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Hepatitis C virus (HCV) is a major public health challenge throughout the world, and there are estimated to be at least 185 million HCV carriers worldwide. HCV is a highly divergent group of viruses classified in 7 major genotypes and a great number of subtypes, and circulating in infected individuals as a continuously evolving quasispecies destined to escape host immune responses and applied antivirals. Although frequencies of the six HCV genotypes vary geographically, HCV Genotype 1 is the most common genotype worldwide and is among the most difficult to treat with interferon therapy. HCV is both an hepatotropic and a lymphotropic virus; and chronic infection could cause, on one hand, chronic hepatitis, cirrhosis and hepatocellular carcinoma and on the other hand several extrahepatic diseases including, mixed cryoglobulinemia and lymphoma.
Fig. 1. Targeting viral entry for treatment of hepatitis B and C virus infections (ACS Infect. Dis. 2015, 1, 9, 420-427).
Great strides in the understanding of HCV virology enabled the development of direct-acting antiviral agents (DAAs), which have improved the standard of care for chronic HCV infection. These therapies enable the elimination of HCV in most (but not all) patient groups. HCV treatment has markedly progressed with the licensing of direct-acting antivirals (DAAs) for HCV cure, yet limited access for the majority of patients is a major challenge. Advances in the understanding of HCV entry revealed it to be a complex process involving many factors, offering several antiviral targets. These include viral envelope proteins E1 and E2, virion-associated lipoprotein ApoE, and cellular factors CD81, SRBI, EGFR, claudin-1, occludin, and the cholesterol transporter NPC1L1. Small molecules targeting SR-BI, EGFR, and NPC1L1 have entered clinical trials, whereas other viral- and host-targeted small molecules, peptides, and antibodies show promise in preclinical models.
As with all viruses, HCV depends on host proteins for viral entry, uncoating, replication, virion assembly and egress. Thus, host-targeting antivirals provide a promising approach for anti-HCV therapeutic development. Indeed, targeting these host cofactors may impose a higher barrier to viral resistance and also offer pan-genotypic coverage of all HCV genotypes and serotypes. More importantly, as certain host molecules are necessary for both virus replication and virus-induced host pathogenesis, host-targeting antivirals may yield anti-HCV therapies that both halt HCV replication and abrogate the other pathogenic effects of HCV. As a natural compound extracted from Phellodendron chinense, γ-Fagarine shows the most potent inhibitory activities on HCV with IC₅₀ values being 20.4 ± 0.4 μg/ml.