ArticleNature communications2024
VLDLR mediates Semliki Forest virus neuroinvasion through the blood-cerebrospinal fluid barrier.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed.
- A conserved E1 stem motif functions as a virulence switch in the emerging Getah virus.Virulence · 2026Article
- The Forgotten Gate: Choroid Plexus and Blood-CSF Barrier in Arboviral Encephalitis.Life (Basel, Switzerland) · 2026Review
- LRP4 is an entry receptor for multiple encephalitic alphaviruses.Nature communications · 2026Article
- Lipoprotein (a) fuels EV71 replication by activating p38 MAPK-autophagy axis.Frontiers in immunology · 2026Article
- Molecular basis of ApoER2-mediated Semliki Forest virus entry.Nature communications · 2025Article
- LRP8 is an entry receptor for tick-borne encephalitis viruses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Engineering a streamlined virus-like particle for programmable tissue-specific gene delivery.Nature communications · 2025Article
- Review
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Article
- Article
- Strategies for delivering drugs across the blood-brain barrier for the treatment of neurodegenerative diseases.Frontiers in drug delivery · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Semliki Forest virus (SFV) is a neuropathogenic alphavirus which is of interest both as a model neurotropic alphavirus and as an oncolytic virus with proven potency in preclinical cancer models. In laboratory mice, peripherally administered SFV infiltrates the central nervous system (CNS) and causes encephalitis of varying severity. The route of SFV CNS entrance is poorly understood but has been considered to occur through the blood-brain barrier. Here we show that neuroinvasion of intravenously administered SFV is strictly dependent on very-low-density-lipoprotein receptor (VLDLR) which acts as an entry receptor for SFV. Moreover, SFV primarily enters the CNS through the blood-cerebrospinal fluid (B-CSF) barrier via infecting choroid plexus epithelial cells which show distinctly high expression of VLDLR. This is the first indication of neurotropic alphavirus utilizing choroid plexus for CNS entry, and VLDLR playing a specific and crucial role for mediating SFV entry through this pathway.
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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.