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HIV B Cell Function SIGNED

Understanding HIV-specific B cell function and viral immunogenicity

Total Cost €

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EC-Contrib. €

0

Partnership

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 HIV B Cell Function project word cloud

Explore the words cloud of the HIV B Cell Function project. It provides you a very rough idea of what is the project "HIV B Cell Function" about.

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Project "HIV B Cell Function" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITY COLLEGE LONDON 

Organization address
address: GOWER STREET
city: LONDON
postcode: WC1E 6BT
website: n.a.

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]
 Total cost 1˙499˙269 €
 EC max contribution 1˙499˙269 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-STG
 Funding Scheme ERC-STG
 Starting year 2018
 Duration (year-month-day) from 2018-06-01   to  2023-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON UK (LONDON) coordinator 1˙499˙269.00

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 Project objective

I will establish how abnormal B cell behaviour contributes to the generation of HIV neutralising antibodies by studying B cell biology: Previous studies show that broadly neutralising HIV antibodies are the most highly-mutated human antibodies ever isolated, with unusually long binding loops and polyreactivity, suggestive of changes to B cell tolerance and germinal centre selection mechanisms. These remarkable antibodies develop only during HIV infection, concurrent with immune dysfunction, not following vaccination. Crucially, the cellular processes whereby these antibodies arise need to be elucidated and I hypothesize that doing so using RNAseq, flow cytometry and imaging B cell activation will answer why only a minority of HIV individuals develop neutralization breadth. Moreover, B cell dysfunction is associated to a range of malignancies and autoimmune diseases and, while much has been learnt from model antigens in mouse models, HIV infection provides a uniquely well-characterised human model to study B cell regulation. Another fundamental question is whether strain-specific antibodies are a stepping-stone to breadth, or a detour that must be eliminated in vaccination. I have shown that the best serum neutralization activity induced via stabilized HIV envelope protein immunization predominantly targets a strain-specific glycan hole, similar to many early responses observed in infection before broad neutralising activity develops. Therefore, I will determine whether non-neutralising and strain-specific antibodies affect the development of breadth by isolating a range of antibodies raised during viral infection from individual donors and comparing binding affinities, clonal ontogenies and B cell receptor activation. Defining the impact of competition between antibody specificities during HIV infection will be directly translatable to developing vaccines for other pathogens where cross-reactivity is a key factor such as Influenza, Dengue and Zika viruses.

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