Pathogenesis of murine coronavirus in the central nervous system.
Pathogenesis of murine coronavirus in the central nervous system.
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DOI：
10.1007/s11481-010-9202-2
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发表时间：
2010-09
影响因子：
6.2
通讯作者：
Weiss, Susan R.
中科院分区：
文献类型：
--
作者：
Bender, Susan J.;Weiss, Susan R.
小鼠冠状病毒（小鼠肝炎病毒，MHV）是一种在小鼠的几个器官系统中诱导疾病的毒株的集合。嗜神经性菌株JHM和A59的感染引起急性脑炎，并且在存活者中引起慢性脱髓鞘，后者用作多发性硬化症的动物模型。MHV受体是一种癌胚抗原相关的细胞粘附分子，CEACAM1a;矛盾的是，CEACAM1a在中枢神经系统（CNS）中表达不足，导致推测其他受体。高神经毒力JHM分离株与毒性较小的变种和弱神经毒力A59株的比较，结合使用反向遗传学，允许映射到单个病毒基因的致病特性。刺突蛋白负责病毒进入，是嗜性和毒力的主要决定因素。其他病毒蛋白质，包括结构性和非结构性蛋白质，也有助于CNS中的发病机制。宿主对MHV反应的研究表明，先天性和适应性反应对于抗病毒防御至关重要。I型干扰素对预防感染后的早期死亡至关重要。在CD4 T细胞的帮助下，CD8 T细胞对于急性疾病期间的病毒清除至关重要，并且在慢性疾病期间持续存在于CNS中。B细胞是防止急性感染清除后病毒在CNS中再活化所必需的。尽管对冠状病毒发病机制的理解取得了进展，但关于病毒进入和在表达低水平受体的细胞类型中传播的机制，以及急性和慢性疾病期间病毒与宿主免疫系统之间的独特相互作用，仍然存在问题。
Murine coronavirus (mouse hepatitis virus, MHV) is a collection of strains that induce disease in several organ systems of mice. Infection with neurotropic strains JHM and A59 causes acute encephalitis, and in survivors, chronic demyelination, the latter of which serves as an animal model for multiple sclerosis. The MHV receptor is a carcinoembryonic antigen-related cell adhesion molecule, CEACAM1a; paradoxically, CEACAM1a is poorly expressed in the central nervous system (CNS), leading to speculation of an additional receptor. Comparison of highly neurovirulent JHM isolates with less virulent variants and the weakly neurovirulent A59 strain, combined with the use of reverse genetics, has allowed mapping of pathogenic properties to individual viral genes. The spike protein, responsible for viral entry, is a major determinant of tropism and virulence. Other viral proteins, both structural and nonstructural, also contribute to pathogenesis in the CNS. Studies of host responses to MHV indicate that both innate and adaptive responses are crucial to antiviral defense. Type I interferon is essential to prevent very early mortality after infection. CD8 T cells, with the help of CD4 T cells, are crucial for viral clearance during acute disease and persist in the CNS during chronic disease. B cells are necessary to prevent reactivation of virus in the CNS following clearance of acute infection. Despite advances in understanding of coronavirus pathogenesis, questions remain regarding the mechanisms of viral entry and spread in cell types expressing low levels of receptor, as well as the unique interplay between virus and the host immune system during acute and chronic disease.
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DOI：
10.1084/jem.90.3.195
发表时间：
1949-08-31
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bailey OT;Pappenheimer AM;Cheever FS;Daniels JB
通讯作者：
Daniels JB
影响因子：
5.4
作者：
Butler, Noah S.;Dandekar, Ajai A.;Perlman, Stanley
通讯作者：
Perlman, Stanley
影响因子：
11.8
作者：
Chiu, SS;Chan, KH;Peiris, JSM
通讯作者：
Peiris, JSM
影响因子：
5.4
作者：
Das Sarma, J;Fu, L;Lavi, E
通讯作者：
Lavi, E
影响因子：
5.3
作者：
Changolkar, Lakshmi N.;Singh, Geetika;Pehrson, John R.
通讯作者：
Pehrson, John R.