Role for tumor necrosis factor-α in JC virus reactivation and progressive multifocal leukoencephalopathy
Document Type
Article
Publication Date
12-24-2010
Publication Title
Journal of Neuroimmunology
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/EBPβ 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-α, we examined a role for TNF-α in JCV regulation. TNF-α stimulated both early and late JCV transcription. Further, the κB element conferred TNF-α response to a heterologous promoter. Immunohistochemistry of HIV+/PML revealed robust labeling for TNF-α and TNFR-1. These data suggest TNF-α stimulation of κB may contribute to JCV reactivation in HIV+/PML.
First Page
46
Last Page
53
PubMed ID
21185609
Volume
233
Issue
1-2
Recommended Citation
Wollebo, Hassen S.; Safak, Mahmut; Del Valle, Luis; Khalili, Kamel; and White, Martyn K., "Role for tumor necrosis factor-α in JC virus reactivation and progressive multifocal leukoencephalopathy" (2010). School of Medicine Faculty Publications. 2304.
https://digitalscholar.lsuhsc.edu/som_facpubs/2304