ArticlePLoS pathogens2006
Borna disease virus blocks potentiation of presynaptic activity through inhibition of protein kinase C signaling.
Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 72 citations in OpenAlex.
- Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.Science advances · 2026Article
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- Review
- Interactions of Equine Viruses with the Host Kinase Machinery and Implications for One Health and Human Disease.Viruses · 2023Review
- Word recognition memory and serum levels of Borna disease virus specific circulating immune complexes in obsessive-compulsive disorder.BMC psychiatry · 2022Article
- Back to the Future: The Role of Infections in Psychopathology. Focus on OCD.Clinical neuropsychiatry · 2022Article
- Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity.iScience · 2022Article
- Engagement of Neurotropic Viruses in Fast Axonal Transport: Mechanisms, Potential Role of Host Kinases and Implications for Neuronal Dysfunction.Frontiers in cellular neuroscience · 2021Article
- Hippocampal expression of a virus-derived protein impairs memory in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Borna disease virus phosphoprotein modulates epigenetic signaling in neurons to control viral replication.Journal of virology · 2015Article
- Early postnatal exposure to lithium in vitro induces changes in AMPAR mEPSCs and vesicular recycling at hippocampal glutamatergic synapses.Journal of biosciences · 2015Article
- Borna disease virus phosphoprotein impairs the developmental program controlling neurogenesis and reduces human GABAergic neurogenesis.PLoS pathogens · 2015Article
- Synaptic Plasticity and Neurological Disorders in Neurotropic Viral Infections.Neural plasticity · 2015Review
- A critical determinant of neurological disease associated with highly pathogenic tick-borne flavivirus in mice.Journal of virology · 2014Article
- Comprehensive analysis of endogenous bornavirus-like elements in eukaryote genomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Review
- The NTPase/helicase domain of hepatitis C virus nonstructural protein 3 inhibits protein kinase C independently of its NTPase activity.Cellular & molecular biology letters · 2013Article
- Apolipoprotein E3 (ApoE3) but not ApoE4 protects against synaptic loss through increased expression of protein kinase C epsilon.The Journal of biological chemistry · 2012Article
- Borna disease virus infects human neural progenitor cells and impairs neurogenesis.Journal of virology · 2012Article
- Rift valley fever virus infection of human cells and insect hosts is promoted by protein kinase C epsilon.PloS one · 2010Article
- Species-specific contribution of the four C-terminal amino acids of influenza A virus NS1 protein to virulence.Journal of virology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection by Borna disease virus (BDV) enables the study of the molecular mechanisms whereby a virus can persist in the central nervous system and lead to altered brain function in the absence of overt cytolysis and inflammation. This neurotropic virus infects a wide variety of vertebrates and causes behavioral diseases. The basis of BDV-induced behavioral impairment remains largely unknown. Here, we investigated whether BDV infection of neurons affected synaptic activity, by studying the rate of synaptic vesicle (SV) recycling, a good indicator of synaptic activity. Vesicular cycling was visualized in cultured hippocampal neurons synapses, using an assay based on the uptake of an antibody directed against the luminal domain of synaptotagmin I. BDV infection did not affect elementary presynaptic functioning, such as spontaneous or depolarization-induced vesicular cycling. In contrast, infection of neurons with BDV specifically blocked the enhancement of SV recycling that is observed in response to stimuli-induced synaptic potentiation, suggesting defects in long-term potentiation. Studies of signaling pathways involved in synaptic potentiation revealed that this blockade was due to a reduction of the phosphorylation by protein kinase C (PKC) of proteins that regulate SV recycling, such as myristoylated alanine-rich C kinase substrate (MARCKS) and Munc18-1/nSec1. Moreover, BDV interference with PKC-dependent phosphorylation was identified downstream of PKC activation. We also provide evidence suggesting that the BDV phosphoprotein interferes with PKC-dependent phosphorylation. Altogether, our results reveal a new mechanism by which a virus can cause synaptic dysfunction and contribute to neurobehavioral disorders.
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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.