CARDIOVIR

Molecular mechanisms and cellular consequences of enterovirus persistence in cardiomyocytes

Coordinatore	UNIVERSITE DE REIMS CHAMPAGNE-ARDENNE    more  Organization address address: BOULEVARD DE LA PAIX 9 VILLA DOUCE city: REIMS postcode: 51100 contact info Titolo: Ms Nome: Nathalie Cognome: Rau Email: send email Telefono: 33326913995 Fax: 33326918714
Nazionalità Coordinatore	France [FR]
Totale costo	156˙863 €
EC contributo	156˙863 €
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-2013-IOF
Funding Scheme	MC-IOF
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-03-01   -   2016-08-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE DE REIMS CHAMPAGNE-ARDENNE  Organization address address: BOULEVARD DE LA PAIX 9 VILLA DOUCE city: REIMS postcode: 51100 contact info Titolo: Ms Nome: Nathalie Cognome: Rau Email: send email Telefono: 33326913995 Fax: 33326918714	FR (REIMS)	coordinator	156˙863.40

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 Obiettivo del progetto (Objective)

'Enteroviruses (EV) are small naked single-stranded positive RNA viruses of approximately 7,400 nucleotides. Their genome is flanked on the 5' end by a non-coding region (NCR), which is crucial for the initiation of the replication and translation of the viral genome. Enteroviruses are common human pathogens, transmitted through fecal-oral and respiratory routes. Although the majority of EV infections remain asymptomatic, these viruses, especially group B coxsackieviruses (CVB), are considered to be a common cause of acute myocarditis in children and young adults, a disease which is a precursor to 10-20% of chronic myocarditis cases as well as dilated cardiomyopathy (DCM, prevalence = 7 cases / 100,000, second leading cause of heart transplantation worldwide after ischemic heart disease). However, the viral molecular mechanisms involved in the progression of acute myocarditis to chronic myocarditis and subsequently to DCM are currently poorly understood, thereby limiting the development of new specific therapeutic strategies. In 2011, our research team (EA-4684 CardioVir/FRS CAP-santé, University of Reims Champagne-Ardenne) reported CVB strains presenting with genomic 5’ terminal deletions ranging in size from 15 to 35 nucleotides in explanted heart tissue collected from patients suffering from idiopathic DCM. These deletions could explain how the virus can persist in the heart long after the acute infection leading to the development of chronic cardiomyopathies. The objectives of this proposal are to determine the mechanisms by which deleted EV ensure the translation and replication of their genomes and to assess the effects of persistent infection on the structures and functions of infected cardiac myocytes. A better understanding of the molecular mechanisms implicated in viral persistence will stimulate the research into new therapeutic strategies to prevent and treat chronic infections caused by EV.'