The pathogenesis of murine coronavirus infection of the central nervous system.

The pathogenesis of murine coronavirus infection of the central nervous system.
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DOI:
10.1615/critrevimmunol.v30.i2.20
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发表时间:
2010
影响因子:
1.3
通讯作者:
Hosking MP
Hosking MP
中科院分区:
医学4区
文献类型:
--
作者:
Lane TE;Hosking MP

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小鼠肝炎病毒(MHV)是一种正链RNA病毒,可引起急性脑脊髓炎,后来演变为慢性暴发性脱髓鞘疾病。在急性感染期间,细胞因子的产生、趋化因子的分泌和免疫细胞向中枢神经系统的浸润是控制病毒复制的关键。尽管有强大的抗病毒T淋巴细胞活性,无菌免疫不能实现,MHV长期存在于少突胶质细胞内。免疫系统的持续浸润和激活,是少突胶质细胞内病毒抗原和RNA滞留的结果,直接导致免疫介导的脱髓鞘的发展,在临床和组织学上与人类脱髓鞘疾病多发性硬化症有显著的相似之处。MHV为研究急性病毒感染时的宿主防御和慢性感染时免疫介导的脱髓鞘提供了一个独特的模型系统。
Mouse hepatitis virus (MHV) is a positive strand RNA virus that causes an acute encephalomyelitis which later resolves into a chronic fulminating demyelinating disease. Cytokine production, chemokine secretion, and immune cell infiltration into the central nervous system are critical to control viral replication during acute infection. Despite potent anti – viral T lymphocyte activity, sterile immunity is not achieved, and MHV chronically persists within oligodendrocytes. Continued infiltration and activation of the immune system, a result of the lingering viral antigen and RNA within oligodendrocytes, lead directly to the development of an immune – mediated demyelination that bears remarkable similarities, both clinically and histologically, to the human demyelinating disease multiple sclerosis. MHV offers a unique model system for studying host defense during acute viral infection and immune – mediated demyelination during chronic infection.
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