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RIG-I knockdown impedes neurogenesis in a murine model of Japanese encephalitis

机译:RIG-I组合式抑制日本脑炎的小鼠模型中的神经发生。

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摘要

Retinoic acid inducible gene I (RIG-I) is a well established pattern recognition receptor (PRR) in neurons infected with Japanese encephalitis virus (JEV) as reported previously from our laboratory. Japanese encephalitis (JE) virus infection in brain has been shown to decrease the proliferation of neural stem/progenitor cells (NSPCs) which has its implications in neurological sequelae in JE survivors. We have found that ablation of RIG-I both in vivo and in vitro models results in significant decrease in NSPC proliferation post JEV infection. We hypothesize that knockdown of RIG-I diminishes the expression of antiviral molecules resulting in an increase in viral replication, which in turn results in enhancement of the expression of cell cycle inhibitors, hence affecting the proliferation of NSPCs.
机译:根据我们实验室先前的报道,视黄酸诱导基因I(RIG-I)是感染日本脑炎病毒(JEV)的神经元中公认的模式识别受体(PRR)。日本脑炎(JE)病毒在大脑中的感染已显示会减少神经干/祖细胞(NSPC)的增殖,这对JE幸存者的神经后遗症具有影响。我们已经发现,在体内和体外模型中RIG-I的切除导致JEV感染后NSPC增殖的显着降低。我们假设敲除RIG-I会减少抗病毒分子的表达,从而导致病毒复制的增加,进而导致细胞周期抑制剂的表达增强,从而影响NSPC的增殖。

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