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当代肠道病毒-D68分离物感染人类脊髓器官

Gabrielle Aguglia¹, Carolyn B Coyne², Terence S Dermody^1,3,4

¹Department of Pediatrics, Division of Infectious Diseases, University of Pittsburgh School of Medicine , Pittsburgh, Pennsylvania, USA.

|August 3, 2023

概括

肠道病毒D68 (EV-D68) 导致儿童,但其机制尚不清楚. 新的人类脊髓器官模型显示,EV-D68感染神经元而不会立即导致细胞死亡,这表明免疫反应有助于.

科学领域:

神经科学是一个神经科学.
病毒学病毒学
干细胞生物学干细胞生物学

背景情况:

肠道病毒D68 (EV-D68) 与严重的呼吸系统疾病和急性软骨髓炎 (AFM) 相关,这是儿童的麻状况.
精确的EV-D68神经侵入和发病机制在很大程度上是未知的.
现有的动物模型由于EV-D68对人类宿主的特异性而存在局限性.

研究的目的:

开发和描述基于人类的模型,用于研究中枢神经系统的EV-D68感染.
研究EV-D68对人类脊髓神经元和相关细胞类型的直接影响.
阐明可能导致AFM的机制.

主要方法:

从诱导多能干细胞 (iPSC) 产生两个不同的人类脊髓有机体 (hSCO) 模型.
感染hSCOs与当代和历史株的EV-D68和埃科病毒11.
在感染的有机体中评估病毒复制,细胞病变效应和细胞亡.

主要成果:

hSCO模型被当代的EV-D68菌株感染,产生了超过两周的传染性病毒.
在hSCOs中,EV-D68感染没有引起显著的直接细胞病变效应或亡.
相比之下,埃科病毒11感染导致hSCOs实质性结构损伤和细胞死亡.

结论:

单独的EV-D68感染可能不足以导致AFM中的神经元死亡.
二次损伤机制,可能涉及免疫反应,可能在EV-D68诱导的发病过程中发挥关键作用.
人类脊髓器官模型为研究EV-D68神经病变发生和开发治疗策略提供了宝贵的平台.

关键词:

急性松性脑膜炎 (AFM) 是一种疾病.肠道病毒病毒.肠道病毒D68 (EV-D68) 是一种病毒.人类模型系统系统诱导多能干细胞的诱导干细胞.有机生物有机物脊髓中的有机体

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