Abstract
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.
Highlights
Hepatitis C virus (HCV) infection is a major world health problem; it has a prevalence of about 2 %, representing 130–170 million infected people worldwide (Shepard et al, 2005)
Since lipoproteins associated with virus particles are essential for lipoprotein lipase (LPL)-mediated virus uptake, these observations suggest that LPL could be a natural modulator of HCV infectivity in vivo and that the LPL effect could depend on the composition of virus-associated lipoproteins
Available data suggest that HCV cell entry is a multi-step process requiring a set of entry molecules
Summary
Hepatitis C virus (HCV) infection is a major world health problem; it has a prevalence of about 2 %, representing 130–170 million infected people worldwide (Shepard et al, 2005). Virus entry is defined as the steps from particle binding to the host cell up to the delivery of the viral genome to its replication site within the target cell, which, in the case of HCV, is the human hepatocyte. This process relies on specific interactions between virus components, mainly envelope proteins and multiple cellular factors. Recent advances in cell culture models have significantly contributed to our understanding of the molecular virology of HCV infection, in particular the entry steps. We will briefly summarize the main model systems used to study HCV cell entry
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