Evidence map›Paper›PMID 25821226›Full record

ArticleThe Journal of infectious diseases2015

Ebola Virus Glycoprotein Promotes Enhanced Viral Egress by Preventing Ebola VP40 From Associating With the Host Restriction Factor BST2/Tetherin.

Jean K Gustin, Ying Bai, Ashlee V Moses, Janet L Douglas

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. A Yeast BiFC-seq Method for Genome-wide Interactome Mapping.Genomics, proteomics & bioinformatics · 2022
    Article
  3. Article
  4. Article
  5. Mechanisms of Immune Evasion by Ebola Virus.Advances in experimental medicine and biology · 2021
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Ebolaviruses: New roles for old proteins.PLoS neglected tropical diseases · 2018
    Review
  12. Article
  13. Immunobiology of Ebola and Lassa virus infections.Nature reviews. Immunology · 2017
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Jean K GustinVaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton.
Ying BaiVaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton.
Ashlee V MosesVaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton.
Janet L DouglasVaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton.
Children's Cancer Therapy Development Institute · USOregon Health & Science University · US

Funding

Characterization of Vpu-mediated degradation of BST-2R01AI090490 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI MOSES, ASHLEE V. · 2010 to 2014
$2.0M
NIAID NIH HHS 5 R01 AI090490-05NIAID NIH HHS R01 AI090490PHS HHS 5 U54 A1081680-05
6 · The paper itself

Abstract

backgroundBST2/tetherin is an innate immune molecule with the unique ability to restrict the egress of human immunodeficiency virus (HIV) and other enveloped viruses, including Ebola virus (EBOV). Coincident with this discovery was the finding that the HIV Vpu protein down-regulates BST2 from the cell surface, thereby promoting viral release. Evidence suggests that the EBOV envelope glycoprotein (GP) also counteracts BST2, although the mechanism is unclear.

resultsWe find that total levels of BST2 remain unchanged in the presence of GP, whereas surface BST2 is significantly reduced. GP is known to sterically mask surface receptors via its mucin domain. Our evaluation of mutant GP molecules indicate that masking of BST2 by GP is probably responsible for the apparent surface BST2 down-regulation; however, this masking does not explain the observed virus-like particle egress enhancement. We discovered that VP40 coimmunoprecipitates and colocalizes with BST2 in the absence but not in the presence of GP.

conclusionsThese results suggest that GP may overcome the BST2 restriction by blocking an interaction between VP40 and BST2. Furthermore, we have observed that GP may enhance BST2 incorporation into virus-like particles. Understanding this novel EBOV immune evasion strategy will provide valuable insights into the pathogenicity of this deadly pathogen.

Indexed as

Antigens, CDBone Marrow Stromal Antigen 2Cell LineDown-RegulationEbolavirusGlycoproteinsGPI-Linked ProteinsHEK293 CellsHumansMucinsMutationReceptors, Cell SurfaceViral Matrix ProteinsViral ProteinsVirus ReleaseAntigens, CDBone Marrow Stromal Antigen 2BST2 protein, humanGlycoproteinsGPI-Linked ProteinsMucinsReceptors, Cell SurfaceViral Matrix ProteinsViral ProteinsVP40 protein, virusBST2Ebola GPEbola virusEbola VP40HIVhost immune restrictiontetherinviral egress

Identifiers

PMID25821226
PMCPMC4564538
OpenAlexW2074876015

What OpenQuestion holds

Textmetadata
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.