Hepatitis C virus (HCV) is a significant cause of chronic liver disease
worldwide. The molecular basis of HCV infection and replication has been extensively
studied, leading to the identification of vital viral proteins and their interactions with
host factors. The HCV genome encodes a single polyprotein cleaved by host and viral
proteases into individual proteins, including the core, envelope glycoproteins (E1 and
E2), p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B. These viral proteins play critical
roles in virus assembly, entry, replication, and evasion of host immune responses. The
HCV envelope glycoproteins E1 and E2 are responsible for virus attachment and entry
into host cells through interactions with various host receptors, including CD81,
scavenger receptor class B type I (SR-BI), and tight junction proteins. The viral protein
NS3 has multiple functions, including protease and helicase activities, which are
critical for viral RNA replication. NS5A is an essential component of the viral
replication complex and regulates viral RNA replication, virion assembly, and
modulation of host immune responses. NS5B is the RNA-dependent RNA polymerase
responsible for viral RNA synthesis. The molecular mechanisms underlying HCVinduced pathogenesis and the development of chronic infection remain poorly
understood. However, recent studies have shed light on the interactions between HCV
and host factors, including the innate and adaptive immune responses and the roles of
viral proteins in modulating these responses. These insights have led to new antiviral
therapies, including direct-acting antivirals (DAAs) that target viral proteins in RNA
replication.
Keywords: Glycoproteins, Hepatitis C virus (HCV), HCV-induced pathogenesis, Polyprotein, Virus assembly, Viral proteins, Viral RNA replication.
