Regulation of autophagy by herpesvirus protein : the involvement in neurodegenerative disorder

为了验证疱疹病毒蛋白通过抑制细胞自噬而诱导神经变性，对表达猪疱疹病毒1型即刻早期蛋白IE180的转基因小鼠进行了检测。IE180转基因小鼠神经细胞中可见选择性自噬途径降解的p62蛋白和异常溶酶体聚集。IE180的表达也可在体外诱导p62的蓄积。将IE180转基因小鼠与GFP-LC3转基因小鼠杂交，获得融合了自噬标记Lc3的绿色荧光蛋白的双转基因小鼠并进行检测。IE180似乎短暂地诱导了自噬的激活，但随后阻止了正常的自噬并导致细胞退化

To verify that protein of herpes virus induce neurodegeneration via inhibition of cellular autophagy, the transgenic mice expressing IE180, immediate early protein of suid herpesvirus 1, were examined. P62 protein, which were degraded via selectively autophagic pathyway, and abnormal lysosome were aggregated in neuronal cells of IE180 transgenic mice. Expression of IE180 also induced accumulation of p62 in vitro. Double transgenic mice crossed IE180 transgenic mice with GFP-LC3 transgenic mice, expressing the green fluorescent protein fused to the autophagic marker LC3, were generated and examined. It seemed that IE180 transiently induced activation of autophagy, but then prevent normal autophagy and result in cell degeneration