Translational compensation of a frameshift mutation affecting herpes simplex virus thymidine kinase is sufficient to permit reactivation from latency.
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Slipping and sliding: frameshift mutations in herpes simplex virus thymidine kinase and drug-resistanceAntiviral drug resistance: mechanisms and clinical implicationsDiverse herpes simplex virus type 1 thymidine kinase mutants in individual human neurons and Ganglia.An unusual internal ribosome entry site in the herpes simplex virus thymidine kinase geneResistance of herpes simplex viruses to nucleoside analogues: mechanisms, prevalence, and managementIn vivo reactivation of latent herpes simplex virus 1 in mice can occur in the brain before occurring in the trigeminal ganglionFailure of thymidine kinase-negative herpes simplex virus to reactivate from latency following efficient establishment.Low-level expression and reversion both contribute to reactivation of herpes simplex virus drug-resistant mutants with mutations on homopolymeric sequences in thymidine kinase.A forward phenotypically driven unbiased genetic analysis of host genes that moderate herpes simplex virus virulence and stromal keratitis in mice.Quantification and analysis of thymidine kinase expression from acyclovir-resistant G-string insertion and deletion mutants in herpes simplex virus-infected cells.Expression of extremely low levels of thymidine kinase from an acyclovir-resistant herpes simplex virus mutant supports reactivation from latently infected mouse trigeminal gangliaNet -1 frameshifting on a noncanonical sequence in a herpes simplex virus drug-resistant mutant is stimulated by nonstop mRNA.A gripping tale of ribosomal frameshifting: extragenic suppressors of frameshift mutations spotlight P-site realignment.Common and new acyclovir resistant herpes simplex virus-1 mutants causing bilateral recurrent herpetic keratitis in an immunocompetent patient.Tranylcypromine reduces herpes simplex virus 1 infection in mice.Thymidine Kinase-Negative Herpes Simplex Virus 1 Can Efficiently Establish Persistent Infection in Neural Tissues of Nude Mice.A functional -1 ribosomal frameshift signal in the human paraneoplastic Ma3 gene.The Impacts of Genome-wide Analyses on our Understanding of Human Herpesvirus Diversity and Evolution.A thymidine kinase-deleted bovine herpesvirus 5 establishes latent infection but reactivates poorly in a sheep modelMapping the sites of latency and reactivation by bovine herpesvirus 5 (BoHV-5) and a thymidine kinase-deleted BoHV-5 in lambs
P2860
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P2860
Translational compensation of a frameshift mutation affecting herpes simplex virus thymidine kinase is sufficient to permit reactivation from latency.
description
2003 nî lūn-bûn
@nan
2003 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
Translational compensation of ...... mit reactivation from latency.
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Translational compensation of ...... mit reactivation from latency.
@en
Translational compensation of ...... mit reactivation from latency.
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type
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Translational compensation of ...... mit reactivation from latency.
@ast
Translational compensation of ...... mit reactivation from latency.
@en
Translational compensation of ...... mit reactivation from latency.
@nl
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Translational compensation of ...... mit reactivation from latency.
@ast
Translational compensation of ...... mit reactivation from latency.
@en
Translational compensation of ...... mit reactivation from latency.
@nl
P2093
P2860
P1433
P1476
Translational compensation of ...... mit reactivation from latency.
@en
P2093
Anthony Griffiths
Brian C Horsburgh
Donald M Coen
Shun-Hua Chen
P2860
P304
P356
10.1128/JVI.77.8.4703-4709.2003
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P577
2003-04-01T00:00:00Z