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诱导神经退行性变，我们对表达suid herpesvirus 1的即时早期蛋白IE180的转基因小鼠进行了检测。通过选择性自噬途径降解的P62蛋白和异常溶酶体聚集在IE180转基因小鼠的神经元细胞中。IE180的表达也诱导了p62在体外的积累。将IE180转基因小鼠与GFP-LC3转基因小鼠杂交，产生双转基因小鼠，表达融合自噬标记LC3的绿色荧光蛋白，并进行检测。IE180似乎短暂地诱导了细胞自噬的激活，但随后阻止了正常的自噬，导致细胞变性

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