ArticleProceedings of the National Academy of Sciences of the United States of America2018
Hippocampal expression of a virus-derived protein impairs memory in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Tau T205 phosphorylation modulates engram cell recruitment and remote memory in mice.Nature communications · 2026Article
- Antagonistic activity against innate immunity determines virulence in mammalian bornaviruses.Npj viruses · 2025Article
- Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits.Nature neuroscience · 2025Article
- Is There such a Thing as Post-Viral Depression?: Implications for Precision Medicine.Biomolecules & therapeutics · 2024Review
- Article
- Word recognition memory and serum levels of Borna disease virus specific circulating immune complexes in obsessive-compulsive disorder.BMC psychiatry · 2022Article
- Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity.iScience · 2022Article
- C-type lectin receptor DCIR contributes to hippocampal injury in acute neurotropic virus infection.Scientific reports · 2021Article
- PPAR Gamma and Viral Infections of the Brain.International journal of molecular sciences · 2021Review
- CARD9 Deficiency Increases Hippocampal Injury Following Acute Neurotropic Picornavirus Infection but Does Not Affect Pathogen Elimination.International journal of molecular sciences · 2021Article
- Early Transcriptional Changes in Rabies Virus-Infected Neurons and Their Impact on Neuronal Functions.Frontiers in microbiology · 2021Article
- Engagement of Neurotropic Viruses in Fast Axonal Transport: Mechanisms, Potential Role of Host Kinases and Implications for Neuronal Dysfunction.Frontiers in cellular neuroscience · 2021Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The analysis of the biology of neurotropic viruses, notably of their interference with cellular signaling, provides a useful tool to get further insight into the role of specific pathways in the control of behavioral functions. Here, we exploited the natural property of a viral protein identified as a major effector of behavioral disorders during infection. We used the phosphoprotein (P) of Borna disease virus, which acts as a decoy substrate for protein kinase C (PKC) when expressed in neurons and disrupts synaptic plasticity. By a lentiviral-based strategy, we directed the singled-out expression of P in the dentate gyrus of the hippocampus and we examined its impact on mouse behavior. Mice expressing the P protein displayed increased anxiety and impaired long-term memory in contextual and spatial memory tasks. Interestingly, these effects were dependent on P protein phosphorylation by PKC, as expression of a mutant form of P devoid of its PKC phosphorylation sites had no effect on these behaviors. We also revealed features of behavioral impairment induced by P protein expression but that were independent of its phosphorylation by PKC. Altogether, our findings provide insight into the behavioral correlates of viral infection, as well as into the impact of virus-mediated alterations of the PKC pathway on behavioral functions.
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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.