SUMOFLU

Interplay between influenza viruses and host SUMO pathways

Coordinatore	UNIVERSITAET ZUERICH    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Switzerland [CH]
Totale costo	1˙482˙452 €
EC contributo	1˙482˙452 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2013-StG
Funding Scheme	ERC-SG
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-02-01   -   2019-01-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITY OF GLASGOW  Organization address address: University Avenue city: GLASGOW postcode: G12 8QQ contact info Titolo: Mr. Nome: Joseph Cognome: Galloway Email: send email Telefono: +44 141 330 3884 Fax: +44 141 330 5611	UK (GLASGOW)	beneficiary	0.00
2	UNIVERSITAET ZUERICH  Organization address address: Raemistrasse 71 city: ZURICH postcode: 8006 contact info Titolo: Dr. Nome: Benjamin Cognome: Hale Email: send email Telefono: +41 44 634 2899 Fax: +41 44 634 4967	CH (ZURICH)	hostInstitution	1˙482˙452.00
3	UNIVERSITAET ZUERICH  Organization address address: Raemistrasse 71 city: ZURICH postcode: 8006 contact info Titolo: Ms. Nome: Monika Cognome: Wiget Email: send email Telefono: +41 44 634 5350	CH (ZURICH)	hostInstitution	1˙482˙452.00

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 Obiettivo del progetto (Objective)

'Influenza viruses cause a significant seasonal disease burden and continually threaten to initiate human pandemics. Antivirals are available for treatment of influenza, however drug-resistant viruses often emerge. Thus, there is urgent need to develop new antivirals with lower chances of selecting resistance. As viruses rely extensively on cellular functions, one way to minimise resistance is to target new antivirals against host factors. This concept requires a fundamental understanding of mechanisms underpinning the interplay between influenza viruses and their hosts.

In this project, we will investigate the role that host SUMO pathways play during influenza virus replication. SUMO proteins are important regulators of cell signalling, and are covalently linked to other proteins in order to alter structure, localization or function. As such, SUMO conjugation regulates many diverse aspects of biology. Our own work shows that global cellular SUMOylation increases during influenza virus infection, and that virus replication is severely impaired when cells are depleted of key enzymes and components required for general SUMO conjugation. Here, we will determine what viral components trigger SUMOylation, and which specific cellular enzymes are involved. We will characterize where in the cell SUMO conjugates accumulate, and for the first time apply large-scale affinity-based quantitative proteomics to the identification of proteins that become SUMO modified during infection. A key aim will be to correlate changes to the SUMO sub-proteome with the function of specific host SUMO-modifying enzymes, thereby establishing the mechanistic role of these modifications during virus replication.

Understanding basic mechanisms underlying SUMOylation during influenza virus infection will provide new insights into the fundamental biology of these important pathogens. The work could also lead to identification of key cellular pathways that can be exploited as novel therapeutic targets'