ArticleJournal of neurovirology2004
The herpes simplex virus type 1 early gene (thymidine kinase) promoter is activated in neurons of brain, but not trigeminal ganglia, of transgenic mice in the absence of viral proteins.
Article in Journal of neurovirology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- An investigation of herpes simplex virus promoter activity compatible with latency establishment reveals VP16-independent activation of immediate-early promoters in sensory neurones.The Journal of general virology · 2011Article
- Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neurons.Journal of virology · 2007Article
- Gamma interferon can block herpes simplex virus type 1 reactivation from latency, even in the presence of late gene expression.Journal of virology · 2005Article
- Neuronal activity regulates viral replication of herpes simplex virus type 1 in the nervous system.Journal of neurovirology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Latent infection of sensory neurons and reactivation are necessary for maintenance of herpes simplex virus type 1 (HSV-1) in its host population. It has been proposed that the HSV-1 early gene, thymidine kinase (TK), may play an important regulatory role in this process. The authors used reporter transgenic mice to test whether sensory ganglia neurons could activate the HSV-1 TK reporter transgene in the absence of viral proteins. The reporter transgene was activated in subsets of neurons in the brain but was not activated in sensory ganglia neurons following a variety of experimental manipulations. These results do not support a role for TK in regulation of the latent viral genome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.