ArticleCell reports2016
Differential Regulation of Interferon Responses by Ebola and Marburg Virus VP35 Proteins.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 97 citations in OpenAlex.
- Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026Article
- 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025Review
- Filovirus infection disrupts epithelial barrier function and ion transport in human iPSC-derived gut organoids.PLoS pathogens · 2025Article
- Ebola virus VP35 NNLNS motif modulates viral RNA synthesis and MIB2-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Opening and closing of a cryptic pocket in VP35 toggles it between two different RNA-binding modes.eLife · 2025Article
- Integrated computational approach revealed the potential inhibitory effect of xanthone derivatives against Marburg virus nucleocapsid.Virusdisease · 2025Article
- Article
- Valorization of a Natural Compound Library in Exploring Potential Marburg Virus VP35 Cofactor Inhibitors via an In Silico Drug Discovery Strategy.Current issues in molecular biology · 2025Article
- Bat organoids reveal antiviral responses at epithelial surfaces.Nature immunology · 2025Article
- Structural insights into the RNA-dependent RNA polymerase complexes from highly pathogenic Marburg and Ebola viruses.Nature communications · 2025Article
- Marburg and Sudan viruses elicit divergent interferon responses and cytokine storm signaling in Egyptian rousette bat macrophages.Frontiers in immunology · 2025Article
- Targeting Myeloid Differentiation Primary Response Protein 88 (MyD88) and Galectin-3 to Develop Broad-Spectrum Host-Mediated Therapeutics against SARS-CoV-2.International journal of molecular sciences · 2024Review
- Novel Antiviral Molecules against Ebola Virus Infection.International journal of molecular sciences · 2023Article
- Emergence of Marburg virus: a global perspective on fatal outbreaks and clinical challenges.Frontiers in microbiology · 2023Review
- Pathogenicity and virulence of Marburg virus.Virulence · 2022Review
- Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines.Pathogens (Basel, Switzerland) · 2022Review
- Ubiquitination of Ebola virus VP35 at lysine 309 regulates viral transcription and assembly.PLoS pathogens · 2022Article
- A cryptic pocket in Ebola VP35 allosterically controls RNA binding.Nature communications · 2022Article
- Cytoplasmic RNA sensors and their interplay with RNA-binding partners in innate antiviral response: theme and variations.RNA (New York, N.Y.) · 2022Review
- Factors affecting RIG-I-Like receptors activation - New research direction for viral hemorrhagic fevers.Frontiers in immunology · 2022Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Suppression of innate immune responses during filoviral infection contributes to disease severity. Ebola (EBOV) and Marburg (MARV) viruses each encode a VP35 protein that suppresses RIG-I-like receptor signaling and interferon-α/β (IFN-α/β) production by several mechanisms, including direct binding to double stranded RNA (dsRNA). Here, we demonstrate that in cell culture, MARV infection results in a greater upregulation of IFN responses as compared to EBOV infection. This correlates with differences in the efficiencies by which EBOV and MARV VP35s antagonize RIG-I signaling. Furthermore, structural and biochemical studies suggest that differential recognition of RNA elements by the respective VP35 C-terminal IFN inhibitory domain (IID) rather than affinity for RNA by the respective VP35s is critical for this observation. Our studies reveal functional differences in EBOV versus MARV VP35 RNA binding that result in unexpected differences in the host response to deadly viral pathogens.
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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.