LIPOHCV
HEPATITIS C VIRUS AND HOST LIPOPROTEIN METABOLISM
| Coordinatore | AGENCIA ESTATAL CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS
Organization address
address: CALLE SERRANO 117 contact info |
| Nazionalità Coordinatore | Spain [ES] |
| 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-2011-CIG |
| Funding Scheme | MC-CIG |
| Anno di inizio | 2011 |
| Periodo (anno-mese-giorno) | 2011-09-01 - 2015-08-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
AGENCIA ESTATAL CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS
Organization address
address: CALLE SERRANO 117 contact info |
ES (MADRID) | coordinator | 100˙000.00 |
Mappa
Word cloud
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
Obiettivo del progetto (Objective)
'Over 3% of the world population is chronically infected by the hepatitis C virus (HCV). Chronic infection is associated with liver disease that leads to fibrosis and cirrhosis and ultimately to hepatocellular carcinoma (HCC). There is no vaccine for HCV and the current treatment is only partially effective and toxic. Consequently, HCV infection is one of the leading causes of liver transplantation worldwide. HCV depends heavily on cellular lipid and lipoprotein metabolism to replicate and produce infectious particles. This dependence coincides with the fact that chronic HCV infection is associated with alterations of the liver lipid metabolism. These alterations are manifested by abnormal accumulation of lipids in hepatocytes (steatosis) in a significant proportion of the patients. In patients responding to interferon treatment, steatosis subsides as the viral titers decrease, suggesting that HCV replication and viral protein expression are a major determinant for these alterations. However, little is known about the molecular mechanisms underlying the interference of HCV infection with lipid metabolism. Understanding how HCV exploits the cellular lipid and lipoprotein biosynthetic machinery might contribute to understanding important aspects of the pathogenesis of chronic HCV infection. In this application, we propose to use a cell culture HCV infection model that we recently developed to study the intersection of cellular lipid and lipoprotein metabolism with basic aspects of HCV infection.'