Herpes simplex virus thymidine kinase expression in trigeminal ganglion infection: correlation of enzyme activity with ganglion virus titer and evidence of in vivo complementation.
Herpes simplex virus thymidine kinase expression in trigeminal ganglion infection: correlation of enzyme activity with ganglion virus titer and evidence of in vivo complementation.
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三叉神经节感染中单纯疱疹病毒胸苷激酶的表达：酶活性与神经节病毒滴度的相关性和体内互补的证据。
DOI：
10.1016/0042-6822(81)90638-3
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发表时间：
1981
期刊：
影响因子：
3.7
通讯作者：
M. E. Dunstan
中科院分区：
文献类型：
--
作者：
R. Tenser;S. Ressel;M. E. Dunstan
使用 1 型单纯疱疹病毒 (HSV-1) 的 3 种胸苷激酶阳性 (TK+) 毒株和 8 种 TK−HSV-1 突变体对小鼠实验性三叉神经节和角膜感染进行了研究。在细胞培养物中对病毒进行了广泛测试，以确定病毒复制或 TK 活性是否对温度敏感 (ts)。 TK-突变体与TK+病毒无异。通过阿拉伯糖胸腺嘧啶测试和胸苷磷酸化测量，很明显，一些 TK-突变体实际上是 TK 活性的中间体 (TK±)。在角膜接种单个病毒后，除了一个例外，观察到 TK−、TK± 和 TK+ 病毒在眼组织中复制（接种后 3 天，2.2 × 103–1.1 × 105 PFU/眼）。然而，TK−突变体很少从三叉神经节中分离出来（<2.5–<5.6 × 10−1PFU/mg），而TK+和较小程度的TK±病毒则经常分离（1.2 × 103–1.2 × 104PFU/mg和3.2 × 100–2.1 × 103PFU/mg）。通过角膜进行体内补充研究接种 TK−−TK− 和 TK−−TK− 病毒混合物。 TK+HSV 补充了 TK-病毒，因为从三叉神经节中分离出大量 TK-HSV（互补指数 >60–>1600）。此外，在接种某些TK−–TK−对后，观察到神经节中的互补（互补指数>2.4–>120）。这些研究支持以下假设：HSV-1 TK 表达对于感觉神经节（神经元）感染来说是必需的，这通过三种方式进行： (ii) 病毒TK活性水平与三叉神经节病毒滴度之间存在相关性； (iii) 当 TK+ 或 TK−HSV 补充时，TK−病毒在三叉神经节中复制。
Experimental trigeminal ganglion and corneal infection in mice was studied with three thymidine kinase-positive (TK+) strains of herpes simplex virus type 1 (HSV-1) and eight TK−HSV-1 mutants. Viruses were extensively tested in cell culture to determine whether any were temperature sensitive (ts) for virus replication or for TK activity. TK−mutants were no moretsthan were TK+viruses. By arabinosylthymine testing and measurement of thymidine phosphorylation, it was apparent that some TK−mutants were, in fact, intermediate for TK activity (TK±). After corneal inoculation of individual viruses it was observed with one exception that TK−, TK±, and TK+viruses replicated in ocular tissues (3 days postinoculation, 2.2 × 103–1.1 × 105PFU/eye). However, TK−mutants were rarely isolated from trigeminal ganglia (<2.5–<5.6 × 10−1PFU/mg), whereas TK+and to a lesser degree TK±viruses were frequently (1.2 × 103–1.2 × 104PFU/mg and 3.2 × 100–2.1 × 103PFU/mg).In vivocomplementation studies were performed by corneal inoculation of TK−−TK−and TK−−TK−virus mixtures. TK+HSV complemented TK−virus since significant amounts of TK−HSV were isolated from trigeminal ganglia (complementation indices were >60–>1600). In addition, after inoculation of certain TK−–TK−pairs, complementation in ganglia was observed (complementation indices were >2.4–>120). These studies support the hypothesis that HSV-1 TK expression is necessary for sensory ganglion (neuron) infection in three ways: HSV-1 TK mutants that replicated in ocular tissues and were nottsmutants did not replicatein vivoin trigeminal ganglia; (ii) there was a correlation between level of viral TK activity and trigeminal ganglion virus titer; and (iii) when complemented by TK+or TK−HSV, TK−virus replicated in trigeminal ganglia.