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Expression of extremely low levels of thymidine kinase from an acyclovir-resistant herpes simplex virus mutant supports reactivation from latently infected mouse trigeminal ganglia.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。
J Virol. 2007 Aug;81(15):8356-60. doi: 10.1128/JVI.00484-07. Epub 2007 May 23.
2
Low-level expression and reversion both contribute to reactivation of herpes simplex virus drug-resistant mutants with mutations on homopolymeric sequences in thymidine kinase.低水平表达和回复均有助于重新激活单纯疱疹病毒耐药突变体，这些突变体在胸苷激酶的同聚物序列上发生了突变。
J Virol. 2006 Jul;80(13):6568-74. doi: 10.1128/JVI.00155-06.
3
Translational compensation of a frameshift mutation affecting herpes simplex virus thymidine kinase is sufficient to permit reactivation from latency.影响单纯疱疹病毒胸苷激酶的移码突变的翻译补偿足以允许从潜伏状态重新激活。
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Quantification and analysis of thymidine kinase expression from acyclovir-resistant G-string insertion and deletion mutants in herpes simplex virus-infected cells.疱疹病毒感染细胞中阿昔洛韦耐药 G 串插入和缺失突变体胸苷激酶表达的定量和分析。
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High-frequency phenotypic reversion and pathogenicity of an acyclovir-resistant herpes simplex virus mutant.一种阿昔洛韦耐药单纯疱疹病毒突变体的高频表型回复和致病性
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Low levels of herpes simplex virus thymidine- thymidylate kinase are not limiting for sensitivity to certain antiviral drugs or for latency in a mouse model.在小鼠模型中，低水平的单纯疱疹病毒胸苷 - 胸苷酸激酶对某些抗病毒药物的敏感性或潜伏状态并无限制作用。
Virology. 1989 Feb;168(2):221-31. doi: 10.1016/0042-6822(89)90261-4.
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Failure of thymidine kinase-negative herpes simplex virus to reactivate from latency following efficient establishment.胸苷激酶阴性单纯疱疹病毒在有效建立潜伏感染后无法从潜伏状态重新激活。
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Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia.胸苷激酶阴性和野生型单纯疱疹病毒在小鼠三叉神经节共感染期间的竞争与互补
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Thymidine kinase-negative herpes simplex virus mutants establish latency in mouse trigeminal ganglia but do not reactivate.胸苷激酶阴性单纯疱疹病毒突变体可在小鼠三叉神经节中建立潜伏感染，但不会再激活。
Proc Natl Acad Sci U S A. 1989 Jun;86(12):4736-40. doi: 10.1073/pnas.86.12.4736.
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A net +1 frameshift permits synthesis of thymidine kinase from a drug-resistant herpes simplex virus mutant.一个净 +1 移码允许从一个耐药单纯疱疹病毒突变体合成胸苷激酶。
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Quantification and analysis of thymidine kinase expression from acyclovir-resistant G-string insertion and deletion mutants in herpes simplex virus-infected cells.疱疹病毒感染细胞中阿昔洛韦耐药 G 串插入和缺失突变体胸苷激酶表达的定量和分析。
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Slipping and sliding: frameshift mutations in herpes simplex virus thymidine kinase and drug-resistance.滑动和滑移：单纯疱疹病毒胸苷激酶中的移码突变与耐药性。
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Resistance of herpes simplex viruses to nucleoside analogues: mechanisms, prevalence, and management.单纯疱疹病毒对核苷类似物的耐药性：机制、流行率和管理。
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A gripping tale of ribosomal frameshifting: extragenic suppressors of frameshift mutations spotlight P-site realignment.一个关于核糖体移码的引人入胜的故事：移码突变的基因外抑制子突显P位点重排。
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本文引用的文献

1
Low-level expression and reversion both contribute to reactivation of herpes simplex virus drug-resistant mutants with mutations on homopolymeric sequences in thymidine kinase.低水平表达和回复均有助于重新激活单纯疱疹病毒耐药突变体，这些突变体在胸苷激酶的同聚物序列上发生了突变。
J Virol. 2006 Jul;80(13):6568-74. doi: 10.1128/JVI.00155-06.
2
Epitopes derived by incidental translational frameshifting give rise to a protective CTL response.由偶然的翻译移码产生的表位引发保护性细胞毒性T淋巴细胞反应。
J Immunol. 2006 Jun 1;176(11):6928-34. doi: 10.4049/jimmunol.176.11.6928.
3
An unusual internal ribosome entry site in the herpes simplex virus thymidine kinase gene.单纯疱疹病毒胸苷激酶基因中一个不同寻常的内部核糖体进入位点。
Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9667-72. doi: 10.1073/pnas.0504132102. Epub 2005 Jun 22.
4
Translational compensation of a frameshift mutation affecting herpes simplex virus thymidine kinase is sufficient to permit reactivation from latency.影响单纯疱疹病毒胸苷激酶的移码突变的翻译补偿足以允许从潜伏状态重新激活。
J Virol. 2003 Apr;77(8):4703-9. doi: 10.1128/jvi.77.8.4703-4709.2003.
5
High-frequency phenotypic reversion and pathogenicity of an acyclovir-resistant herpes simplex virus mutant.一种阿昔洛韦耐药单纯疱疹病毒突变体的高频表型回复和致病性
J Virol. 2003 Feb;77(3):2282-6. doi: 10.1128/jvi.77.3.2282-2286.2003.
6
Resistance of herpesviruses to antiviral drugs: clinical impacts and molecular mechanisms.疱疹病毒对抗病毒药物的耐药性：临床影响及分子机制
Drug Resist Updat. 2002 Apr;5(2):88-114. doi: 10.1016/s1368-7646(02)00021-3.
7
Reactivation of acyclovir-resistant thymidine kinase-deficient herpes simplex virus harbouring single base insertion within a 7 Gs homopolymer repeat of the thymidine kinase gene.在胸苷激酶基因的7个鸟嘌呤同聚物重复序列内存在单碱基插入的对阿昔洛韦耐药的胸苷激酶缺陷型单纯疱疹病毒的再激活。
J Med Virol. 2000 Oct;62(2):247-50.
8
Recurrent acyclovir-resistant herpes simplex in an immunocompromised patient: can strain differences compensate for loss of thymidine kinase in pathogenesis?一名免疫功能低下患者复发性阿昔洛韦耐药单纯疱疹：毒株差异能否在发病机制中弥补胸苷激酶缺失？
J Infect Dis. 1998 Sep;178(3):618-25. doi: 10.1086/515375.
9
Phenotypic and genotypic characterization of acyclovir-resistant herpes simplex viruses from immunocompromised patients.免疫功能低下患者中阿昔洛韦耐药单纯疱疹病毒的表型和基因型特征
J Infect Dis. 1998 Aug;178(2):297-303. doi: 10.1086/515626.
10
Human thymidine kinase can functionally replace herpes simplex virus type 1 thymidine kinase for viral replication in mouse sensory ganglia and reactivation from latency upon explant.人胸苷激酶可在功能上替代单纯疱疹病毒1型胸苷激酶，用于在小鼠感觉神经节中的病毒复制以及在植入后从潜伏状态重新激活。
J Virol. 1998 Aug;72(8):6710-5. doi: 10.1128/JVI.72.8.6710-6715.1998.

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.

DOI:10.1128/JVI.00484-07
PMID:17522225
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1951311/
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。