ArticleFrontiers in aging neuroscience2016
Herpes Simplex Virus-Type1 (HSV-1) Impairs DNA Repair in Cortical Neurons.
Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 31 citations in OpenAlex.
- Herpes simplex virus type 1 R-loops are targets for APOBEC-mediated mutagenesis.Genome biology · 2026Article
- CD163+ perivascular macrophages in schizophrenia: a research framework for testing macrophage-related mechanisms.Frontiers in psychiatry · 2026Article
- Unveiling the Involvement of Herpes Simplex Virus-1 in Alzheimer's Disease: Possible Mechanisms and Therapeutic Implications.Molecular neurobiology · 2025Review
- The DNA repair protein DNA-PKcs modulates synaptic plasticity via PSD-95 phosphorylation and stability.EMBO reports · 2024Article
- Asymptomatic herpes simplex virus brain infection elicits cellular senescence phenotypes in the central nervous system of mice suffering multiple sclerosis-like disease.Communications biology · 2024Article
- Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System.Viruses · 2023Review
- Interleukin 1β triggers synaptic and memory deficits in Herpes simplex virus type-1-infected mice by downregulating the expression of synaptic plasticity-related genes via the epigenetic MeCP2/HDAC4 complex.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Contribution of viral and bacterial infections to senescence and immunosenescence.Frontiers in cellular and infection microbiology · 2023Review
- Nuclear antiviral innate responses at the intersection of DNA sensing and DNA repair.Trends in microbiology · 2022Review
- Recurrent Herpes Simplex Virus Type 1 (HSV-1) Infection Modulates Neuronal Aging Marks in In Vitro and In Vivo Models.International journal of molecular sciences · 2021Article
- Viral interactions with non-homologous end-joining: a game of hide-and-seek.The Journal of general virology · 2020Review
- Multiple Herpes Simplex Virus-1 (HSV-1) Reactivations Induce Protein Oxidative Damage in Mouse Brain: Novel Mechanisms for Alzheimer's Disease Progression.Microorganisms · 2020Article
- Contributions of DNA Damage to Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Coalescing replication compartments provide the opportunity for recombination between coinfecting herpesviruses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Early neuronal accumulation of DNA double strand breaks in Alzheimer's disease.Acta neuropathologica communications · 2019Article
- Modeling Herpes Simplex Virus 1 Infections in Human Central Nervous System Neuronal Cells Using Two- and Three-Dimensional Cultures Derived from Induced Pluripotent Stem Cells.Journal of virology · 2019Article
- Recurrent herpes simplex virus-1 infection induces hallmarks of neurodegeneration and cognitive deficits in mice.PLoS pathogens · 2019Article
- Herpes Simplex Virus Type 1 Infection of the Central Nervous System: Insights Into Proposed Interrelationships With Neurodegenerative Disorders.Frontiers in cellular neuroscience · 2019Review
- The Major Tegument Protein of Bovine Herpesvirus 1, VP8, Interacts with DNA Damage Response Proteins and Induces Apoptosis.Journal of virology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several findings suggest that Herpes simplex virus-1 (HSV-1) infection plays a role in the neurodegenerative processes that characterize Alzheimer's disease (AD), but the underlying mechanisms have yet to be fully elucidated. Here we show that HSV-1 productive infection in cortical neurons causes the accumulation of DNA lesions that include both single (SSBs) and double strand breaks (DSBs), which are reported to be implicated in the neuronal loss observed in neurodegenerative diseases. We demonstrate that HSV-1 downregulates the expression level of Ku80, one of the main components of non-homologous end joining (NHEJ), a major pathway for the repair of DSBs. We also provide data suggesting that HSV-1 drives Ku80 for proteasomal degradation and impairs NHEJ activity, leading to DSB accumulation. Since HSV-1 usually causes life-long recurrent infections, it is possible to speculate that cumulating damages, including those occurring on DNA, may contribute to virus induced neurotoxicity and neurodegeneration, further suggesting HSV-1 as a risk factor for neurodegenerative conditions.
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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 Socratic graph.