Deletion of glycoprotein gE reduces the propagation of pseudorabies virus in the nervous system of mice after intranasal inoculation
Deletion of glycoprotein gE reduces the propagation of pseudorabies virus in the nervous system of mice after intranasal inoculation
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DOI：
10.1006/viro.1996.0247
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发表时间：
1996-05-01
期刊：
影响因子：
3.7
通讯作者：
Flamand, A
中科院分区：
文献类型：
--
作者：
Babic, N;Klupp, B;Flamand, A
用非必需糖蛋白E(GE)缺失、表达LacZ基因的伪狂犬病病毒(PRV)突变体(GE(-)β-Gal(+)PRV)及其挽救的病毒经鼻接种小鼠。Ge(-)β-Gal(+)PRV的半数致死剂量与亲本Kaplan株相似，但小鼠存活时间更长，没有出现伪狂犬病症状。在鼻黏膜中，GE(-)β-Gal(+)PRV的复制效率低于挽救的病毒。Ge(-)β-Gal(+)PRV可感染支配鼻黏膜的三叉神经细胞和交感神经元。然而，在三叉神经通路中没有发生跨神经元向二级细胞群的转移，而在交感神经通路中则严重减少。突变体也不能在副交感神经系统中繁殖。相反，GE拯救的病毒与野生型PRV一样，通过三叉神经、交感神经和副交感神经途径传播。这些发现提供了进一步的证据，即GE的缺失比病毒在一级神经元中的穿透和增殖更具特异性地影响PRV的跨神经元转移。(C)1996年学术出版社。
A pseudorabies virus (PrV) mutant, deficient in the nonessential glycoprotein E (gE) and expressing the LacZ gene (gE(-) beta gal(+) PrV), and its rescued virus were inoculated intranasally in mice. The median lethal dose of gE(-) beta gal(+) PrV was similar to that of the parental Kaplan strain, but mice survived longer and did not develop symptoms of pseudorabies. In the nasal mucosa, gE(-) beta gal(+) PrV replicated less efficiently than rescued virus. gE(-) beta gal(+) PrV could infect first-order trigeminal and sympathetic neurons innervating the nasal mucosa. However, transneuronal transfer to second-order cells groups did not occur in trigeminal pathways and was severely reduced in sympathetic pathways. The mutant was also unable to propagate in the parasympathetic system. In contrast, gE-rescued virus was transferred transneuronally in trigeminal, sympathetic, and parasympathetic pathways, like wild-type PrV. These findings provide further evidence that deletion of gE specifically affects transneuronal transfer of PrV more than penetration and multiplication of the virus in first-order neurons. (C) 1996 Academic Press, Inc.