Evidence map›Paper›PMID 27189922›Full record

ReviewJournal of molecular biology2016

Rodent-Adapted Filoviruses and the Molecular Basis of Pathogenesis.

Logan Banadyga, Michael A Dolan, Hideki Ebihara

Abstract readReview
In one paragraph

Review in Journal of molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  6. Evaluating Countermeasures Against Marburg Virus Using a Mouse Model.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  7. 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 · 2024
    Article
  8. Review
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  12. Article
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  18. Review
  19. A Forgotten Episode of Marburg Virus Disease: Belgrade, Yugoslavia, 1967.Microbiology and molecular biology reviews : MMBR · 2020
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Logan BanadygaLaboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.
Michael A DolanBioinformatics and Computational Biosciences Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Hideki EbiharaLaboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. Electronic address: ebiharah@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Molecular Basis of Host-Filovirus Interactions in PathogenesisZIAAI001136 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI EBIHARA, HIDEKI · 2011 to 2016
$3.5M
Intramural NIH HHS ZIA AI001136
6 · The paper itself

Abstract

Ebola, Marburg, and Ravn viruses, all filoviruses, are the causative agents of severe hemorrhagic fever. Much of what we understand about the pathogenesis of filovirus disease is derived from work with animal models, including nonhuman primates, which are considered the "gold standard" filovirus model since they faithfully recapitulate the clinical hallmarks of filovirus disease. However, rodent models, including the mouse, guinea pig, and hamster, also exist for Ebola, Marburg, and Ravn viruses, and although they may not reproduce all the clinical signs of filovirus disease, thanks to their relative ease of use and low cost, they are often the first choice for initial descriptions of virus pathogenesis and evaluation of antiviral prophylactics and therapeutics. Since filoviruses do not cause significant disease in adult, immunocompetent rodents, these models rely on "rodent-adapted" viruses that have been passaged several times through their host until virulence and lethality are achieved. In the process of adaptation, the viruses acquire numerous nucleotide/amino acid mutations that contribute to virulence in their rodent host. Interestingly, virus protein 24 (VP24) and nucleoprotein (NP) appear to be major virulence factors for ebolaviruses in rodents, whereas VP40 appears to be the major virulence factor for marburgviruses. By characterizing these mutations and understanding the molecular mechanisms that lead to the acquisition of virulence, we can gain better insight into the pathogenic processes that underlie filovirus disease in humans. These processes, and the viral and/or cellular proteins that contribute to them, will make attractive targets for the development of novel therapeutics and counter-measures.

Indexed as

Adaptation, BiologicalDisease Models, AnimalAnimalsCricetinaeFiloviridaeFiloviridae InfectionsGuinea PigsMiceVirulenceEbola virusFilovirusMarburg viruspathogenesisrodent adaptation

Identifiers

PMID27189922
PMCPMC5010511
OpenAlexW2390167325

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.