JC polyomavirus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248428 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human and animal viruses possess remarkable capabilities in hijacking host processes to facilitate viral infection. Viruses use various strategies to target antiviral response mechanisms while promoting cellular phenotypic states that benefit viral replication. Viruses that replicate and assemble in the nucleus, including human pathogenic DNA viruses, need to balance maximal use of the host DNA replication machinery while at the same time avoid damage to the nucleus before generating a large number of viruses that will support the spread of infection. We have identified a novel mechanism of virus interference with the cell nucleus that involves virus-mediated modulation of nuclear mechanical properties. One of the most widespread human viruses, the JC polyomavirus, interferes with nuclear architecture to form virus-occupied space and substantially reduces the rigidity of the infected human cell nucleus. The JC virus's impact on nuclear rigidity is mediated by the viral nonstructural protein, Agnoprotein (Agno). The Agno interference with nuclear mechanics is governed by structurally diverse mimics of host proteins that support chromatin interaction with the key chromatin regulator, heterochromatin protein 1 alpha (HP1α), and is critical for JC virus infection in vitro. The ability to control chromatin organization and thus nuclear mechanics reveals a previously unknown virus strategy of hijacking the mechanism controlling nuclear physical properties to maximize virus production within the nucleus.
2024-12-31 | GSE271609 | GEO
Project description:JC polyomavirus (JCPyV) established a persistent infection, but BK polyomavirus (BKPyV) killed the cells in 15 days. To identify the cellular factors responsible for controlling JCPyV infection and promoting viral persistence, we profiled the transcriptomes of JCPyV- and BKPyV-infected cells at several time points postinfection. We found that interferon-stimulated genes (ISGs) were only activated in the JCPyV and not in the BKPyV-infected cells.
2019-08-15 | GSE135833 | GEO
Project description:Distinct JC polyomavirus strains in patients with progressive multifocal leukoencephalopathy
| PRJEB15261 | ENA
Project description:JC polyomavirus (circular genome) contains two opposite coding regions separated by the regulator non-coding control region (NCCR). NCCR rearrangements and missense mutations in the viral capsid protein VP1 gene differentiate JCV prototype genomes recovered from PML lesions from archetype urine strains. To further investigate the emerging variability of JCV populations in PML, we deep sequenced JCV whole genome recovered from CNS and/or urine samples from HIV- and non HIV-infected PML patients, using single-molecule real-time sequencing (PacBio, Pacific Biosciences). Phylogenetic analysis showed that PML strains distributed among 6 of 7 known genotypes. Whole genome single molecule sequencing provides insight in the genesis of JCV neurotropic populations.
2022-01-12 | E-MTAB-11077 | biostudies-arrayexpress
Project description:Supra-epigenomic impact of the human JC polyomavirus
| PRJNA1132281 | ENA
Project description:JC polyomavirus (JCPyV) is the causative agent of progressive multifocal leukoencephalopathy (PML), a devastating demyelinating disease of the central nervous system that results in the widespread formation of lesions across the brain parenchyma. The virus is opportunistic and remains in a benign state in the kidneys and lymphoid organs of more than half of the global human adult population. However, in rare cases of severe or selective immune suppression, JCPyV can establish a lytic infection of glial cells in the brain. While PML has traditionally been characterized as a lytic infection of oligodendrocytes, more recent findings suggest an important role for astrocytes during the initial stages of disease. Because of the exceptional species and tissue specificity of the virus, appropriate models of JCPyV infection in the brain are lacking, thus hampering progress towards the development of novel antiviral strategies and biomarkers of disease activity. Here, using iPSC-derived astrocytes infected with JCPyV and analyzed by LC-MS/MS, we show that the virus strongly influences the cell biology, inducing an unique proteomic signature that sharply contrasts with mock-infected cells.
2023-08-28 | PXD044144 | Pride
Project description:JC polyomavirus (JCPyV) is the causative agent of progressive multifocal leukoencephalopathy (PML), a devastating demyelinating disease of the central nervous system that results in the widespread formation of lesions across the brain parenchyma. The virus is opportunistic and remains in a benign state in the kidneys and lymphoid organs of more than half of the global human adult population. However, in rare cases of severe or selective immune suppression, JCPyV can establish a lytic infection of glial cells in the brain. While PML has traditionally been characterized as a lytic infection of oligodendrocytes, more recent findings suggest an important role for astrocytes during the initial stages of disease. Because of the exceptional species and tissue specificity of the virus, appropriate models of JCPyV infection in the brain are lacking, thus hampering progress towards the development of novel antiviral strategies and biomarkers of disease activity. Towards the aim of biomarker development extracellular vesicles (EVs) were isolated from JCPyV-infected and mock-infected human iPSC-derived astrocytes and analyzed by LC-MS/MS. As a inflammatory control, EVs were also isolated from cytokine-stimulated iPSC-derived astrocytes. We demonstrate that the proteomic signature associated with EVs from JCPyV-infected astrocytes reflect what was observed on a cellular level for infected astrocytes while being strikingly different from that of EVs generated under inflammatory conditions.
2023-08-28 | PXD044784 | Pride
Project description:Identification of quasispecies in JC virus genome in patients with progressive multifocal leukoencephalopathy by deep sequencing
| PRJDB4940 | ENA
Project description:BackgroundPolyomavirus JC (JCV) causes the CNS demyelinating disease progressive multifocal leukoencephalopathy (PML), which occurs almost exclusively in people with immune deficiencies, such as HIV-1/AIDS patients. JCV infection is very common and usually occurs early in life. After primary infection, virus is controlled by the immune system but, rarely when immune function is impaired, it can re-emerge and multiply in the astrocytes and oligodendrocytes in the brain and cause PML. Thus a central question in PML pathogenesis is the nature of the molecular mechanisms maintaining JCV in a latent state and then allowing reactivation.MethodsSince transcription can be regulated by epigenetic mechanisms including DNA methylation and histone acetylation, we investigated their role in JCV regulation by employing inhibitors of epigenetic events.ResultsThe histone deacetylase inhibitors trichostatin A (TSA) and sodium butyrate powerfully stimulated JCV early and late transcription while the DNA methylation inhibitor 5-azacytidine had no effect. Analysis of JCV mutants showed that this effect was mediated by the KB element of the JCV control region, which binds transcription factors NF-κB p65, NFAT4 and C/EBPβ and mediates stimulation by TNF-α. Stimulation of transcription by p65 was additive with TSA as was cotransfection with transcriptional coactivators/acetyltransferase p300 whereas depletion of endogenous p65 by RNA interference inhibited the effect of TSA. EMSA with a KB oligonucleotide showed p65 expression, TNF-α stimulation or TSA treatment each caused a gel shift that was further shifted by antibody to p65.ConclusionsWe conclude that JCV is regulated epigenetically by protein acetylation events and that these involve the NF-κB p65 binding site in the JCV control region.
| S-EPMC3765676 | biostudies-literature