HSV-1 BOTTLENECK

Herpes simplex virus-1 bottleneck during genome replication

 Coordinatore TEL AVIV UNIVERSITY 

 Organization address address: RAMAT AVIV
city: TEL AVIV
postcode: 69978

contact info
Titolo: Ms.
Nome: Lea
Cognome: Pais
Email: send email
Telefono: 97236408774
Fax: 97236409697

 Nazionalità Coordinatore Israel [IL]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-2012-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-03-01   -   2017-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    TEL AVIV UNIVERSITY

 Organization address address: RAMAT AVIV
city: TEL AVIV
postcode: 69978

contact info
Titolo: Ms.
Nome: Lea
Cognome: Pais
Email: send email
Telefono: 97236408774
Fax: 97236409697

IL (TEL AVIV) coordinator 100˙000.00

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mutations    infection    viral    replication    bottleneck    herpesvirus    genomes   

 Obiettivo del progetto (Objective)

'Infection with herpes simplex virus-1 (HSV-1) can lead to diverse outcomes ranging from asymptomatic infection to life threatening encephalitis. Emergence of drug resistant viral isolates, leading to treatment failure, is caused by rapid generation of mutations. For DNA viruses (such as herpesviruses) it is assumed that recombination and complementation can provide important mechanisms for generating and maintaining genome diversity. We therefore suggest that the phenomenon (We recently identified) that only a limited number of incoming herpesvirus genomes are able to initiate expression and replication, may have a role in regulating the number of mutations. In the proposed project we will characterize this bottleneck mechanism in order to test this hypothesis. We will identify the steps in the infection process in which this bottleneck occurs. We will find host and viral proteins that regulate the number of viral genomes being expressed and replicated. Finally, we will develop methods for testing the evolutionary benefits of this bottleneck. This project will uncover new regulatory elements involved in herpesvirus replication and may, as well, reveal more general concepts in virology.'

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