ArticleExperimental eye research2022
Regulation of herpes simplex virus type 1 latency-reactivation cycle and ocular disease by cellular signaling pathways.
Article in Experimental eye research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- HSV-1 reactivation as an emergent property of neuronal stress: implications for traumatic brain injury.Journal of neuroinflammation · 2026Review
- Non-neuronal sites of latency for alphaherpesviruses.Journal of virology · 2026Review
- Regional and Temporal Patterns of Long-Term Pseudorabies Virus Detection and Neuropathology in the Murine CNS.Pathogens (Basel, Switzerland) · 2026Article
- Mechanistic Perspectives on Herpes Simplex Virus Inhibition by Phenolic Acids and Tannins: Interference with the Herpesvirus Life Cycle.International journal of molecular sciences · 2025Review
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- Olfactory and trigeminal routes of HSV-1 CNS infection with regional microglial heterogeneity.Journal of virology · 2024Article
- Article
- Flavonoids with Anti-Herpes Simplex Virus Properties: Deciphering Their Mechanisms in Disrupting the Viral Life Cycle.Viruses · 2023Review
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
Following acute infection, herpes simplex virus type 1 (HSV-1) establishes life-long latency in sensory and other neurons. Recurrent ocular HSV-1 outbreaks are generally due to reactivation from latency. The HSV-1 latency-reactivation cycle is a complex virus-host relationship. The viral encoded latency-associated transcript (LAT) is abundantly expressed in latency and encodes several micro-RNAs and other small non-coding RNAs, which may regulate expression of key viral and cellular genes. Certain cellular signaling pathways, including Wnt/β-catenin and mTOR pathway, mediate certain aspect of the latency-reactivation cycle. Stress, via activation of the glucocorticoid receptor and other stress induced cellular transcription factors, are predicted to trigger reactivation from latency by stimulating viral gene expression and impairing immune responses and inflammation. These observations suggest stress and certain cellular signaling pathways play key roles in regulating the latency-reactivation cycle and recurrent ocular disease.
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What OpenQuestion holds
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.