FIGURE 2 | Potential targets for antiviral intervention in the HCV life cycle and their location in the HCV genome.

From the following article:

The way forward in HCV treatment — finding the right path

Michael P. Manns, Graham R. Foster, Jürgen K. Rockstroh, Stefan Zeuzem, Fabien Zoulim & Michael Houghton

Nature Reviews Drug Discovery 6, 991-1000 (December 2007)

doi:10.1038/nrd2411

The way forward in HCV treatment |[mdash]| finding the right path

Hepatitis C virus (HCV) is a single-stranded RNA virus belonging to the Flaviviridae family75. a | Genomic organization of proteins encoded by HCV, comprising the structural proteins core (C), envelope 1 (E1), envelope 2 (E2), and P7 (presumed to be an ion channel) and the non-structural proteins (NS2, NS3, NS4A, NS4B, NS5A and NS5B), which are mainly enzymes essential to the viral life cycle. b | The nucleocapsid of the HCV genome is surrounded by an envelope that facilitates attachment and penetration into host cells. Upon enty into the host cell by endocytosis, the virus undergoes a fusion and uncoating step. Its RNA genome is translated into a polyprotein of approximately 3,000 amino acids5, that is processed by cellular and viral proteases (including NS3) to yield four structural and six non-structural proteins50. The non-structural protein NS5B, a RNA-dependent RNA polymerase, catalyses the replication of the viral genome; negative-strand RNA intermediates are formed, which, in turn, serve as templates for the synthesis of new positive-strand RNAs. These are either encapsulated to form new viruses or used as mRNA for viral protein synthesis. The newly formed viral particles are released by exocytosis97. Each HCV structure represents a potential antiviral target for drug and vaccine development46, 98. For example, protease inhibitors target the NS3/4 protease, which is essential for viral polyprotein processing; polymerase inhibitors target the NS5B RNA-dependent RNA polymerase, which is essential for viral RNA replication; cyclophilin inhibitors block cyclophilin-induced stimulation of RNA-binding activity of NS5B; and alpha-glucosidase inhibitors block the action of a host enzyme required for viral assembly, release and infectivity. Examples of drugs that are or have been in clinical development are included. Fig. 1b modified with permission from Nature Ref. 99 © (2005) Macmillan Publishers Ltd.

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