Jakob J, Roos R P
Department of Neurology/MC2030, University of Chicago Medical Center, Illinois 60637, USA.
J Neurovirol. 1996 Apr;2(2):70-7. doi: 10.3109/13550289609146540.
Theiler's murine encephalomyelitis virus (TMEV) strains are divided into two subgroups on the basis of their differing disease phenotypes. Members of the GDVII subgroup, such as GDVII strain, produce an acute lethal polioencephalomyelitis. In contrast, members of the TO subgroup, such as DA strain, induce a persistent infection with chronic demyelination; this white matter disease serves as an experimental model of multiple sclerosis (MS) due to their similar pathology and because the immune system in both diseases appears to contribute to the demyelination. The availability of full-length infectious TMEV clones, the relative simplicity of the TMEV genome, and the availability of the mouse as a host provide the opportunity to identify molecular determinants and disease mechanisms that are responsible for neurovirulence, demyelination and virus persistence, and makes this a valuable system for pathogenesis studies.
泰勒氏鼠脑脊髓炎病毒（TMEV）毒株根据其不同的疾病表型分为两个亚组。GDVII亚组的成员，如GDVII毒株，会引发急性致死性脑脊髓灰质炎。相比之下，TO亚组的成员，如DA毒株，会引发伴有慢性脱髓鞘的持续性感染；这种白质疾病因其相似的病理学特征以及两种疾病的免疫系统似乎都对脱髓鞘有影响，而成为多发性硬化症（MS）的实验模型。全长感染性TMEV克隆的可得性、TMEV基因组相对简单以及小鼠作为宿主的可得性，为确定导致神经毒力、脱髓鞘和病毒持续性的分子决定因素和疾病机制提供了机会，使其成为发病机制研究的一个有价值的系统。
