ArticleNature communications2021
Highly efficient intercellular spreading of protein misfolding mediated by viral ligand-receptor interactions.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- When Viruses Talk through Extracellular Vesicles: a New Perspective on Sars-Cov-2-Induced Neurodegeneration.Journal of extracellular vesicles · 2026Article
- Golgi Fragmentation as a Potential Link Between SARS-CoV-2 Infection and Alzheimer's Disease: Mechanisms and Implications for Neurodegeneration in Long COVID.Sub-cellular biochemistry · 2026Review
- Gangliosides modulate the secretion of extracellular vesicles and their misfolded protein cargo.Science advances · 2025Article
- The age-dependent neuroglial interaction with peripheral immune cells in coronavirus-induced neuroinflammation with a special emphasis on COVID-19.Biogerontology · 2025Review
- Aggregating amyloid resources: A comprehensive review of databases on amyloid-like aggregation.Computational and structural biotechnology journal · 2024Review
- Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies.Signal transduction and targeted therapy · 2024Review
- The evolving roles of extracellular vesicles in embryo-maternal communication.Communications biology · 2024Review
- Review
- New views on the complex interplay between degeneration and autoimmunity in multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- Exploring the Potential Long-term Impact of SARS-CoV-2 on Protein Misfolding and Amyloid-related Conditions.Protein and peptide letters · 2024Review
- Extracellular vesicles derived from stressed beta cells mediate monocyte activation and contribute to islet inflammation.Frontiers in immunology · 2024Article
- Alzheimer's disease and its treatment-yesterday, today, and tomorrow.Frontiers in pharmacology · 2024Review
- Dual-targeting inhibition of TNFR1 for alleviating rheumatoid arthritis by a novel composite nucleic acid nanodrug.International journal of pharmaceutics: X · 2023Article
- Viruses and amyloids - a vicious liaison.Prion · 2023Review
- Mechanisms and pathology of protein misfolding and aggregation.Nature reviews. Molecular cell biology · 2023Review
- Pervasive aggregation and depletion of host and viral proteins in response to cysteine-reactive electrophilic compounds.bioRxiv : the preprint server for biology · 2023Article
- Neuroprotective Agents with Therapeutic Potential for COVID-19.Biomolecules · 2023Review
- The elusive role of herpesviruses in Alzheimer's disease: current evidence and future directions.NeuroImmune pharmacology and therapeutics · 2023Review
- Reactivated endogenous retroviruses promote protein aggregate spreading.Nature communications · 2023Article
- Long COVID as a Tauopathy: Of "Brain Fog" and "Fusogen Storms".International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein aggregates associated with neurodegenerative diseases have the ability to transmit to unaffected cells, thereby templating their own aberrant conformation onto soluble homotypic proteins. Proteopathic seeds can be released into the extracellular space, secreted in association with extracellular vesicles (EV) or exchanged by direct cell-to-cell contact. The extent to which each of these pathways contribute to the prion-like spreading of protein misfolding is unclear. Exchange of cellular cargo by both direct cell contact or via EV depends on receptor-ligand interactions. We hypothesized that enabling these interactions through viral ligands enhances intercellular proteopathic seed transmission. Using different cellular models propagating prions or pathogenic Tau aggregates, we demonstrate that vesicular stomatitis virus glycoprotein and SARS-CoV-2 spike S increase aggregate induction by cell contact or ligand-decorated EV. Thus, receptor-ligand interactions are important determinants of intercellular aggregate dissemination. Our data raise the possibility that viral infections contribute to proteopathic seed spreading by facilitating intercellular cargo transfer.
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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.