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本文引用的文献
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Translational compensation of a frameshift mutation affecting herpes simplex virus thymidine kinase is sufficient to permit reactivation from latency.
J Virol. 2003 Apr;77(8):4703-9. doi: 10.1128/jvi.77.8.4703-4709.2003.
2
Identification, localization, and regulation of expression of the UL24 protein of herpes simplex virus type 1.
J Virol. 2002 Nov;76(21):10821-8. doi: 10.1128/jvi.76.21.10821-10828.2002.
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Neither LAT nor open reading frame P mutations increase expression of spliced or intron-containing ICP0 transcripts in mouse ganglia latently infected with herpes simplex virus.
J Virol. 2002 May;76(10):4764-72. doi: 10.1128/jvi.76.10.4764-4772.2002.
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ICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency.
J Virol. 2001 Apr;75(7):3240-9. doi: 10.1128/JVI.75.7.3240-3249.2001.
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Persistent elevated expression of cytokine transcripts in ganglia latently infected with herpes simplex virus in the absence of ganglionic replication or reactivation.
Virology. 2000 Dec 5;278(1):207-16. doi: 10.1006/viro.2000.0643.
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Optimized viral dose and transient immunosuppression enable herpes simplex virus ICP0-null mutants To establish wild-type levels of latency in vivo.
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Replication of herpes simplex virus type 1 within trigeminal ganglia is required for high frequency but not high viral genome copy number latency.
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Recurrent acyclovir-resistant herpes simplex in an immunocompromised patient: can strain differences compensate for loss of thymidine kinase in pathogenesis?
J Infect Dis. 1998 Sep;178(3):618-25. doi: 10.1086/515375.
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The probability of in vivo reactivation of herpes simplex virus type 1 increases with the number of latently infected neurons in the ganglia.
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The latent herpes simplex virus type 1 genome copy number in individual neurons is virus strain specific and correlates with reactivation.
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