ArticleNeurobiology of disease2025
Phosphorylated-tau associates with HSV-1 chromatin and correlates with nuclear speckles decondensation in low-density host chromatin regions.
Article in Neurobiology of disease, 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
8 citing papers in PubMed.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Nuclear speckles: a fundamental layer of gene regulation.Trends in cell biology · 2026Review
- Dynamics of Paraspeckle Components in Herpes Simplex Virus 1 (HSV-1)-Infected Human Neuronal Cells.Viruses · 2026Article
- Neurosenescence, inflammaging and neuroinflammation in neurodegenerative disorders.Frontiers in aging · 2026Review
- From infection to dysfunction: viral triggers and antiviral immune factors in Alzheimer's disease pathology.Frontiers in immunology · 2026Review
- HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025Review
- The Role of Nitric Oxide in HSV-1 Infection: The Use of an Inducible Nitric Synthase Inhibitor Aminoguanidine to Treat Neuroinflammation.Microorganisms · 2025Article
- Herpes simplex virus-1 infection alters microtubule-associated protein Tau splicing and promotes Tau pathology in neural models of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Abnormal tau phosphorylation is a key mechanism in neurodegenerative diseases. Evidence implicates infectious agents, such as Herpes Simplex Virus 1 (HSV-1), as co-factors in the onset or the progression of neurodegenerative diseases, including Alzheimer's disease. This has led to divergence in the field regarding the contribution of viruses in the etiology of neurodegenerative diseases. Research indicates that viruses may function as risk factors driving neurodegenerative disease rather than playing a causative role. Investigating HSV-1 in abnormal tau phosphorylation is important for understanding the role of infectious agents in neurodegeneration. We generated cellular models of HSV-1 acute, latent infection, and viral reactivation from latency in cortical brain organoids and investigated the interplay between tau phosphorylation and HSV-1 infection by employing human induced pluripotent stem cell (iPSC)-derived monolayer neuronal cultures and brain organoids. Acute infection with HSV-1 strains 17syn
Indexed as
Identifiers
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.