Hepatitis C virus production requires apolipoprotein A-I and affects its association with nascent low-density lipoproteins.
type: Distribution
access URL: https://riip.hal.science/pasteur-00980167
format: HTML
issued: 2026-05-05T14:18:18.454953
modified: 2026-05-05T14:18:18.433076

test_moissonnage_selune
type: Agent

Hepatitis C virus production requires apolipoprotein A-I and affects its association with nascent low-density lipoproteins.
type: Dataset
contact point: Organization
  fn: CCSD
keyword: journal-articles
keyword: mesh-adult
keyword: mesh-hepatitis-c
keyword: mesh-virion
keyword: sdvmpvirlife-sciences-q-biomicrobiology-and-parasitologyvirology
keyword: mesh-virus-replication
keyword: mesh-proteomics
keyword: mesh-apolipoprotein-a-i
keyword: mesh-lipoproteins-ldl
keyword: mesh-electrophoresis-gel-two-dimensional
keyword: mesh-female
keyword: mesh-down-regulation
keyword: mesh-humans
keyword: mesh-male
keyword: mesh-middle-aged
keyword: infoeu-reposemanticsarticle
keyword: mesh-hepacivirus
keyword: mesh-case-control-studies
keyword: mesh-cells-cultured
landing page: 0017-5749
description: BACKGROUND/AIMS: The life cycle of hepatitis C virus (HCV) is intimately linked to the lipid metabolism of the host. In particular, HCV exploits the metabolic machinery of the lipoproteins in several steps of its life cycle such as circulation in the bloodstream, cell attachment and entry, assembly and release of viral particles. However, the details of how HCV interacts with and influences the metabolism of the host lipoproteins are not well understood. A study was undertaken to investigate whether HCV directly affects the protein composition of host circulating lipoproteins. METHODS: A proteomic analysis of circulating very low-, low- and high-density lipoproteins (VLDL, LDL and HDL), isolated from either in-treatment naïve HCV-infected patients or healthy donors (HD), was performed using two-dimensional gel electrophoresis and tandem mass spectrometry (MALDI-TOF/TOF). The results obtained were further investigated using in vitro models of HCV infection and replication. RESULTS: A decreased level of apolipoprotein A-I (apoA-I) was found in the LDL fractions of HCV-infected patients. This result was confirmed by western blot and ELISA analysis. HCV cellular models (JFH1 HCV cell culture system (HCVcc) and HCV subgenomic replicons) showed that the decreased apoA-I/LDL association originates from hepatic biogenesis rather than lipoprotein catabolism occurring in the circulation, and is not due to a downregulation of the apoA-I protein concentration. The sole non-structural viral proteins were sufficient to impair the apoA-I/LDL association. Functional evidence was obtained for involvement of apoA-I in the viral life cycle such as RNA replication and virion production. The specific siRNA-mediated downregulation of apoA-I led to a reduction in both HCV RNA and viral particle levels in culture. CONCLUSIONS: This study shows that HCV induces lipoprotein structural modification and that its replication and production are linked to the host lipoprotein metabolism, suggesti…
issued: 2026-05-05T14:18:18.452822
language: en
modified: 2026-05-05T14:18:18.452828