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StressEBOV SIGNED

Ebola virus manipulation of the cellular stress responses

Total Cost €

0

EC-Contrib. €

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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.

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

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.
fax: n.a.
 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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