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. 2015 Jan 12;2(1):35–45. doi: 10.1016/j.gendis.2015.01.001

Figure 1.

Figure 1

Anti-HCV drugs targeting viral life cycle. (1) HCV viral particle interacts with several entry factors such as, SR-B1, CD81, CLDN1 and OCLN to enter the hepatocytes. Entry inhibitor, ITX-5061 inhibits the uptake of viral particles through SR-B1. (2) Once inside the cell, virus releases its genome by the process of uncoating. (3) The viral RNA is translated and the resulting polyprotein is processed at the endoplasmic reticulum. NS3/4A protease inhibitors inhibit viral protein synthesis and impair interferon signaling pathway. (4) Replication takes place in ER-derived membrane compartment, called as membranous web composed of single-, double-, multi-membraned vesicles and lipid droplets. miR-122 binding to viral genome enhances viral replication and translation. Drugs targeting NS5A and NS5B block viral replication. CypA interacts with NS5A and required for viral replication. Nucleocapsid is formed after interaction of core and NS5A protein with lipid droplets. The p7, NS2 and NS3-NS4A proteins are also involved in coordination of virus assembly. (5) HCV virion morphogenesis is coupled to the very-low density lipoproteins (VLDL) secretory pathway, and virus particles are released as lipoviroparticles (LVPs). Viral proteins and host factors that are the targets of direct-acting antivirals (DAAs) in advanced clinical development are indicated in the legend. CLDN1, claudin 1; CypA, cyclophilin A; miR, microRNA; OCLN, occludin; SR-B1, scavenger receptor class B member 1; LD, lipid droplets.