Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteins

Hua Huang, Fang Sun, David M. Owen, Weiping Li, Yan Chen, Michael Gale, Jin Ye

Research output: Contribution to journalArticle

396 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)5848-5853
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number14
Publication statusPublished - Apr 3 2007



  • Apolipoprotein B
  • Microsomal triglyceride transfer protein

ASJC Scopus subject areas

  • Genetics
  • General

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