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 |