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The hepatitis C virus internal ribosome entry site RNA (HCV IRES) is a highly conserved, structured RNA region of approximately 340 nucleotides located within the 5′ untranslated region (UTR) of the HCV genome[1][2][6]. It mediates cap-independent initiation of protein translation by direct recruitment of the host cell's 40S ribosomal subunit, bypassing the need for many canonical eukaryotic initiation factors[5][6]. The HCV IRES forms several distinct secondary and tertiary structural domains that interact with both initiation factors and ribosomal subunits, enabling efficient translation of the viral polyprotein[2][3][5]. Because of its essential role in the viral life cycle and unique RNA-driven mechanism, the HCV IRES represents a validated antiviral target, and selective small molecules that bind specific IRES subdomains can inhibit viral translation and represent promising therapeutic strategies[4][5].
Inhibition of viral translation initiation by stabilizing non-productive conformations of the IRES RNA, thereby blocking ribosome recruitment and viral protein synthesis
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