Prosniak M, Hooper D C, Dietzschold B, Koprowski H
Center for Neurovirology, Department of Microbiology and Immunology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107-6799, USA.
Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2758-63. doi: 10.1073/pnas.051630298.
A variety of molecular genetic approaches were used to study the effect of rabies virus (RV) infection on host gene expression in mouse brain. The down-regulation of gene expression was found to be a major effect of RV infection by using subtraction hybridization. However, a combination of techniques identified approximately 39 genes activated by infection. These included genes involved in regulation of cell metabolism, protein synthesis, synaptic activity, and cell growth and differentiation. Northern blot analysis to monitor temporal activation of several of these genes following infection revealed essentially two patterns of activation: (i) an early response with up-regulation beginning within 3 days after infection and correlating with transcription of RV nuclear protein; and (ii) a late response with enhanced expression occurring at days 6-7 after infection and associated with peak RV replication. The gene activation patterns and the known functions of their products suggest that a number of host genes may be involved in the replication and spread of RV in the brain.
采用多种分子遗传学方法研究狂犬病病毒（RV）感染对小鼠脑内宿主基因表达的影响。通过消减杂交发现基因表达下调是RV感染的主要效应。然而，综合多种技术鉴定出约39个被感染激活的基因。这些基因包括参与细胞代谢调控、蛋白质合成、突触活动以及细胞生长和分化的基因。通过Northern印迹分析监测感染后其中几个基因的时间激活情况，发现基本上有两种激活模式：（i）早期反应，感染后3天内开始上调并与RV核蛋白转录相关；（ii）晚期反应，感染后6 - 7天表达增强并与RV复制高峰相关。基因激活模式及其产物的已知功能表明，许多宿主基因可能参与RV在脑内的复制和传播。
