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Review
. 2009 Jan 1;14(9):3274-85.
doi: 10.2741/3450.

Hepatitis C virus entry: molecular mechanisms and targets for antiviral therapy

Mirjam B Zeisel  1 , Heidi Barth, Catherine Schuster, Thomas F Baumert
Affiliations
Review

Hepatitis C virus entry: molecular mechanisms and targets for antiviral therapy

Mirjam B Zeisel et al. Front Biosci (Landmark Ed). .

Abstract

With an estimated 170 million infected individuals, hepatitis C virus (HCV) has a major impact on public health. The liver is the primary target organ of HCV, and the hepatocyte is its primary target cell. Attachment of the virus to the cell surface followed by viral entry is the first step in a cascade of interactions between the virus and the target cell that is required for successful entry into the cell and initiation of infection. Using recombinant HCV envelope glycoproteins and HCV pseudotype particles, several cell surface molecules have been identified interacting with HCV during viral binding and entry. These include CD81, highly sulfated heparan sulfate, the low-density lipoprotein receptor, scavenger receptor class B type I and claudin-1. Treatment options for chronic HCV infection are limited and a vaccine to prevent HCV infection is not available. Interfering with HCV entry holds promise for drug design and discovery as the understanding of molecular mechanisms underlying HCV interaction with the host cell is advancing. The complexity of the virus entry process offers several therapeutic targets.

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Figures

Fig. 1
Fig. 1. HCV entry: targets for antiviral therapy
Both virus and host cell components involved in virus entry may serve as targets for the development of HCV entry inhibitors. Viral entry may be inhibited (1) by blocking interaction between the virus and the target cell, (2) by interfering with post binding events, and (3) by interfering with viral fusion. Future anti-HCV therapies might be combinations of drugs targeting distinct steps of HCV infection, i. e. entry inhibitors, protease inhibitors and polymerase inhibitors that might have complementary effects and delay the emergence of drug resistance.
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