Evidence map›Paper›PMID 31356611›Full record

ArticlePLoS neglected tropical diseases2019

Inhibition of Ebola Virus by a Molecularly Engineered Banana Lectin.

Evelyn M Covés-Datson, Julie Dyall, Lisa Evans DeWald, Steven R King, Derek Dube, Maureen Legendre, Elizabeth Nelson, Kelly C Drews, Robin Gross, Dawn M Gerhardt and 10 more

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The Journal of general virology · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Targeting glycans for CAR therapy: The advent of sweet CARs.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  15. Article
  16. Lectins and lectibodies: potential promising antiviral agents.Cellular & molecular biology letters · 2022
    Review
  17. Plant lectins as prospective antiviral biomolecules in the search for COVID-19 eradication strategies.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  18. Article
  19. Review
  20. Frontiers in cellular and infection microbiology · 2022
    Review
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

20 authors at 3 institutions in 1 country.

Evelyn M Covés-DatsonMedical Scientist Training Program, University of Michigan, Ann Arbor, Michigan, United States of America.
Julie DyallIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Lisa Evans DeWaldIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Steven R KingDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America.
Derek DubeDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America.
Maureen LegendreDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America.
Elizabeth NelsonDepartment of Cell Biology, University of Virginia, Charlottesville, Virginia, United States of America.
Kelly C DrewsDepartment of Pathology, University of Virginia, Charlottesville, Virginia, United States of America.
Robin GrossIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Dawn M GerhardtIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Lisa TorzewskiIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Elena PostnikovaIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Janie Y LiangIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Bhupal BanDepartment of Cell Biology, University of Virginia, Charlottesville, Virginia, United States of America.
Jagathpala ShettyAntibody Engineering and Technology Core, University of Virginia, Charlottesville, Virginia, United States of America.
Lisa E HensleyIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Peter B JahrlingIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Gene G OlingerIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, United States of America.
Judith M WhiteDepartment of Cell Biology, University of Virginia, Charlottesville, Virginia, United States of America.ORCID 0000-0002-0532-996X
David M MarkovitzDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America.
National Institutes of Health · USUniversity of Michigan · USUniversity of Virginia · US

Funding

MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
Molecular Mechanisms of Microbial Pathogenesis Training ProgramT32AI007528 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARRUTHERS, VERNON BRUCE · 1998 to 2024
$6.8M
Combinations of Approved Drugs to Combat Ebola VirusR01AI114776 · NIAID · UNIVERSITY OF VIRGINIA · PI WHITE, JUDITH M. · 2015 to 2017
$1.5M
Elucidating the role of potassium channels in HIV-1-induced bystander CD4+ T cell deathF31AI136615 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COVES-DATSON, EVELYN · 2018 to 2018
$31k
NIAID NIH HHS F31 AI136615NIAID NIH HHS HHSN272200700016INIAID NIH HHS R01 AI114776NIAID NIH HHS T32 AI007528NIGMS NIH HHS T32 GM007863
6 · The paper itself

Abstract

Ebolaviruses cause an often rapidly fatal syndrome known as Ebola virus disease (EVD), with average case fatality rates of ~50%. There is no licensed vaccine or treatment for EVD, underscoring the urgent need to develop new anti-ebolavirus agents, especially in the face of an ongoing outbreak in the Democratic Republic of the Congo and the largest ever outbreak in Western Africa in 2013-2016. Lectins have been investigated as potential antiviral agents as they bind glycans present on viral surface glycoproteins, but clinical use of them has been slowed by concerns regarding their mitogenicity, i.e. ability to cause immune cell proliferation. We previously engineered a banana lectin (BanLec), a carbohydrate-binding protein, such that it retained antiviral activity but lost mitogenicity by mutating a single amino acid, yielding H84T BanLec (H84T). H84T shows activity against viruses containing high-mannose N-glycans, including influenza A and B, HIV-1 and -2, and hepatitis C virus. Since ebolavirus surface glycoproteins also contain many high-mannose N-glycans, we assessed whether H84T could inhibit ebolavirus replication. H84T inhibited Ebola virus (EBOV) replication in cell cultures. In cells, H84T inhibited both virus-like particle (VLP) entry and transcription/replication of the EBOV mini-genome at high micromolar concentrations, while inhibiting infection by transcription- and replication-competent VLPs, which measures the full viral life cycle, in the low micromolar range. H84T did not inhibit assembly, budding, or release of VLPs. These findings suggest that H84T may exert its anti-ebolavirus effect(s) by blocking both entry and transcription/replication. In a mouse model, H84T partially (maximally, ~50-80%) protected mice from an otherwise lethal mouse-adapted EBOV infection. Interestingly, a single dose of H84T pre-exposure to EBOV protected ~80% of mice. Thus, H84T shows promise as a new anti-ebolavirus agent with potential to be used in combination with vaccination or other agents in a prophylactic or therapeutic regimen.

Indexed as

AnimalsAntiviral AgentsCell Line, TumorEbolavirusEscherichia coliFemaleGenetic EngineeringHEK293 CellsHemorrhagic Fever, EbolaHumansImmunoglobulin Variable RegionMiceMice, Inbred C57BLMusaPlant LectinsVirus ReplicationAntiviral AgentsImmunoglobulin Variable RegionPlant Lectins

Identifiers

PMID31356611
PMCPMC6687191
OpenAlexW2964397977

What OpenQuestion holds

Textmetadata
LicenceCC0
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.