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StressEBOV SIGNED

Ebola virus manipulation of the cellular stress responses

Total Cost €

0

EC-Contrib. €

0

Partnership

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 Outcomes and results

 StressEBOV project word cloud

Explore the words cloud of the StressEBOV project. It provides you a very rough idea of what is the project "StressEBOV" about.

killed    knockout    overexpression    entire    firstly    strand    flow    sensing    stress    ebov    nonsegmented    characterised    people    approved    transcribed    sensors    replication    vp35biotin    treatment    life    competent    limited    cytoplasmic    interaction    fundamental    proteins    causes    negative    vp35    transcription    depletion    microscopy    cytometric    cas9    biochemical    tested    ligase    virus    trvlps    mutants    counteract    antiviral    unknown    protein    replicated    cycle    acquisition    pkr    treatments    epidemic    trap    viral    trigger    11    image    particles    imagestream    therapeutic    laboratories    secondly    purification    bsl2    polymerase    sg    africa    rna    fever    proximity    western    tagging    automated    proteomic    regulation    gfp    validated    haemorraghic    ebola    inhibits    candidate    infection    reverse    bioid2    filovirus    fusion    interactome    drugs    genetic    vaccines    latter    severe    counteraction    cofactors    granule    pathogenic    crispr    poorly    trvlp    bsl4    rnas    panel    rig    sgs    tetracistronic    genome    co    live    cellular    cell    summary   

Project "StressEBOV" data sheet

The following table provides information about the project.

Coordinator		 KING'S COLLEGE LONDON 

Organization address
address: STRAND
city: LONDON
postcode: WC2R 2LS
website: www.kcl.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
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 Coordinator Country United Kingdom [UK]
 Project website https://www.kcl.ac.uk/lsm/research/divisions/diiid/departments/infectious/research/neil/lab1
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-04-01   to  2019-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON UK (LONDON) coordinator 183˙454.00

Map

 Project objective

Ebola virus (EBOV) is a highly pathogenic filovirus that causes severe haemorraghic fever and killed over 11,000 people during the recent epidemic in Western Africa. Although potential vaccines and drugs are being tested, no treatment has been approved. Therefore, understanding the cellular regulation of EBOV replication is fundamental to develop novel treatments. EBOV is a nonsegmented negative-strand RNA virus for which research is limited to BSL4 laboratories. However, a recent reverse genetic system using tetracistronic transcription- and replication-competent virus-like particles (trVLPs) allows modelling of the entire EBOV life cycle under BSL2 conditions. The EBOV genome is transcribed and replicated by the viral polymerase complex but the regulation of these processes remains poorly characterised. EBOV RNAs can also trigger antiviral responses via cytoplasmic RNA-sensors RIG-I and PKR, the latter also promoting stress granule (SG) formation. While EBOV inhibits RNA-sensing, the impact of SGs on EBOV is unknown. Therefore, I will investigate the role of cellular stress responses on EBOV replication and their potential counteraction by the EBOV VP35 protein using the trVLP system. Firstly, I will analyse the impact of SGs on EBOV replication by overexpression and CRISPR/Cas9 depletion of SG proteins. Using a panel of VP35 mutants, I will also investigate its potential to counteract SGs by automated flow cytometric image acquisition (Imagestream). Secondly, I will identify the EBOV polymerase complex interactome during infection using two distinct proteomic approaches: co-purification with a VP35-GFP fusion protein(GFP-trap) and VP35biotin-ligase proximity tagging (BioID2). Candidate VP35 cofactors will be validated by biochemical interaction, CRISPR-knockout and live cell microscopy to determine their role in EBOV replication. In summary, this project will increase the understanding of EBOV replication and identify new therapeutic targets.

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