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当代肠道病毒 D68 分离株感染人类脊髓类器官。

Contemporary enterovirus-D68 isolates infect human spinal cord organoids.

机构信息

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

Department of Molecular Genetics and Microbiology, Duke University School of Medicine , Durham, North Carolina, USA.

出版信息

mBio. 2023 Aug 31;14(4):e0105823. doi: 10.1128/mbio.01058-23. Epub 2023 Aug 3.

Abstract

Enterovirus D68 (EV-D68) is a nonpolio enterovirus associated with severe respiratory illness and acute flaccid myelitis (AFM), a polio-like illness causing paralysis in children. AFM outbreaks have been associated with increased circulation and genetic diversity of EV-D68 since 2014, although the virus was discovered in the 1960s. The mechanisms by which EV-D68 targets the central nervous system are unknown. Since enteroviruses are human pathogens that do not routinely infect other animal species, establishment of a human model of the central nervous system is essential for understanding pathogenesis. Here, we describe two human spinal cord organoid (hSCO)-based models for EV-D68 infection derived from induced, pluripotent stem cell (iPSC) lines. One hSCO model consists primarily of spinal motor neurons, while the another model comprises multiple neuronal cell lineages, including motor neurons, interneurons, and glial cells. These hSCOs can be productively infected with contemporary strains, but not a historic strain, of EV-D68 and produce extracellular virus for at least 2 weeks without appreciable cytopathic effect. By comparison, infection with hSCO with another enterovirus, echovirus 11, causes significant structural destruction and apoptosis. Together, these findings suggest that EV-D68 infection is not the sole mediator of neuronal cell death in the spinal cord in those with AFM and that secondary injury from the immune response likely contributes to pathogenesis. IMPORTANCE AFM is a rare condition that causes significant morbidity in affected children, often contributing to life-long sequelae. It is unknown how EV-D68 causes paralysis in children, and effective therapeutic and preventative strategies are not available. Mice are not native hosts for EV-D68, and thus, existing mouse models use immunosuppressed or neonatal mice, mouse-adapted viruses, or intracranial inoculations. To complement existing models, we report two hSCO models for EV-D68 infection. These three-dimensional, multicellular models comprised human cells and include multiple neural lineages, including motor neurons, interneurons, and glial cells. These new hSCO models for EV-D68 infection will contribute to understanding how EV-D68 damages the human spinal cord, which could lead to new therapeutic and prophylactic strategies for this virus.

摘要

肠道病毒 D68(EV-D68)是一种与严重呼吸道疾病和急性弛缓性脊髓炎(AFM)相关的非脊髓灰质炎肠道病毒,这是一种类似小儿麻痹症的疾病,会导致儿童瘫痪。自 2014 年以来,随着 EV-D68 的循环和遗传多样性增加,已经出现了 AFM 疫情,尽管该病毒早在 20 世纪 60 年代就被发现。EV-D68 针对中枢神经系统的机制尚不清楚。由于肠道病毒是不会常规感染其他动物物种的人类病原体,因此建立中枢神经系统的人类模型对于理解发病机制至关重要。在这里,我们描述了两种源自诱导多能干细胞(iPSC)系的基于人脊髓神经球(hSCO)的 EV-D68 感染模型。一种 hSCO 模型主要由脊髓运动神经元组成,而另一种模型则包含多种神经元细胞谱系,包括运动神经元、中间神经元和神经胶质细胞。这些 hSCO 可以被当代的 EV-D68 株有效感染,但不能被历史株感染,并且在没有明显细胞病变效应的情况下至少 2 周产生细胞外病毒。相比之下,用另一种肠道病毒柯萨奇病毒 11 感染 hSCO 会导致明显的结构破坏和细胞凋亡。总的来说,这些发现表明,在患有 AFM 的患者中,EV-D68 感染并不是脊髓神经元死亡的唯一介导因素,免疫反应的二次损伤可能导致发病机制。

重要性 AFM 是一种罕见的疾病,会导致受影响的儿童出现严重的发病率,通常会导致终身后遗症。目前尚不清楚 EV-D68 如何导致儿童瘫痪,也没有有效的治疗和预防策略。小鼠不是 EV-D68 的天然宿主,因此现有的小鼠模型使用免疫抑制或新生小鼠、小鼠适应病毒或颅内接种。为了补充现有模型,我们报告了两种用于 EV-D68 感染的 hSCO 模型。这些三维、多细胞模型由人类细胞组成,包括多种神经谱系,包括运动神经元、中间神经元和神经胶质细胞。这些用于 EV-D68 感染的新型 hSCO 模型将有助于了解 EV-D68 如何损害人类脊髓,这可能为该病毒带来新的治疗和预防策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0010/10470749/6abe671b929e/mbio.01058-23.f001.jpg

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