ArticleJournal of virology1995
Quantification of transcripts from the ICP4 and thymidine kinase genes in mouse ganglia latently infected with herpes simplex virus.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 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.
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Who cites it
137 citing papers in PubMed, 227 citations in OpenAlex.
- HSV-1 reactivation as an emergent property of neuronal stress: implications for traumatic brain injury.Journal of neuroinflammation · 2026Review
- Targeted mutagenesis of the ICP4 transactivation domain generates a protective DIVA vaccine against duck plague.Poultry science · 2026Article
- Partial or complete blocking of gD binding to HVEM affects primary and latent HSV-1 infection as well as eye disease in HSV-1 infected mice.PLoS pathogens · 2026Article
- Regional and Temporal Patterns of Long-Term Pseudorabies Virus Detection and Neuropathology in the Murine CNS.Pathogens (Basel, Switzerland) · 2026Article
- Article
- Lytic promoter activity during herpes simplex virus latency is dependent on genome location.Journal of virology · 2024Article
- A Journey through the Minefield of the Discovery and Characterization of Latency-Related RNA/Latency-Associated Transcript.Viruses · 2024Review
- Reanalysis of single-cell RNA sequencing data does not support herpes simplex virus 1 latency in non-neuronal ganglionic cells in mice.Journal of virology · 2024Article
- Binding of herpesvirus entry mediator (HVEM) and HSV-1 gD affect reactivation but not latency levels.PLoS pathogens · 2023Article
- The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome.Journal of virology · 2023Review
- Regulation of alphaherpesvirus protein via post-translational phosphorylation.Veterinary research · 2022Review
- Disrupting Neurons and Glial Cells Oneness in the Brain-The Possible Causal Role of Herpes Simplex Virus Type 1 (HSV-1) in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- How an increase in the copy number of HSV-1 during latency can cause Alzheimer's disease: the viral and cellular dynamics according to the microcompetition model.Journal of neurovirology · 2021Article
- PML-NB-dependent type I interferon memory results in a restricted form of HSV latency.EMBO reports · 2021Article
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- Persistent Herpes Simplex Virus Type 1 Infection of Enteric Neurons Triggers CD8Frontiers in cellular and infection microbiology · 2021Article
- Trivalent Glycoprotein Subunit Vaccine Prevents Neonatal Herpes Simplex Virus Mortality and Morbidity.Journal of virology · 2020Article
- Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020Review
- Herpes Simplex Virus Latency Is Noisier the Closer We Look.Journal of virology · 2020Review
- Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.PloS one · 2020Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus establishes latency in nervous tissue in which it is maintained for the life of the mammalian host, with occasional reactivation leading to subsequent spread. Latency-associated transcripts are abundant during latency, but viral proteins and productive cycle RNAs have not been detected. Using sensitive, quantitative PCR assays, we have quantified certain viral RNAs specific to productive-cycle genes in mouse ganglia latently infected with herpes simplex virus type 1. Sense-strand RNA specific to the essential immediate-early gene, ICP4, was present in most ganglia in variable amounts relative to the amount of viral DNA, with one to seven molecules of RNA per viral genome in about 20% of ganglia. In contrast, the amount of latency-associated transcripts was much less variable, at an average of 4 x 10(4) molecules per viral genome. The amounts of ICP4-specific RNA were similar at 30 and 60 days postinfection, and at least some of these transcripts initiated within a region consistent with utilization of the ICP4 promoter. RNA specific to the thymidine kinase gene, whose transcription in productive infection is dependent on ICP4, was present in latently infected ganglia at a maximum level of 3.2 x 10(6) molecules per ganglion (500 molecules per viral genome). ICP4-specific and tk-specific RNAs measured from the same samples showed a positive correlation extending over 2 orders of magnitude. We conclude that ICP4-specific RNA is expressed in the absence of detectable reactivation and discuss possible implications of our findings for latent gene expression.
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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.