ArticleJournal of virology2011
Marburg virus VP40 antagonizes interferon signaling in a species-specific manner.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 78 citations in OpenAlex.
- Viral interferon antagonism shapes host tropism.PLoS pathogens · 2025Review
- Marburg virus glycoprotein mRNA vaccine is more protective than a virus-like particle-forming mRNA vaccine.The Journal of clinical investigation · 2025Article
- Article
- Identification of potential VP40 inhibitor of Marburg virus through molecular docking, pharmacokinetic analysis and molecular dynamics simulation.Scientific reports · 2025Article
- Jamaican fruit bats' competence for Ebola but not Marburg virus is driven by intrinsic differences.Nature communications · 2025Article
- Lack of Lloviu Virus Disease Development in Ferret Model.Emerging infectious diseases · 2024Article
- Molecular determinants of cross-species transmission in emerging viral infections.Microbiology and molecular biology reviews : MMBR · 2024Review
- Emerging and reemerging infectious diseases: global trends and new strategies for their prevention and control.Signal transduction and targeted therapy · 2024Review
- Novel antiviral approaches for Marburg: a promising therapeutics in the pipeline.Frontiers in microbiology · 2024Review
- Sandfly Fever Viruses Attenuate the Type I Interferon Response by Targeting the Phosphorylation of JAK-STAT Components.Frontiers in immunology · 2022Article
- Hemorrhagic fever viruses: Pathogenesis, therapeutics, and emerging and re-emerging potential.Frontiers in microbiology · 2022Review
- High-Throughput Screening Assay to Identify Small Molecule Inhibitors of Marburg Virus VP40 Protein.ACS infectious diseases · 2020Article
- Impact of Měnglà Virus Proteins on Human and Bat Innate Immune Pathways.Journal of virology · 2020Article
- Immune correlates of postexposure vaccine protection against Marburg virus.Scientific reports · 2020Article
- Marburg virus pathogenesis - differences and similarities in humans and animal models.Virology journal · 2019Review
- Global virus outbreaks: Interferons as 1st responders.Seminars in immunology · 2019Review
- Current status of small molecule drug development for Ebola virus and other filoviruses.Current opinion in virology · 2019Review
- Role of Type I Interferons on Filovirus Pathogenesis.Vaccines · 2019Review
- Filovirus Virulence in Interferon α/β and γ Double Knockout Mice, and Treatment with Favipiravir.Viruses · 2019Article
- Virus and host interactions critical for filoviral RNA synthesis as therapeutic targets.Antiviral research · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Marburgviruses are zoonotic pathogens that cause lethal hemorrhagic fever in humans and nonhuman primates. However, they do not cause lethal disease in immunocompetent mice unless they are adapted to this species. The adaptation process can therefore provide insight into the specific virus-host interactions that determine virulence. In primate cells, the Lake Victoria marburgvirus Musoke strain (MARV) VP40 matrix protein antagonizes alpha/beta interferon (IFN-α/β) and IFN-γ signaling by inhibiting the activation of the cellular tyrosine kinase Jak1. Here, VP40 from the Ravn strain (RAVV VP40)-from a distinct Marburg virus clade-is demonstrated to also inhibit IFN signaling in human cells. However, neither MARV nor RAVV VP40 effectively inhibited IFN-signaling in mouse cells, as assessed by assays of the antiviral effects of IFN-α/β and the IFN-α/β-induced phosphorylation of Jak1, STAT1, and STAT2. In contrast, the VP40 from a mouse-adapted RAVV (maRAVV) did inhibit IFN signaling. Effective Jak1 inhibition correlated with the species from which the cells were derived and did not depend upon whether Jak1 was of human or mouse origin. Of the seven amino acid changes that accumulated in VP40 during mouse adaptation, two (V57A and T165A) are sufficient to allow efficient IFN signaling antagonism by RAVV VP40 in mouse cells. The same two changes also confer efficient IFN antagonist function upon MARV VP40 in mouse cells. The mouse-adaptive changes did not affect the budding of RAVV VP40 in mouse cells, suggesting that this second major function of VP40 did not undergo adaptation. These data identify an apparent determinant of RAVV host range and virulence and define specific genetic determinants of this function.
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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.