022Review
- JCPyV NCCR analysis in PML patients with different risk factors: exploring common rearrangements as essential changes for neuropathogenesis.Virology journal · 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
- Human Polyomavirus JCPyV and Its Role in Progressive Multifocal Leukoencephalopathy and Oncogenesis.Frontiers in oncology · 2019Review
- Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders.Brain sciences · 2016Review
- Human polyomaviruses and incidence of cutaneous squamous cell carcinoma in the New Hampshire skin cancer study.Cancer medicine · 2016Article
- Virological Mechanisms in the Coinfection between HIV and HCV.Mediators of inflammation · 2015Review
- Immune surveillance and response to JC virus infection and PML.Journal of neurovirology · 2014Review
- Effects of Tat proteins and Tat mutants of different human immunodeficiency virus type 1 clades on glial JC virus early and late gene transcription.The Journal of general virology · 2013Article
- Human polyomavirus reactivation: disease pathogenesis and treatment approaches.Clinical & developmental immunology · 2013Review
- New insights on human polyomavirus JC and pathogenesis of progressive multifocal leukoencephalopathy.Clinical & developmental immunology · 2013Review
- Article
- Molecular biology, epidemiology, and pathogenesis of progressive multifocal leukoencephalopathy, the JC virus-induced demyelinating disease of the human brain.Clinical microbiology reviews · 2012Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
JC virus (JCV) is the aetiological agent of progressive multifocal leukoencephalopathy (PML), a fatal, demyelinating disease of the brain affecting people with AIDS. Although immunosuppression is involved in infection of the brain by JCV, a direct influence of human immunodeficiency virus type 1 (HIV-1) has also been established. The Tat protein of HIV-1 has been implicated in activation of the cytokine transforming growth factor (TGF)-beta in HIV-1-infected cells and in stimulating JCV gene transcription and DNA replication in oligodendroglia, the primary central nervous system cell type infected by JCV in PML. This study demonstrated that Tat can cooperate with SMAD proteins, the intracellular effectors of TGF-beta, at the JCV DNA control region (CR) to stimulate JCV gene transcription. Tat stimulated JCV early gene transcription in KG-1 oligodendroglial cells when expressed via transfection or added exogenously. Using chromatin immunoprecipitation, it was shown that exogenous Tat enhanced binding of SMAD2, -3 and -4 and their binding partner Fast1 to the JCV CR in living cells. When SMAD2, -3 and -4 were expressed together, Tat, expressed from plasmid pTat, stimulated transcription from both early and late gene promoters, with the early promoter exhibiting stimulation of >100-fold. Tat, SMAD4 and JCV large T-antigen were all visualized in oligodendroglial cells at the border of an active PML lesion in the cerebral frontal lobe. These results revealed a positive reinforcement system in which the SMAD mediators of the TGF-beta system act cooperatively with Tat to stimulate JCV gene transcription.
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