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CARDIOVIR: Molecular mechanisms and cellular consequences of enterovirus persistence in cardiomyocytes.

Total cost: EUR 156 863,4

EU contribution: EUR 156 863,4

Topic(s):FP7-PEOPLE-2013-IOF - Marie Curie Action: "International Outgoing Fellowships for Career Development"

Subjects : Life Sciences

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-sant, 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.




EU contribution: EUR 156 863,4



Participation ended



51100 REIMS


Administrative contact: Nathalie Rau

Tel.: +33326913995

Fax: +33326918714

Project completion date : 2016-08-31 12:00:00

Major organization : UNIVERSITE DE POITIERS

Address : Rue De L Hotel Dieu 15 Hotel Pinet

86034 Poitiers Cedex

Country :France

Url :

Financier : European Union (EU),

Financier address : European Union (EU)

Rue de la Loi 200/Wetstraat 200,

B-1049 Bruxelles/Brussels,


Tel: 32-2-2999696, 2993085

Fax: 32-2-2961749


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Publication:Mena Report
Date:Feb 16, 2016
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