单纯疱疹病毒胸苷激酶缺陷型突变体在小鼠中的致病性。
The pathogenicity of thymidine kinase-deficient mutants of herpes simplex virus in mice.
作者信息
Field H J, Wildy P
出版信息
J Hyg (Lond). 1978 Oct;81(2):267-77. doi: 10.1017/s0022172400025109.
Abstract
The pathogenicity for mice of two mutants of herpes simplex virus (type 1 and type 2), which fail to induce thymidine kinase, were compared with their respective parent strains. The mutants were much less virulent than the parents following either intracerebral or peripheral inoculation. The replication of the virus at the site of inoculation and its progression into the nervous system were studied. Following a very large inoculum in the ear, the type 1 mutant was found to establish a latent infection in the cervical dorsal root ganglia. Mice inoculated intracerebrally with small doses of the mutant viruses were solidly immune to challenge with lethal doses of the parent strain.
摘要
对两种单纯疱疹病毒（1型和2型）突变体（它们不能诱导胸苷激酶）对小鼠的致病性与其各自的亲本菌株进行了比较。无论是脑内接种还是外周接种，突变体的毒性都比亲本小得多。研究了病毒在接种部位的复制及其向神经系统的进展。在耳部接种非常大量的病毒后，发现1型突变体在颈背根神经节中建立了潜伏感染。用小剂量突变病毒脑内接种的小鼠对致死剂量的亲本菌株攻击具有牢固的免疫力。
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