| Virus Name | JC Virus |
| Virus Short Name | JC |
| Order | Unassigned |
| Virus Family | Polyomaviridae |
| Virus Subfamily | N.A. |
| Genus | Polyomavirus |
| Species | JC polyomavirus |
| Host | Mammals, human |
| Cell Tropism | Respiratory system, kidneys, or brain |
| Associated Disease | Progressive multifocal leukoencephalopathy |
| Mode of Transmission | N.A. |
| VIPR DB link | N.A. |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/129/polyomaviridae |
| Virus Host DB link | N.A. |
| Paper Title | Role for tumor necrosis factor-alpha in JC virus reactivation and progressive multifocal leukoencephalopathy |
| Author's Name | Hassen S. Wollebo, Mahmut Safak, Luis Del Valle, Kamel Khalili and Martyn K. White |
| Journal Name | Journal Of Neuroimmunology |
| Pubmed ID | 21185609 |
| Abstract | JCV causes the CNS demyelinating disease progressive multifocal leukoencephalopathy (PML). After primary infection, JCV persists in a latent state, where viral protein expression and replication are not detectable. NF-κB and C/EBPbeta regulate the JCV promoter via a control element, κB, suggesting proinflammatory cytokines may reactivate JCV to cause PML, e.g., in HIV-1/AIDS. Since HIV-1 induces cytokines in brain, including TNF-alpha, we examined a role for TNF-alpha in JCV regulation. TNF-alpha stimulated both early and late JCV transcription. Further, the κB element conferred TNF-alpha response to a heterologous promoter. Immunohistochemistry of HIV+/PML revealed robust labeling for TNF-alpha and TNFR-1. These data suggest TNF-alpha stimulation of κB may contribute to JCV reactivation in HIV+/PML. |
| Used Model | TC620 cells |
| DOI | 10.1016/j.jneuroim.2010.11.013 |