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HGB-StIC SIGNED

Human Genetic Basis of Severe Staphylococcal Infections in Childhood

Total Cost €

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EC-Contrib. €

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Partnership

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Project "HGB-StIC" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITAIR MEDISCH CENTRUM UTRECHT 

Organization address
address: HEIDELBERGLAAN 100
city: UTRECHT
postcode: 3584 CX
website: www.umcutrecht.nl

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 Netherlands [NL]
 Total cost 260˙929 €
 EC max contribution 260˙929 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-GF
 Starting year 2019
 Duration (year-month-day) from 2019-01-01   to  2021-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAIR MEDISCH CENTRUM UTRECHT NL (UTRECHT) coordinator 260˙929.00
2    THE ROCKEFELLER UNIVERSITY NOT FOR PROFIT CORPORATION US (NEW YORK) partner 0.00

Map

 Project objective

Staphylococcus aureus is one of the most important bacterial pathogens impacting human health. Beta-barrel pore-forming toxins (BB-PFTs) are major virulence factors of S. aureus that destroy phagocytes, key effectors of immunity during staphylococcal infection, in a receptor-specific manner. Acquired immunity to a specific compound of S. aureus, LTA, can rescue an inborn error of the TLR2 pathway (TIRAP deficiency). I hypothesize that severe staphylococcal infections during childhood, at least in some patients, can result from single gene inborn errors of immunity. Some of these disorders may affect immunity to BB-PFTs and the TLR2 pathway. In this project, a cohort of ±70 patients with severe S. aureus infections during childhood will be investigated for mutations responsible for a poor outcome of infection. I will perform whole exome sequencing in these patients and their parents. I will search for mutations in genes encoding BB-PFT-receptors and the TLR2 pathway. I will also search for mutations in a genome-wide approach, testing various genetic models and taking advantage, when appropriate, of genome-wide linkage. I will then functionally characterize the candidate mutations. Depending on the gene identified, a set of experiments will be performed to investigate the functional consequences of the morbid gene on immunity against S. aureus, and I will further characterize the specific host-pathogen interaction. This project will not only shed light on the pathogenesis of S. aureus, but will also provide the basis for new avenues of vaccine and treatment strategies. By investigating human host counterparts in a genome-wide setting, this study is the first unbiased and systematic assessment linking S. aureus virulence factors with host genetic predisposition.

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The information about "HGB-STIC" are provided by the European Opendata Portal: CORDIS opendata.

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