Practice question

Internal ribosome entry sites enable cap-independent initiation through highly structured RNA segments in the 5' untranslated region that directly engage 40S subunits without requiring eIF4E-cap interaction. Viral genomes frequently harbor IRES elements because infection often triggers cleavage of eIF4G and shutdown of host capped translation. Poliovirus, encephalomyocarditis virus, hepatitis C virus, and dicistroviruses contain archetypal IRES structures that hijack cellular ribosomes using internal recruitment and trans-acting factors. Cellular IRES usage remains limited to stress conditions such as mitosis, apoptosis, and hypoxia, making viral mRNA the predominant physiological context for IRES-mediated translation mechanisms.