A comparative study of pseudorabies virus (PRV) strains with defects in thymidine kinase and glycoprotein genes
A comparative study of pseudorabies virus (PRV) strains with defects in thymidine kinase and glycoprotein genes
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DOI：
10.1053/jcpa.2000.0406
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发表时间：
2000-08-01
影响因子：
0.8
通讯作者：
Silini, R
中科院分区：
文献类型：
--
作者：
Ferrari, M;Mettenleiter, TC;Silini, R
在两个实验的过程中，检查了两个伪造病毒突变体的猪的毒力和神经性触及毒性（6c2tk菌株（ - ），胸苷激酶（TK）功能缺陷； - ）/ge（ - ），在TK和糖蛋白I和e）中存在缺陷以及野生型父菌株（86/27V）。在鼻内接种后的不同时间，通过包括病毒分离，聚合酶链反应测定和免疫组织化学的方法检查了扁桃体，肺和不同水平的三叉神经和嗅觉神经途径的样品。两种突变病毒的毒力降低，如中度的临床体征和病变所表明的，并且仅零星的病毒分离。此外，与野生型母菌株不同，突变病毒未通过皮质类固醇治疗从潜在状态重新激活。此外，与野生型菌株相比，突变菌株向中枢神经系统（嗅觉和三叉神经神经途径）的迁移减少了。因此，编码TK酶和GI/GE复合物的基因中的突变与毒力降低，外周靶组织的复制减少以及迁移到嗅觉和三叉神经途径有关。 （c）2000 Harcourt Publishers Ltd.
In the course of two experiments, an examination was made of the virulence and neuroinvasiveness for pigs of two pseudorabies virus mutants (strain 6C2TK(-), with a defect in thymidine kinase (TK) function; and strain 6C2TK(-), gI(-)/gE(-), with defects in TK and glycoproteins I and E) and of the wild-type parent strain (86/27V). At various times after intranasal inoculation, pigs were killed and samples of tonsil, lung and different levels of the trigeminal and olfactory nervous pathways were examined by methods that included viral isolation, polymerase chain reaction assay and immunohistochemistry. Both mutant viruses were of reduced virulence, as indicated by no more than moderate clinical signs and lesions, and only sporadic isolation of virus; moreover, unlike the wild-type parent strain, the mutant viruses were not reactivated from the latent state by corticosteroid treatment. In addition, migration of the mutant strains to the central nervous system (olfactory and trigeminal nervous pathways) was reduced as compared with that of the wild-type strain. Thus, mutations in the genes encoding the TK enzyme and the gI/gE complex were associated with reduced virulence, reduced replication in peripheral target tissues, and reduced migration to the olfactory and trigeminal pathways. (C) 2000 Harcourt Publishers Ltd.