Abstract：
Enterovirus D68 (EV-D68) is one of hundreds of non-polio enteroviruses that typically cause cold-like respiratory illness. The first EV-D68 outbreak in the United States in 2014 aroused widespread concern among the public and health authorities. The infection was found to be associated with increased surveillance of acute flaccid myelitis, a neurological condition that causes limb paralysis in conjunction with spinal cord inflammation. In vitro studies utilising two-dimensional (2D) and three-dimensional (3D) culture systems have been employed to elucidate the pathogenic mechanism of EV-D68. Various animal models have also been developed to investigate viral tropism and distribution, pathogenesis, and immune responses during EV-D68 infection. EV-D68 infections have primarily been investigated in respiratory, intestinal and neural cell lines/tissues, as well as in small-size immunocompetent rodent models that were limited to a young age. Some studies have implemented strategies to overcome the barriers by using immunodeficient mice or virus adaptation. Although the existing models may not fully recapitulate both respiratory and neurological disease observed in human EV-D68 infection, they have been valuable for studying pathogenesis and evaluating potential vaccine or therapeutic candidates. In this review, we summarise the methodologies and findings from each experimental model and discuss their applications and limitations.
摘要：
肠道病毒D68(EV-D68)是通常引起感冒样呼吸道疾病的数百种非脊髓灰质炎肠道病毒之一。2014年首次在美国爆发的EV-D68引起了公众和卫生当局的广泛关注。发现感染与急性弛缓性脊髓炎的监测增加有关，导致肢体瘫痪和脊髓发炎的神经系统疾病。利用二维（2D）和三维（3D）培养系统的体外研究已用于阐明EV-D68的致病机制。还开发了各种动物模型来研究病毒的嗜性和分布，发病机制，和EV-D68感染期间的免疫反应。EV-D68感染主要在呼吸道进行了调查，肠和神经细胞系/组织，以及仅限于年轻年龄的小型免疫能力啮齿动物模型。一些研究已经实施了通过使用免疫缺陷小鼠或病毒适应来克服障碍的策略。尽管现有模型可能无法完全概括在人类EV-D68感染中观察到的呼吸道和神经系统疾病，它们对于研究发病机制和评估潜在的疫苗或治疗候选物很有价值.在这次审查中,我们总结了每个实验模型的方法和发现，并讨论了它们的应用和局限性。
