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肠道病毒71型(EV71))已被证明是引起近年来亚洲-太平洋地区频发的手足口病重症并导致患者死亡的最主要病原体.但是,其是如何感染神经系统并导致严重神经系统病理损伤的分子机制尚不明确.在前期针对EV71感染星状胶质细胞的研究工作基础上,本研究利用针对恒河猴细胞内磷酸化/去磷酸化系统的共212个磷酸酶基因的siRNA库,分别下调了分离自恒河猴大脑并经纯化培养的星状胶质细胞内相应的磷酸酶的表达,并在此背景条件下比较了EV71在该细胞中的增殖特征,并对若干可以通过其表达水平及其活性的变化而直接影响EV71增殖的磷酸酶做了进一步分析.结果表明,恒河猴星状胶质细胞中若干与调控信号通路相关的酪氨酸磷酸酶和丝/苏氨酸磷酸酶对EV71的增殖具有调控作用,而病毒亦可能通过与这些磷酸酶的相互作用对所感染的星状胶质细胞的免疫反应性产生相应的影响.
Enterovirus 71 (EV71)) has been shown to be the most important causative agent causing severe HFMD and death in Asia-Pacific in recent years, but how it infects the nervous system and causes severe neurological pathologies The molecular mechanism of injury is still unclear.On the basis of previous studies on EV71 infection of astrocytes, we used a siRNA library of 212 phosphatase genes targeting rhesus monkey phosphorylation / dephosphorylation system , Respectively, down-regulated rhesus monkey brain and purified culture of astrocytes in the corresponding phosphatase expression, and in this context compared EV71 proliferation characteristics in the cells, and several can pass Its expression level and activity changes directly affect the EV71 proliferation of phosphatase for further analysis.The results show that a number of rhesus monkey astrocytes and regulatory signal transduction pathway tyrosine phosphatase and silk / Acid phosphatases have a regulatory effect on the proliferation of EV71, and the virus may also produce a corresponding immunoreactivity to infected astrocytes through their interaction with these phosphatases influences.