Semin Liver Dis 2005; 25(1): 93-104
DOI: 10.1055/s-2005-864785
Copyright © 2005 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Hepatitis C Virus Particles and Lipoprotein Metabolism

Patrice André1 , Gabriel Perlemuter2 , Agata Budkowska3 , Christian Bréchot4 , Vincent Lotteau5
  • 1Professeur, INSERM, Lyon, France
  • 2INSERM Avenir, Clarmart, France
  • 3Chef de laboratoire, Unité des Hepacivirus, Institut Pasteur, Paris, France
  • 4Professeur, Unité Mixte Pasteur/INSERM, Faculté de Médecine Necker Enfants malades, Paris, France
  • 5Directeur de Recherche, INSERM, Lyon, France
Further Information

Publication History

Publication Date:
25 February 2005 (online)

ABSTRACT

The majority of infectious hepatitis C particles are present in the low-density fractions from plasma of infected patients, suggesting an association of the virus with lipoproteins and the use of lipoprotein receptors for cell entry. Although classical hepatitis C virus (HCV) virions have been reported by some investigators, their role in the HCV life cycle has not been clearly identified. Moreover, two other forms of particles have been characterized: low-density lipo-viro-particles (LVPs) and high-density particles. The latter are nonenveloped nucleocapsids that have immunoglobulin G Fcγ binding capacity. LVPs are spherical particles enriched in triglycerides. At a minimum, they contain apolipoprotein B, HCV RNA, and core protein. The main source of LVPs is likely to be the enterocytes rather than the hepatocytes, suggesting an interaction between chylomicron and LVP assembly. In experimental systems, HCV core protein inhibits the microsomal triglyceride transfer protein, binds to apolipoprotein AII, and induces accumulation of cytoplasmic lipid droplets. A model of LVP and HCV core-lipid droplet generation is proposed.

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Patrice AndréM.D. 

Professeur, INSERM U503, IFR 128 Biosciences Lyon Gerland

21 avenue Tony Garnier, 69365 Lyon cedex 07, France

Email: andre@cervi-lyon.inserm.fr