Extracellular lipid-free apolipoprotein E inhibits HCV replication and induces ABCG1-dependent cholesterol efflux.
Fiche publication
Date publication
mai 2017
Journal
Gut
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas, Dr CROUCHET Emilie, Dr VERRIER Eloi
Tous les auteurs :
Crouchet E, Lefèvre M, Verrier ER, Oudot MA, Baumert TF, Schuster C
Lien Pubmed
Résumé
The HCV life cycle and the lipid metabolism are inextricably intertwined. In the blood, HCV virions are associated with lipoproteins, forming lipoviroparticles (LVPs), which are the most infectious form of the virus. Apolipoprotein E (apoE), a key LVP component, plays an essential role in HCV entry, assembly and egress. ApoE is also a cell host factor involved in lipoprotein homeostasis. Although the majority of apoE is associated with lipoproteins, a lipid-free (LF) form exists in blood. However, the role of LF-apoE in both lipid metabolism and HCV life cycle is poorly understood.
Mots clés
ATP Binding Cassette Transporter, Sub-Family G, Member 1, metabolism, Apolipoprotein A-I, biosynthesis, Apolipoproteins E, metabolism, Cell Line, Tumor, Cholesterol, metabolism, Dose-Response Relationship, Drug, Hepacivirus, growth & development, Hepatocytes, metabolism, Humans, Life Cycle Stages, drug effects, Lipoproteins, HDL, biosynthesis, Membrane Microdomains, Virus Internalization, Virus Replication, drug effects
Référence
Gut. 2017 05;66(5):896-907