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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/E416    most recent 00091.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Petit, J.-M. Articles by Hillon, P. Search for Related Content PubMed PubMed Citation Articles by Petit, J.-M. Articles by Hillon, P.

Cell surface expression of LDL receptor in chronic hepatitis C: correlation with viral load

¹Institut National de la Santé et de la Recherche Médicale CRI-866, ²Services de Diabétologie et Endocrinologie, and ³Laboratoire de Virologie, Dijon, France

Submitted 8 February 2007 ; accepted in final form 25 April 2007

The LDL receptor (LDL-R) has been proposed as the viral receptor for Hepatitis C virus (HCV). This hypothesis has been based exclusively on in vitro studies. In human mononuclear cells, LDL-R gene expression has been demonstrated to be parallel and be coordinately regulated to gene expression in the human liver. The purpose of the current study was to determine the mononuclear cell surface expression of the LDL receptor in patients with HCV chronic infection according to viral load. Sixty-eight consecutive untreated chronic hepatitis C patients were studied to determine the mononuclear cell surface expression of the LDL-R. LDL-Rs were quantified at the surface of mononuclear cells in fresh blood samples taken after fasting using flow cytometry. LDL-R expression was significantly associated with LDL-cholesterol (r = –0.25; P = 0.03) and HCV-viral load (r = 0.37, P = 0.002). In multivariate analysis, the LDL-R expression was significantly associated with HCV viral load, whereas genotype, age, body mass index, and fibrosis were not. In conclusion, our data provided by a human study, suggest that the LDL-R may be one of the receptors implicated in HCV replication.

fibrosis; lipoproteins; cytometry