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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.008300-0
Journal of General Virology 2009;90:1055.

A more recent version of this article appeared on May 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.008300-0
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Hepatitis C virus cell entry: role of lipoproteins and cellular receptors

Michela E. Burlone1 and Agata Budkowska2,3

1 University of Eastern Piedmont 'A. Avogadro', Department of Clinical and Experimental Medicine,;
2 Pasteur Institute, Hepacivirus and Innate Immunity

3 E-mail: 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 Flaviviridae family. HCV cell entry is a multi-step process, involving several viral and cellular factors triggering virus uptake into the hepatocyte. Tetraspanin CD81, human scavenger receptor SR-BI, and tight junction molecules Claudin-1 and occludin are main receptors mediating HCV entry. In addition, virus may use glycosaminoglycans and/or low density receptor 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 VLDL. 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 in the initiation of infection. This review summarises the current knowledge about HCV receptors, mechanisms of HCV cell entry and the role of lipoproteins involved in this process.

Received 28 October 2008; accepted 19 February 2009.




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