Hepatitis C virus replication and host antiviral pathways (HCV-Host Pathways)

Hepatitis C virus (HCV) replication and host antiviral pathways represent the dynamic interaction between the viral life cycle and the human innate immune system [Horner & Gale, Nature Medicine, 2013]. The virus utilizes host cell machinery to replicate its positive-sense RNA genome within specialized cytoplasmic compartments called membranous webs, primarily involving the NS3/4A protease, NS5A protein, and NS5B polymerase [Moradpour & Penin, 2013; UniProt P26664]. Host cells recognize viral infection through pattern recognition receptors like RIG-I and TLR3, which trigger signaling cascades to produce type I and III interferons [NCBI, 2020]. HCV has evolved sophisticated evasion mechanisms, such as the NS3/4A-mediated cleavage of host adapter proteins MAVS and TRIF, to blunt these antiviral responses [PubMed, 2014]. Modern therapeutic strategies utilize Direct-Acting Antivirals (DAAs) to specifically inhibit viral enzymes, achieving high rates of sustained virologic response compared to older host-modulating interferon therapies [Feld & Foster, Nature Reviews, 2018]. Chronic disruption of these pathways by the virus leads to persistent hepatic inflammation, which can progress to cirrhosis and hepatocellular carcinoma [NIH, 2022; StatPearls, 2023].

Other names

HCV life cycleHepatitis C virus-host cell interactionsHCV replication complexHCV-host interactome

Inhibition of viral NS3/4A protease, NS5A phosphoprotein, or NS5B polymerase; induction of host interferon-stimulated genes (ISGs) and modulation of innate immune signaling.