ArticleJournal of virology2002
PrP(c) expression influences the establishment of herpes simplex virus type 1 latency.
Article in Journal of virology, 2002. 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, 22 citations in OpenAlex.
- Differential expression of cellular prion protein (PrPJournal of neurovirology · 2024Article
- Stress and viral insults do not trigger E200K PrP conversion in human cerebral organoids.PloS one · 2022Article
- Prion protein protects mice from lethal infection with influenza A viruses.PLoS pathogens · 2018Article
- Prion Protein PRNP: A New Player in Innate Immunity? The Aβ Connection.Journal of Alzheimer's disease reports · 2017Article
- A proautophagic antiviral role for the cellular prion protein identified by infection with a herpes simplex virus 1 ICP34.5 mutant.Journal of virology · 2013Article
- All quiet on the neuronal front: NMDA receptor inhibition by prion protein.The Journal of cell biology · 2008Article
- Poliovirus type 1 infection of murine PRNP-knockout neuronal cells.Journal of neurovirology · 2005Article
- Microglia from Creutzfeldt-Jakob disease-infected brains are infectious and show specific mRNA activation profiles.Journal of virology · 2002Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PrP(c) is a glycophosphatidylinositol-linked cell-surface protein expressed principally by neural tissue. The normal function of this protein is unestablished, although a role in either transmembrane signaling, cell-cell adhesion, or copper metabolism has been proposed. In this study we have investigated the effect of the neurotropic virus herpes simplex virus type 1 (HSV-1) in strains of mice which express different levels of PrP(c). Viral gene expression under the control of the HSV-1 early promoter IE110, detected either by in situ hybridization for RNA transcripts or by beta-galactosidase (beta-Gal) activity from an inserted lacZ gene, showed that the magnitude of HSV replication was retarded in PrP-/- mice. This was reflected in the lower level of acute viral titers in tissues from these virus-inoculated mice. However, HSV-inoculated PrP-/- mice contained higher levels of latent virus in both peripheral and central nervous tissue than those seen in mice which express PrP(c). Our observations show that lack of PrP(c) expression favors the establishment of HSV latency whereas HSV replication proceeds more efficiently in neuronal tissue that expresses this protein. The data further suggest that PrP(c) may be involved in a metabolic pathway that culminates in apoptosis of neurons that have been infected by neurotropic viruses.
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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 OpenQuestion graph.