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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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 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.

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

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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