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Hepatitis C virus (HCV) antigens are a group of structural and non-structural proteins produced from a single viral polyprotein of approximately 3,000 amino acids [1, 7]. This polyprotein is cleaved by host and viral proteases into ten functional units: Core, E1, E2, p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B, each playing a critical role in the viral life cycle [7, 8]. For instance, E1 and E2 mediate host cell entry, while non-structural proteins like NS5B catalyze the replication of the viral RNA genome [2, 11]. In patients with chronic hepatitis C, these antigens contribute to persistent inflammation, liver cirrhosis, and an increased risk of hepatocellular carcinoma by interfering with host immune signaling [20, 23]. These proteins serve as the primary targets for direct-acting antivirals (DAAs), which have transformed HCV into a curable disease [6, 17]. Therapeutic agents specifically inhibit the NS3/4A protease, the NS5A replication complex protein, or the NS5B RNA-dependent RNA polymerase, thereby halting the production of new viral particles [14, 16].
Direct-acting antivirals target specific Hepatitis C virus (HCV) antigens to disrupt the viral life cycle. NS3/4A inhibitors block the protease responsible for polyprotein cleavage; NS5A inhibitors interfere with viral replication complex formation and assembly; and NS5B inhibitors target the RNA-dependent RNA polymerase to terminate viral genome replication.
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