Hepatitis C virus entry and replication interfaces (HCV entry/replication interfaces)

The Hepatitis C virus (HCV) entry and replication interfaces encompass the molecular interactions between viral proteins and host factors necessary for infection and viral production (Lindenbach & Rice, 2013, Nature). Entry is a multi-step process involving the viral E1/E2 envelope glycoproteins and host receptors such as CD81, scavenger receptor class B type I (SR-BI), Claudin-1, and Occludin (Ding et al., 2014, Journal of Virology). Once inside, the viral RNA is replicated within a specialized membrane-associated structure called the membranous web by the replication complex, which includes the NS3/4A protease, NS5A phosphoprotein, and NS5B RNA-dependent RNA polymerase (Moradpour & Penin, 2013, Cold Spring Harbor Perspectives in Medicine). These interfaces are the primary targets for direct-acting antivirals (DAAs), which have transformed HCV from a chronic condition to a curable one (Manns et al., 2017, Nature Reviews Disease Primers). Drugs like Sofosbuvir and Velpatasvir work by binding to these viral proteins, effectively halting the viral life cycle (FDA, 2016, Epclusa Label). Understanding these interfaces is crucial for overcoming drug resistance, which often arises from mutations at the drug-binding sites within these protein complexes (Pawlotsky, 2016, Gastroenterology).

Other names

HCV entry factorsHCV replication complexHCV protein-protein interactionsHCV host-cell interfacesHCV membranous web

Inhibition of NS3/4A serine protease, NS5A protein (replication complex assembly), and NS5B RNA-dependent RNA polymerase; blockade of viral entry receptors.