Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 14, Pages 5848-5853Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0700760104
Keywords
apolipoprotein B; microsomal triglyceride; transfer protein
Categories
Funding
- NHLBI NIH HHS [P01 HL020948, HL-20948] Funding Source: Medline
- NIAID NIH HHS [AI-060389, R01 AI060389, R56 AI060389] Funding Source: Medline
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Hepatitis C virus (HCV) and triglyceride-rich very low-density lipoproteins (VLDLs) both are secreted uniquely by hepatocytes and circulate in blood in a complex. Here, we isolated from human hepatoma cells the membrane vesicles in which HCV replicates. These vesicles, which contain the HCV replication complex, are highly enriched in proteins required for VLDL assembly, including apolipoprotein B (apoB), apoE, and microsomal triglyceride transfer protein. in hepatoma cells that constitutively produce infectious HCV, HCV production is reduced by two agents that block VLDL assembly: an inhibitor of microsomal triglyceride transfer protein and siRNA directed against apoB. These results provide a possible explanation for the restriction of HCV production to the liver and suggest new cellular targets for treatment of HCV infection.
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