CARDIOVIR

Molecular mechanisms and cellular consequences of enterovirus persistence in cardiomyocytes

 Coordinatore 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

 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

Mappa


 Word cloud

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

heart    dcm    chronic    mechanisms    infections    genome    viruses    ev    strategies    deletions    disease    molecular    acute    myocarditis    therapeutic    cvb    nucleotides    enteroviruses    replication    infection    viral    translation   

 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.'

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