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Originally published as JGV in Press, 10.1099/vir.0.008300-0 on March 4, 2009 J Gen Virol 90 (2009), 1055-1070; DOI 10.1099/vir.0.008300-0

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Review

Hepatitis C virus cell entry: role of lipoproteins and cellular receptors

Michela E. Burlone1,2 and Agata Budkowska1

1 Pasteur Institute, Hepacivirus and Innate Immunity, 25/28 Rue du Dr Roux, 75724 Paris Cedex 15, France
2 University of Eastern Piedmont ‘A. Avogadro’, Department of Clinical and Experimental Medicine, Via Solaroli 17, 28100 Novara, Italy

Correspondence
Agata Budkowska
agata.budkowska{at}pasteur.fr

Hepatitis C virus (HCV), a major cause of chronic liver disease, is a single-stranded positive sense virus of the family Flaviviridae. HCV cell entry is a multi-step process, involving several viral and cellular factors that trigger virus uptake into the hepatocyte. Tetraspanin CD81, human scavenger receptor SR-BI, and tight junction molecules Claudin-1 and occludin are the main receptors that mediate HCV entry. In addition, the virus may use glycosaminoglycans and/or low density receptors on host cells as initial attachment factors. A unique feature of HCV is the dependence of virus replication and assembly on host cell lipid metabolism. Most notably, during HCV assembly and release from the infected cells, virus particles associate with lipids and very-low-density lipoproteins. Thus, infectious virus circulates in patient sera in the form of triglyceride-rich particles. Consequently, lipoproteins and lipoprotein receptors play an essential role in virus uptake and the initiation of infection. This review summarizes the current knowledge about HCV receptors, mechanisms of HCV cell entry and the role of lipoproteins in this process.






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