Hepatitis C virus and host liver-related pathways (HCV-Host Pathways)

The Hepatitis C virus (HCV) and host liver-related pathways represent the integrated biological network involved in the viral life cycle and the resulting hepatic pathology [1]. HCV is a member of the Flaviviridae family that exploits host liver-specific factors, such as the microRNA miR-122 and the chaperone protein cyclophilin A, to facilitate its entry, RNA replication, and assembly [2, 5]. The viral genome encodes a polyprotein that is processed into structural and non-structural proteins, including the NS3/4A protease, NS5A protein, and NS5B RNA-dependent RNA polymerase, which serve as the primary targets for direct-acting antiviral (DAA) therapy [1, 4]. Chronic activation of these pathways leads to persistent inflammation, oxidative stress, and metabolic dysregulation within the liver, often progressing to cirrhosis and hepatocellular carcinoma [3]. Therapeutic intervention aims to disrupt these viral-host interactions to achieve a sustained virologic response (SVR), effectively curing the infection [4]. However, the complexity of these pathways necessitates careful consideration of drug-drug interactions and the potential for viral resistance [1]. Sources: [1] Manns, M. P., et al. (2017) Nature Reviews Disease Primers; [2] Lindenbach, B. D., & Rice, C. M. (2013) Springer; [3] NIH/NIDDK (2023) Hepatitis C; [4] Feld, J. J., & Foster, G. R. (2016) Journal of Hepatology; [5] Janssen, H. L., et al. (2013) NEJM.

Other names

HCV-host interactomeHepatitis C viral replication pathwaysHCV infection machineryHCV-host cell interactions

Inhibition of viral NS3/4A protease, NS5A replication complex, and NS5B polymerase; modulation of host factors like miR-122 and cyclophilin A to disrupt the viral life cycle.