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如果it2限制了小鼠冠状病毒传播到脊髓白质及其相关的髓质病理

Madhav Sharma¹, Debanjana Chakravarty¹, Afaq Hussain¹

¹Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata , Mohanpur, West Bengal, India.

Journal of virology

|July 28, 2023

概括

干扰素诱导的蛋白质与四基重复2 (Ifit2) 限制神经向型冠状病毒的传播. 如果it2缺乏导致严重的脊髓脱髓化和持续的病毒载量,突出显示了ifit2在预防慢性神经疾病中的作用.

科学领域:

神经病毒学神经病毒学
免疫学免疫学免疫学
病理学病理学病理学

背景情况:

干扰素诱导的蛋白质与四基重复2 (Ifit2) 是干扰素刺激的基因,对于限制病毒感染至关重要.
在急性病毒性脑炎中Ifit2的作用已经确立,但它对神经向性病毒感染的慢性脱髓化阶段的影响仍然不太了解.
神经型小鼠β-冠状病毒RSA59引起急性脑炎和慢性脱髓化,作为研究病毒诱导的神经疾病的模型.

研究的目的:

研究Ifit2在急性和慢性阶段的RSA59感染的神经病理结果中的作用.
确定Ifit2缺乏对病毒传播,免疫细胞透和中枢神经系统中血脑屏障完整性的影响.
阐明Ifit2对控制病毒载量和预防慢性脱髓化有何作用.

主要方法:

在Ifit2缺乏和野生型小鼠中注射RSA59的内注射.
在感染后的急性 (5日) 和慢性 (30日) 阶段进行神经病理学评估.
分析病毒传播,微质激活 (CX3CR1),淋巴细胞透 (CD4+,CD8+T细胞),淋巴结激活 (IFNγ) 和血脑屏障 (BBB) 完整性 (Claudin-5,ZO-1).

主要成果:

如果it2缺乏导致RSA59在脊髓中广泛扩散,T细胞透受损,CD4+T细胞激活减少,淋巴结中的IFNγ表达减少.
虽然BBB完整性在Ifit2缺乏的小鼠中得到了更好的保护,但与野生型小鼠相比,它们在慢性阶段表现出严重的脱髓化和持久的病毒载荷.
在急性阶段,在Ifit2缺乏的小鼠中观察到急性微质激活受损和CX3CR1表达减少.

结论:

如果it2在限制神经变型冠状病毒传播和促进病毒控制所需的急性神经炎症方面发挥着关键作用.
如果it2缺乏会加剧病毒的传播,并导致严重的慢性脱髓化,这表明它有保护作用,防止长期的神经损伤.
这些发现凸显了Ifit2在对神经向病毒的宿主免疫力方面的重要性,以及它在预防多发性硬化症等疾病方面的潜在作用.

关键词:

如果it2如果it2如果it2 冠状病毒冠状病毒病毒脱化是脱化的一种.干扰素 - 玛干扰素微质细胞中的微质细胞

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