ArticleJournal of virology2013
Ebola virus does not block apoptotic signaling pathways.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026Article
- Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines.Pathogens (Basel, Switzerland) · 2022Review
- PET imaging of TSPO expression in immune cells can assess organ-level pathophysiology in high-consequence viral infections.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Ebola Virus Requires Phosphatidylserine Scrambling Activity for Efficient Budding and Optimal Infectivity.Journal of virology · 2021Article
- Article
- HER2-mediated enhancement of Ebola virus entry.PLoS pathogens · 2020Article
- Investigating the Cellular Transcriptomic Response Induced by the Makona Variant of Ebola Virus in Differentiated THP-1 Cells.Viruses · 2019Article
- Ebola Virus VP40 Modulates Cell Cycle and Biogenesis of Extracellular Vesicles.The Journal of infectious diseases · 2018Article
- Role of Transmembrane Protein 16F in the Incorporation of Phosphatidylserine Into Budding Ebola Virus Virions.The Journal of infectious diseases · 2018Article
- Ebola virus requires a host scramblase for externalization of phosphatidylserine on the surface of viral particles.PLoS pathogens · 2018Article
- A comparison of host gene expression signatures associated with infection in vitro by the Makona and Ecran (Mayinga) variants of Ebola virus.Scientific reports · 2017Article
- Differential transcriptional responses to Ebola and Marburg virus infection in bat and human cells.Scientific reports · 2016Article
- Ebola Virus Does Not Induce Stress Granule Formation during Infection and Sequesters Stress Granule Proteins within Viral Inclusions.Journal of virology · 2016Article
- Activation of innate antiviral immune response via double-stranded RNA-dependent RLR receptor-mediated necroptosis.Scientific reports · 2016Article
- Ebola VP40 in Exosomes Can Cause Immune Cell Dysfunction.Frontiers in microbiology · 2016Article
- Molecular mechanisms of Ebola virus pathogenesis: focus on cell death.Cell death and differentiation · 2015Review
- The multiple roles of sGP in Ebola pathogenesis.Viral immunology · 2015Review
- Review
- Human Ebola virus infection in West Africa: a review of available therapeutic agents that target different steps of the life cycle of Ebola virus.Infectious diseases of poverty · 2014Article
- Filovirus Strategies to Escape Antiviral Responses.Current topics in microbiology and immunologyReview
Corrections and comments
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Authors and funding
11 authors at 8 institutions in 4 countries.
Funding
Abstract
Since viruses rely on functional cellular machinery for efficient propagation, apoptosis is an important mechanism to fight viral infections. In this study, we sought to determine the mechanism of cell death caused by Ebola virus (EBOV) infection by assaying for multiple stages of apoptosis and hallmarks of necrosis. Our data indicate that EBOV does not induce apoptosis in infected cells but rather leads to a nonapoptotic form of cell death. Ultrastructural analysis confirmed necrotic cell death of EBOV-infected cells. To investigate if EBOV blocks the induction of apoptosis, infected cells were treated with different apoptosis-inducing agents. Surprisingly, EBOV-infected cells remained sensitive to apoptosis induced by external stimuli. Neither receptor- nor mitochondrion-mediated apoptosis signaling was inhibited in EBOV infection. Although double-stranded RNA (dsRNA)-induced activation of protein kinase R (PKR) was blocked in EBOV-infected cells, induction of apoptosis mediated by dsRNA was not suppressed. When EBOV-infected cells were treated with dsRNA-dependent caspase recruiter (dsCARE), an antiviral protein that selectively induces apoptosis in cells containing dsRNA, virus titers were strongly reduced. These data show that the inability of EBOV to block apoptotic pathways may open up new strategies toward the development of antiviral therapeutics.
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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.