期刊
VIRUS RESEARCH
卷 111, 期 1, 页码 55-60出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.virusres.2005.03.010
关键词
neurovirulence; pathogenesis; rabies; virulence
类别
Recent reports have suggested that rabies virus phosphoprotein (P) interaction with dynein minus-end-directed microtubule motor proteins may be of fundamental importance in the axonal transport of rabies virus. A deletion of I I amino acids was introduced into recombinant rabies virus SAD-L 16 (L 16) that modified the dynein light chain (LC8) binding site of the rabies virus P, producing mutant L-AP11. This mutant is a useful tool for determining the role of P-LC8 interaction in viral spread and pathogenesis. Seven-day-old ICR mice were inoculated into a hindlimb thigh muscle with L16 or L-Delta P11. Histopathological and immunohistochemical analyses of their brains were performed at serial time points in order to determine the pattern of viral spread. L 16 spread to the brain and caused a severe encephalitis with apoptotic neuronal changes. L-AP11 infected specific brain areas (brainstem and hippocampus) 1-2 days later than L16 and involved a smaller number of neurons in some brain regions. However, the neuronal apoptotic changes produced by both viruses were similar in most brain regions. Following peripheral inoculation, deletions modifying the LC8 binding site had an effect on delaying viral spread, but did not significantly alter the pattern of rabies virus encephalitis. The precise role of the rabies virus P-dynein interaction in the axonal transport of rabies virus, particularly the importance of this interaction during natural infection, merits further study. (c) 2005 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据