Sakudo Akikazu, Onodera Takashi, Ikuta Kazuyoshi
Department of Virology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Neurosci Lett. 2008 Jan 24;431(1):81-5. doi: 10.1016/j.neulet.2007.11.026. Epub 2007 Dec 4.
Our previous studies have shown that the persistent expression of Borna disease virus phosphoprotein (BDV P) in mice leads to behavioral abnormalities resembling those in BDV-infected animals. In this study, we investigated whether the neurobehavioral abnormalities genetically induced by BDV P influence experimental prion disease. The effect of the phosphoprotein on prion diseases was evaluated based on the incubation time and survival curve, as well as the abnormal isoform of prion protein (PrP(Sc)) levels in brains of BDV P Tg mice treated with proteinase K (PK) treatment and subjected to western blotting. Increased expression of the BDV P transgene had no effect on the PrP(Sc) level, incubation time, or survival curve. The abnormalities induced by BDV P are different from those induced by prion diseases, indicating that the signaling cascades induced by the phosphoprotein differ from those induced by prion diseases.
我们之前的研究表明，博尔纳病病毒磷蛋白（BDV P）在小鼠中的持续表达会导致行为异常，类似于感染BDV的动物。在本研究中，我们调查了由BDV P基因诱导的神经行为异常是否会影响实验性朊病毒病。基于潜伏期和生存曲线，以及经蛋白酶K（PK）处理并进行蛋白质印迹分析的BDV P转基因小鼠大脑中朊病毒蛋白（PrP(Sc)）异常异构体的水平，评估了磷蛋白对朊病毒病的影响。BDV P转基因表达的增加对PrP(Sc)水平、潜伏期或生存曲线没有影响。BDV P诱导的异常与朊病毒病诱导的异常不同，这表明磷蛋白诱导的信号级联与朊病毒病诱导的信号级联不同。
