ArticleThe Journal of infectious diseases2018
Ebola Virus VP40 Modulates Cell Cycle and Biogenesis of Extracellular Vesicles.
Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 52 citations in OpenAlex.
- Ebola virus matrix protein VP40 triggers inflammatory responses linked to the ebolavirus virulence.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- Article
- Dual Role of Extracellular Vesicles as Orchestrators of Emerging and Reemerging Virus Infections.Cell biochemistry and biophysics · 2025Review
- Rational design of self-amplifying virus-like vesicles with Ebola virus glycoprotein as vaccines.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Characterizing changes in transcriptome and kinome responses in testicular cells during infection by Ebola virus.Npj viruses · 2024Article
- Harnessing crosstalk between extracellular vesicles and viruses for disease diagnostics and therapeutics.Extracellular vesicles and circulating nucleic acids · 2024Review
- Navigating the Complex Landscape of Ebola Infection Treatment: A Review of Emerging Pharmacological Approaches.Infectious diseases and therapy · 2024Review
- Extracellular vesicles in bacterial and fungal diseases - Pathogenesis to diagnostic biomarkers.Virulence · 2023Review
- Exosomal transmission of viruses, a two-edged biological sword.Cell communication and signaling : CCS · 2023Review
- Extracellular Vesicles and Viruses: Two Intertwined Entities.International journal of molecular sciences · 2023Review
- Extracellular vesicle storm during the course of Ebola virus infection in primates.Frontiers in cellular and infection microbiology · 2023Article
- Multifunctional role of exosomes in viral diseases: From transmission to diagnosis and therapy.Cellular signalling · 2022Review
- WWOX-Mediated Degradation of AMOTp130 Negatively Affects Egress of Filovirus VP40 Virus-Like Particles.Journal of virology · 2022Article
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- Article
- Retroviral infection of human neurospheres and use of stem Cell EVs to repair cellular damage.Scientific reports · 2022Article
- Article
- A Comprehensive Insight into the Role of Exosomes in Viral Infection: Dual Faces Bearing Different Functions.Pharmaceutics · 2021Review
- Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
Abstract
Background: Ebola virus (EBOV) mainly targets myeloid cells; however, extensive death of T cells is often observed in lethal infections. We have previously shown that EBOV VP40 in exosomes causes recipient immune cell death. Methods: Using VP40-producing clones, we analyzed donor cell cycle, extracellular vesicle (EV) biogenesis, and recipient immune cell death. Transcription of cyclin D1 and nuclear localization of VP40 were examined via kinase and chromatin immunoprecipitation assays. Extracellular vesicle contents were characterized by mass spectrometry, cytokine array, and western blot. Biosafety level-4 facilities were used for wild-type Ebola virus infection studies. Results: VP40 EVs induced apoptosis in recipient T cells and monocytes. VP40 clones were accelerated in growth due to cyclin D1 upregulation, and nuclear VP40 was found bound to the cyclin D1 promoter. Accelerated cell cycling was related to EV biogenesis, resulting in fewer but larger EVs. VP40 EV contents were enriched in ribonucleic acid-binding proteins and cytokines (interleukin-15, transforming growth factor-β1, and interferon-γ). Finally, EBOV-infected cell and animal EVs contained VP40, nucleoprotein, and glycoprotein. Conclusions: Nuclear VP40 upregulates cyclin D1 levels, resulting in dysregulated cell cycle and EV biogenesis. Packaging of cytokines and EBOV proteins into EVs from infected cells may be responsible for the decimation of immune cells during EBOV pathogenesis.
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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.