将泰勒氏小鼠脑脊髓炎病毒DA株VP1的环II替换为GDVII株的环II，会改变神经毒力、病毒持续性和脱髓鞘。
Replacement of loop II of VP1 of the DA strain with loop II of the GDVII strain of Theiler's murine encephalomyelitis virus alters neurovirulence, viral persistence, and demyelination.
作者信息
Wada Y, McCright I J, Whitby F G, Tsunoda I, Fujinami R S
机构信息
Department of Neurology and Pathology, University of Utah, Salt Lake City, Utah 84132, USA.
出版信息
J Virol. 1998 Sep;72(9):7557-62. doi: 10.1128/JVI.72.9.7557-7562.1998.
Abstract
Theiler's murine encephalomyelitis viruses, which are murine picornaviruses, can cause central nervous system inflammatory disease. To study the role of loop II in capsid protein VP1, two mutant viruses of strain DA in which DA loop II amino acids were replaced with strain GDVII amino acids were constructed. Infection of mice with the two mutant viruses led to dramatically different patterns of disease.
摘要
泰勒氏鼠脑脊髓炎病毒属于鼠微小核糖核酸病毒，可引发中枢神经系统炎性疾病。为研究衣壳蛋白VP1中loop II的作用，构建了两株DA毒株的突变病毒，其中DA毒株的loop II氨基酸被GDVII毒株的氨基酸所取代。用这两种突变病毒感染小鼠，会导致截然不同的疾病模式。
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