An in vitro model of hepatitis C virus genotype 3a-associated triglycerides accumulation

Karim Abid, Valerio Pazienza, Andrea De Gottardi, Laura Rubbia-Brandt, Beatrice Conne, Paolo Pugnale, Christine Rossi, Alessandra Mangia, Francesco Negro

Research output: Contribution to journalArticlepeer-review


Background/Aims: The hepatitis C virus (HCV) induces lipid accumulation in vitro and in vivo. Although clinical observations are consistent with a direct effect of HCV genotype 3a on lipid metabolism, experimental systems have focused on the expression of HCV proteins of genotype 1. To extend these observations, we established an in vitro model expressing the HCV core of different genotypes. Methods: The HCV core protein from patients with severe (genotype 3a) or no (genotypes 1b, 2a, 3h, 4h and 5a) liver steatosis was expressed in Huh7 cells. Core protein expression (by immunohistochemistry and immunoblot) and triglycerides accumulation (by Oil Red O stain and enzymatic measurement) were evaluated 48 h after transfection. Results: Although triglyceride accumulation occurred with genotypes 1b, 3a and 3h, the genotype 3a core protein expression resulted in the highest level of accumulation (i.e. about 3-fold with respect to 1b, and 2-fold with respect to 3h). This effect was not related to core protein expression levels and was abolished by culturing cells in lipid-free medium. Conclusions: Consistent with observations in chronic hepatitis C patients, the in vitro expression of HCV genotype 3a core protein is the ideal candidate model for studying the mechanisms of HCV-associated steatosis.

Original languageEnglish
Pages (from-to)744-751
Number of pages8
JournalJournal of Hepatology
Issue number5
Publication statusPublished - May 2005


  • Chronic hepatitis
  • Genotypes
  • Hepatitis C virus
  • Liver fibrosis
  • Steatosis

ASJC Scopus subject areas

  • Gastroenterology


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