ArticleiScience2022
Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Long-Term Survival of Borna Disease Virus 1 (BoDV-1)-Encephalitis: An Exceptional Case with Valuable Insights for Pathophysiology and Disease Management.Infectious diseases and therapy · 2026Article
- BoDV-1 Infection Is Associated with Altered Prion Protein Glycoform Maturation and Reduced ETS1-MGAT5/GnTV Pathway Activity in Rat C6 Astroglial Cells.Microorganisms · 2026Article
- Monolithic 3D Nanoelectrode Arrays on CMOS Circuitry for Scalable, High-Resolution Neural Recording.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits.Nature neuroscience · 2025Article
- Ex vivo study of neuroinvasive and neurotropic viruses: what is current and what is next.FEMS microbiology reviews · 2025Review
- Analysis of BoDV-1 status, EEG resting-state alpha activity and pro-inflammatory cytokines in adults with and without major depressive disorder.Frontiers in psychology · 2024Article
- Viral infections in etiology of mental disorders: a broad analysis of cytokine profile similarities - a narrative review.Frontiers in cellular and infection microbiology · 2024Review
- Case report: Fatal Borna virus encephalitis manifesting with basal brain and brainstem symptoms.Frontiers in neurology · 2023Article
- Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Borna disease viruses (BoDV) have recently emerged as zoonotic neurotropic pathogens. These persistent RNA viruses assemble nuclear replication centers (vSPOT) in close interaction with the host chromatin. However, the topology of this interaction and its consequences on neuronal function remain unexplored. In neurons, DNA double-strand breaks (DSB) have been identified as novel epigenetic mechanisms regulating neurotransmission and cognition. Activity-dependent DSB contribute critically to neuronal plasticity processes, which could be impaired upon infection. Here, we show that BoDV-1 infection, or the singled-out expression of viral Nucleoprotein and Phosphoprotein, increases neuronal DSB levels. Of interest, inducing DSB promoted the recruitment anew of vSPOT colocalized with DSB and increased viral RNA replication. BoDV-1 persistence decreased neuronal activity and response to stimulation by dampening the surface expression of glutamate receptors. Taken together, our results propose an original mechanistic cross talk between persistence of an RNA virus and neuronal function, through the control of DSB levels.
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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.