ALPHA

"Alphavirus-specific mechanisms of OAS/RNAse L pathway inhibition, study of non-structural proteins and search for inhibitors."

Coordinatore	UNIVERSITE D'AIX MARSEILLE    more  Organization address address: Boulevard Charles Livon 58 city: Marseille postcode: 13284 contact info Titolo: Ms. Nome: Celine Cognome: Damon Email: send email Telefono: +334 91 99 85 95
Nazionalità Coordinatore	France [FR]
Totale costo	201˙932 €
EC contributo	201˙932 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2011-IEF
Funding Scheme	MC-IEF
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-07-01   -   2014-06-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE D'AIX MARSEILLE  Organization address address: Boulevard Charles Livon 58 city: Marseille postcode: 13284 contact info Titolo: Ms. Nome: Celine Cognome: Damon Email: send email Telefono: +334 91 99 85 95	FR (Marseille)	coordinator	201˙932.40

Mappa

 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

 Obiettivo del progetto (Objective)

'Emerging and re-emerging Infectious Diseases (EIDs) are defined as 'infections that have newly appeared in a population or have existed previously but are rapidly increasing in incidence or geographic range'. Over the last decades, a number of new emerging diseases, such as HIV/AIDS and SARS, as well as re emerging diseases that increase in incidence or whose geographic range is changing, such as chikungunya or dengue fever, continue to pose a significant threat to populations in Europe and world wide. Some of these EID are caused by the Alphavirus which are emergent arthropod borne viruses with a worldwide distribution. One of the most established antiviral pathways induced by dsRNAs is the Interferon inducible 2’5’ oligoadenylate synthetase (OAS) / endoribonuclease L (RNAse L) system. OAS is activated upon binding to dsRNA and generates, from ATP, short 2’-5’ linked oligoadenylates (2’5’A) which activate a latent RNAse L. RNAse L cleaves ribosomal and viral RNA, inducing apoptosis and blocking viral infection. In turn, viruses developed means to escape the host antiviral response. Studies on Ebola, HCV, Influenza, Vaccinia and HIV showed that viral nsPs can inhibit RNAse L/OAS system through direct binding to one of these enzymes or through the sequestration of dsRNA, 2’5’A or other cellular mediators. However, mechanisms involved in the anti-apoptotic action of several RNA viruses including alphaviruses are unknown. I will unravel the molecular aspects of the viral evasion produced via the inhibition of OAS/ RNAse L pathway by non-structural proteins of alphavirus. Subsequenlty, I will determine the structure and biophysical properties of these nsPs. The ultimate goal is to know which nsPs or subdomains of these proteins are important in the inhibition of OAS/ RNAse L pathway through molecular and cell biology experiments and relate to the structure obtained by crystalography possibiliting the design of future inhibitors targeting these proteins or sub-domains.'