肿瘤坏死因子-α在 JC 病毒激活和进行性多灶性白质脑病中的作用。
Role for tumor necrosis factor-α in JC virus reactivation and progressive multifocal leukoencephalopathy.
机构信息
Center for Neurovirology, Department of Neuroscience, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA 19140, USA.
出版信息
J Neuroimmunol. 2011 Apr;233(1-2):46-53. doi: 10.1016/j.jneuroim.2010.11.013. Epub 2010 Dec 24.
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.
摘要
JCV 会导致中枢神经系统脱髓鞘疾病进行性多灶性白质脑病（PML）。原发性感染后，JCV 处于潜伏状态，此时无法检测到病毒蛋白的表达和复制。NF-κB 和 C/EBPβ 通过一个控制元件 κB 调节 JCV 启动子，这表明促炎细胞因子可能会重新激活 JCV 导致 PML，例如在 HIV-1/AIDS 中。由于 HIV-1 会在大脑中诱导细胞因子，包括 TNF-α，我们研究了 TNF-α 在 JCV 调节中的作用。TNF-α 刺激了早期和晚期 JCV 转录。此外，κB 元件赋予了 TNF-α 对异源启动子的反应。HIV+/PML 的免疫组织化学显示 TNF-α 和 TNFR-1 的强烈标记。这些数据表明，TNF-α 对 κB 的刺激可能导致 HIV+/PML 中 JCV 的重新激活。
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