ArticleProceedings of the National Academy of Sciences of the United States of America2012
Structural basis for Marburg virus VP35-mediated immune evasion mechanisms.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 118 citations in OpenAlex.
- Experimental Treatment with Favipiravir for Ebola Virus Disease (the JIKI Trial): A Historically Controlled, Single-Arm Proof-of-Concept Trial in Guinea.PLoS medicine · 2016Trial
- Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026Article
- 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025Review
- Guardians of immunity: neutrophils and their role in Ebola virus infection.Annals of medicine and surgery (2012) · 2025Review
- Opening and closing of a cryptic pocket in VP35 toggles it between two different RNA-binding modes.eLife · 2025Article
- 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
- Structural insights into the RNA-dependent RNA polymerase complexes from highly pathogenic Marburg and Ebola viruses.Nature communications · 2025Article
- Immunogenicity, Pathogenesis, and Host's Immuno-Responses to Marburg Virus Infection.Pathogens (Basel, Switzerland) · 2025Review
- Marburg and Sudan viruses elicit divergent interferon responses and cytokine storm signaling in Egyptian rousette bat macrophages.Frontiers in immunology · 2025Article
- Article
- Molecular determinants of cross-species transmission in emerging viral infections.Microbiology and molecular biology reviews : MMBR · 2024Review
- Design of a novel multi-epitope vaccine against Marburg virus using immunoinformatics studies.BMC biotechnology · 2024Article
- Viral evasion of the interferon response at a glance.Journal of cell science · 2023Review
- Article
- Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines.Pathogens (Basel, Switzerland) · 2022Review
- Ebola and Marburg virus VP35 coiled-coil validated as antiviral target by tripartite split-GFP complementation.iScience · 2022Article
- A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations.Frontiers in immunology · 2022Review
- Factors affecting RIG-I-Like receptors activation - New research direction for viral hemorrhagic fevers.Frontiers in immunology · 2022Review
- Designing of a Multi-epitope Vaccine against the Structural Proteins of Marburg Virus Exploiting the Immunoinformatics Approach.ACS omega · 2021Article
- Functional Importance of Hydrophobic Patches on the Ebola Virus VP35 IFN-Inhibitory Domain.Viruses · 2021Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Filoviruses, marburgvirus (MARV) and ebolavirus (EBOV), are causative agents of highly lethal hemorrhagic fever in humans. MARV and EBOV share a common genome organization but show important differences in replication complex formation, cell entry, host tropism, transcriptional regulation, and immune evasion. Multifunctional filoviral viral protein (VP) 35 proteins inhibit innate immune responses. Recent studies suggest double-stranded (ds)RNA sequestration is a potential mechanism that allows EBOV VP35 to antagonize retinoic-acid inducible gene-I (RIG-I) like receptors (RLRs) that are activated by viral pathogen-associated molecular patterns (PAMPs), such as double-strandedness and dsRNA blunt ends. Here, we show that MARV VP35 can inhibit IFN production at multiple steps in the signaling pathways downstream of RLRs. The crystal structure of MARV VP35 IID in complex with 18-bp dsRNA reveals that despite the similar protein fold as EBOV VP35 IID, MARV VP35 IID interacts with the dsRNA backbone and not with blunt ends. Functional studies show that MARV VP35 can inhibit dsRNA-dependent RLR activation and interferon (IFN) regulatory factor 3 (IRF3) phosphorylation by IFN kinases TRAF family member-associated NFkb activator (TANK) binding kinase-1 (TBK-1) and IFN kB kinase e (IKKe) in cell-based studies. We also show that MARV VP35 can only inhibit RIG-I and melanoma differentiation associated gene 5 (MDA5) activation by double strandedness of RNA PAMPs (coating backbone) but is unable to inhibit activation of RLRs by dsRNA blunt ends (end capping). In contrast, EBOV VP35 can inhibit activation by both PAMPs. Insights on differential PAMP recognition and inhibition of IFN induction by a similar filoviral VP35 fold, as shown here, reveal the structural and functional plasticity of a highly conserved virulence factor.
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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.