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董兆鹏, 王倩, 张振杰, Michael J. Carr, 李栋, 史卫峰. 2018: 柯萨奇病毒B4诱导急性心肌炎和大脑皮层神经元水肿小鼠模型的建立. 动物学研究, 39(1): 52-57. DOI: 10.24272/j.issn.2095-8137.2017.056
引用本文: 董兆鹏, 王倩, 张振杰, Michael J. Carr, 李栋, 史卫峰. 2018: 柯萨奇病毒B4诱导急性心肌炎和大脑皮层神经元水肿小鼠模型的建立. 动物学研究, 39(1): 52-57. DOI: 10.24272/j.issn.2095-8137.2017.056
Zhao-Peng Dong, Qian Wang, Zhen-Jie Zhang, Michael J. Carr, Dong Li, Wei-Feng Shi. 2018: Murine model of acute myocarditis and cerebral cortical neuron edema induced by coxsackievirus B4. Zoological Research, 39(1): 52-57. DOI: 10.24272/j.issn.2095-8137.2017.056
Citation: Zhao-Peng Dong, Qian Wang, Zhen-Jie Zhang, Michael J. Carr, Dong Li, Wei-Feng Shi. 2018: Murine model of acute myocarditis and cerebral cortical neuron edema induced by coxsackievirus B4. Zoological Research, 39(1): 52-57. DOI: 10.24272/j.issn.2095-8137.2017.056

柯萨奇病毒B4诱导急性心肌炎和大脑皮层神经元水肿小鼠模型的建立

Murine model of acute myocarditis and cerebral cortical neuron edema induced by coxsackievirus B4

  • 摘要: 柯萨奇病毒B4(CV-B4)感染在全球各地均有报道,大量研究表明胰腺炎和1型糖尿病的发生与CV-B4感染密切相关。另外,有报道显示心肌炎及重症中枢神经系统感染并发症也与CV-B4感染有关,但其发病机制尚不清楚。在本研究中,我们建立了CV-B4感染ICR小鼠模型并检测了CV-B4感染是否具有致急性心肌炎以及中枢神经系统感染倾向。结果表明,感染过程中CV-B4感染组和阴性对照组小鼠全部存活且均未观察到明显的临床症状。然而,在CV-B4感染小鼠的心肌和脑组织分别观察到了明显的急性心肌炎和大脑皮层神经元水肿的病理改变;而且感染2天后在小鼠脑和心肌组织中检测到了较高的CV-B4病毒载量。此外,与阴性对照组相比CV-B4感染组小鼠血清中IFN-γ和IL-6表达水平显著升高,这提示IFN-γ和IL-6可能在CV-B4感染导致的病理损伤过程中发挥一定作用。本研究所建立的CV-B4感染模型成功复制了由CV-B4诱导的急性心肌炎和大脑皮层神经元水肿,这对于CV-B4疫苗筛选及抗病毒药物效果评估具有一定的意义。

     

    Abstract: Globally, coxsackievirus B4 (CV-B4) has been continuously isolated and evidence suggests an association with the development of pancreatitis and type I diabetes. In addition, CV-B4 is also associated with myocarditis and severe central nervous system (CNS) complications, which remain poorly studied and understood. In the present study, we established an ICR mouse model of CV-B4 infection and examined whether CV-B4 infection resulted in a predisposition to myocarditis and CNS infection. We found high survival in both the treatment and control group, with no significant differences in clinical outcomes observed. However, pathological lesions were evident in both brain and heart tissue of the CV-B4-infected mice. In addition, high viral loads were found in the neural and cardiac tissues as early as 2 d postinfection. Expressions of IFN-γ and IL-6 in sera were significantly higher in CV-B4-infected mice compared to uninfected negative controls, suggesting the involvement of these cytokines in the development of histopathological lesions. Our murine model successfully reproduced the acute myocarditis and cerebral cortical neuron edema induced by CV-B4, and may be useful for the evaluation of vaccine candidates and potential antivirals against CV-B4 infection.

     

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