来自阿昔洛韦耐药单纯疱疹病毒突变体的极低水平胸苷激酶表达支持从潜伏感染的小鼠三叉神经节中重新激活。
Expression of extremely low levels of thymidine kinase from an acyclovir-resistant herpes simplex virus mutant supports reactivation from latently infected mouse trigeminal ganglia.
作者信息
Besecker Michael I, Furness Caroline L, Coen Donald M, Griffiths Anthony
机构信息
Department of Virology and Immunology, Southwest Foundation for Biomedical Research, San Antonio, TX 78227, USA.
出版信息
J Virol. 2007 Aug;81(15):8356-60. doi: 10.1128/JVI.00484-07. Epub 2007 May 23.
Abstract
A single-cytosine-deletion in the herpes simplex virus gene encoding thymidine kinase (TK) was previously found in an acyclovir-resistant clinical isolate. A laboratory strain engineered to carry this mutation did not generate sufficient TK activity for detection by plaque autoradiography, which detected 0.25% wild-type activity. However, a drug sensitivity assay suggested that extremely low levels of TK are generated by this virus. The virus was estimated to express 0.09% of wild-type TK activity via a ribosomal frameshift 24 nucleotides upstream of the mutation. Remarkably, this appeared to be sufficient active TK to support a low level of reactivation from latently infected mouse trigeminal ganglia.
摘要
先前在一株阿昔洛韦耐药的临床分离株中发现，单纯疱疹病毒编码胸苷激酶（TK）的基因存在单个胞嘧啶缺失。构建携带此突变的实验室菌株后，通过噬斑放射自显影检测发现其产生的TK活性不足以被检测到，仅能检测到0.25%的野生型活性。然而，药物敏感性试验表明，该病毒产生的TK水平极低。据估计，该病毒通过突变上游24个核苷酸处的核糖体移码表达出0.09%的野生型TK活性。值得注意的是，这似乎足以产生有活性的TK，以支持潜伏感染小鼠三叉神经节的低水平再激活。
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