BACKGROUND Neural stem cells (NSCs) residing in the central nervous system play an important role in neurogenesis. Several viruses can infect these neural progenitors and cause severe neurological diseases. The innate immune responses against the neurotropic viruses in these tissue-specific stem cells remain unclear. METHODS Human NSCs were transfected with viral RNA mimics or infected with neurotropic virus for detecting the expression of antiviral interferons (IFNs) and downstream IFN-stimulated antiviral genes. RESULTS NSCs are able to produce interferon-β (IFN-β) (type I) and λ1 (type III) after transfection with poly(I:C) and that downstream IFN-stimulated antiviral genes, such as ISG56 and MxA, and the viral RNA sensors RIG-I, MDA5, and TLR3, can be expressed in NSCs under poly(I:C) or IFN-β stimulation. In addition, our results show that the pattern recognition receptors RIG-I and MDA5, as well as the endosomal pathogen recognition receptor TLR3, but not TLR7 and TLR8, are involved in the activation of IFN-β transcription in NSCs. Furthermore, NSCs infected with the neurotropic viruses, Zika and Japanese encephalitis viruses, are able to induce RIG-I-mediated IFN-β expression. CONCLUSION Human NSCs have the ability to activate IFN signals against neurotropic viral pathogens.

中文翻译：

---

激活人类神经干细胞中的 I 型干扰素抗病毒反应。


背景技术存在于中枢神经系统中的神经干细胞(NSC)在神经发生中发挥重要作用。几种病毒可以感染这些神经祖细胞并引起严重的神经系统疾病。这些组织特异性干细胞中针对嗜神经病毒的先天免疫反应仍不清楚。方法用病毒RNA模拟物转染人NSC或用嗜神经病毒感染，以检测抗病毒干扰素（IFN）和下游IFN刺激的抗病毒基因的表达。结果 NSC 在转染 Poly(I:C) 后能够产生干扰素-β (IFN-β)（I 型）和 λ1（III 型）以及下游 IFN 刺激的抗病毒基因，如 ISG56 和 MxA，以及病毒 RNA 传感器 RIG-I、MDA5 和 TLR3 可在 Poly(I:C) 或 IFN-β 刺激下在 NSC 中表达。此外，我们的结果表明，模式识别受体 RIG-I 和 MDA5 以及内体病原体识别受体 TLR3（但不包括 TLR7 和 TLR8）参与 NSC 中 IFN-β 转录的激活。此外，感染神经病毒、寨卡病毒和日本脑炎病毒的 NSC 能够诱导 RIG-I 介导的 IFN-β 表达。结论 人类 NSC 能够激活针对嗜神经病毒病原体的 IFN 信号。