Evidence map›Paper›PMID 30700020›Full record

ArticleInternational journal of molecular sciences2019

Characterizing Cellular Responses During Oncolytic Maraba Virus Infection.

Golnoush Hassanzadeh, Thet Naing, Tyson Graber, Seyed Mehdi Jafarnejad, David F Stojdl, Tommy Alain, Martin Holcik

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Oncolytic viruses against cancer, promising or delusion?Medical oncology (Northwood, London, England) · 2023
    Review
  4. The Role of Bcl-xL Protein in Viral Infections.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. A Retrospective on eIF2A-and Not the Alpha Subunit of eIF2.International journal of molecular sciences · 2020
    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

7 authors at 2 institutions in 2 countries.

Golnoush HassanzadehMolecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON K1H 8L1, Canada. ghassanz@ualberta.ca.
Thet NaingMolecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON K1H 8L1, Canada. ThetFatica@cunet.carleton.ca.
Tyson GraberMolecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON K1H 8L1, Canada. rnaguru@gmail.com.ORCID 0000-0002-5337-3404
Seyed Mehdi JafarnejadCentre for Cancer Research and Cell Biology (CCRCB), Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7AE, UK. sm.jafarnejad@qub.ac.uk.
David F StojdlMolecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON K1H 8L1, Canada. dave@arc.cheo.ca.
Tommy AlainMolecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON K1H 8L1, Canada. tommy@arc.cheo.ca.
Martin HolcikMolecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON K1H 8L1, Canada. martinholcik@cunet.carleton.ca.ORCID 0000-0002-1922-5299
Children's Hospital of Eastern Ontario · CAQueen's University Belfast · GB

Funding

National Sciences and Engineering Research Council RGPIN 250100-2010
6 · The paper itself

Abstract

The rising demand for powerful oncolytic virotherapy agents has led to the identification of Maraba virus, one of the most potent oncolytic viruses from Rhabdoviridae family which displays high selectivity for killing malignant cells and low cytotoxicity in normal cells. Although the virus is readied to be used for clinical trials, the interactions between the virus and the host cells is still unclear. Using a newly developed interferon-sensitive mutant Maraba virus (MG1), we have identified two key regulators of global translation (4E-BP1 and eIF2α) as being involved in the regulation of protein synthesis in the infected cells. Despite the translational arrest upon viral stress, we showed an up-regulation of anti-apoptotic Bcl-xL protein that provides a survival benefit for the host cell, yet facilitates effective viral propagation. Given the fact that eIF5B canonically regulates 60S ribosome subunit end joining and is able to replace the role of eIF2 in delivering initiator tRNA to the 40S ribosome subunit upon the phosphorylation of eIF2α we have tested whether eIF5B mediates the translation of target mRNAs during MG1 infection. Our results show that the inhibition of eIF5B significantly down-regulates the level of

Indexed as

bcl-X ProteinEukaryotic Initiation Factor-2Eukaryotic Initiation FactorsHumansOncolytic VirotherapyOncolytic VirusesPhosphorylationProtein BiosynthesisRibosome Subunits, Large, EukaryoticRNA, Messengerbcl-X ProteinEukaryotic Initiation Factor-2eukaryotic initiation factor-5BEukaryotic Initiation FactorsRNA, MessengerBcl-xLeIF5BIRESMG-1translationXIAP

Identifiers

PMID30700020
PMCPMC6387032
OpenAlexW2594477378

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.