ArticleJournal of neurovirology2003
The herpes simplex virus type 1 ICP0 promoter is activated by viral reactivation stimuli in trigeminal ganglia neurons of transgenic mice.
Article in Journal of neurovirology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Photoimmunology: how ultraviolet radiation affects the immune system.Nature reviews. Immunology · 2019Review
- Rodent Papillomaviruses.Viruses · 2017Review
- De Novo Herpes Simplex Virus VP16 Expression Gates a Dynamic Programmatic Transition and Sets the Latent/Lytic Balance during Acute Infection in Trigeminal Ganglia.PLoS pathogens · 2016Article
- The Skin Microbiome: Is It Affected by UV-induced Immune Suppression?Frontiers in microbiology · 2016Article
- Association between unprotected ultraviolet radiation exposure and recurrence of ocular herpes simplex virus.American journal of epidemiology · 2014Article
- Article
- DNA damage promotes herpes simplex virus-1 protein expression in a neuroblastoma cell line.Journal of neurovirology · 2013Article
- Detection of ICP0 protein in tear fluid of individuals with active herpetic epithelial keratitis.Japanese journal of ophthalmology · 2011Article
- 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
- A 16 bp upstream sequence from the rat tyrosine hydroxylase promoter supports long-term expression from a neurofilament promoter, in a helper virus-free HSV-1 vector system.Brain research · 2011Article
- Activities of ICP0 involved in the reversal of silencing of quiescent herpes simplex virus 1.Journal of virology · 2011Article
- Virus reactivation: a panoramic view in human infections.Future virology · 2011Article
- Reversal of heterochromatic silencing of quiescent herpes simplex virus type 1 by ICP0.Journal of virology · 2011Article
- Role of nuclear factor Y in stress-induced activation of the herpes simplex virus type 1 ICP0 promoter.Journal of virology · 2010Article
- ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.Journal of virology · 2006Article
- Stress up-regulates neuronal expression of the herpes simplex virus type 2 large subunit of ribonucleotide reductase (R1; ICP10) by activating activator protein 1.Journal of neurovirology · 2005Article
- 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
- 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.Journal of neurovirology · 2004Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) causes a latent infection in sensory ganglia neurons in humans and in the mouse model. The ability of the virus to latently infect neurons and reactivate is central to the ability of HSV-1 to remain in the human population and spread to new hosts. It is possible that neuronal transcriptional proteins control latency and reactivation by modulating activation of the HSV-1 immediate-early (IE) gene ICP0. We have previously shown that factors in trigeminal ganglia neurons can differentially activate the IE ICP0 promoter and the IE ICP4 promoter in developing trigeminal ganglia neurons of transgenic mice. Ultraviolet (UV) irradiation and hyperthermic stress have been shown to result in HSV-1 reactivation from sensory neurons in the mouse model. Reporter transgenic mice were exposed to UV irradiation or hyperthermia to test whether stimuli that are known to reactivate HSV-1 could activate viral IE promoters in the absence of viral proteins. Measurement of beta-galactosidase activity in trigeminal ganglia from these transgenic mice indicated that the ICP0 promoter activity was significantly increased by both UV irradiation and hyperthermia. The IE genes ICP4 and ICP27 and the late gene gC reporter transgenes failed to be activated in parallel experiments. These results suggest that the ICP0 promoter is a target for activation by host transcription factors in sensory neurons that have undergone damage. It further suggests the possibility that activation of ICP0 gene expression by neuronal transcription factors may be important in reactivation of HSV-1 in neurons.
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