Key result
Mutation of the HCV IRES domain IIb alters the configuration of the viral RNA in the 40S subunit decoding groove and decreases translation initiation efficiency by approximately 50% compared to wild-type.
Population
Hepatitis C virus (HCV) internal ribosome entry site (IRES) RNA and 40S ribosomal subunit complex
Comparison
Mutation of domain IIb of the IRES vs Wild-type IRES
Design
Preclinical
Authors
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Hypothesis-generating for IRES-40S interactions in HCV; leaves open targeted antiviral development.
Domain IIb of the HCV IRES structurally communicates with the start codon region upon 40S subunit binding, which is critical for driving viral protein synthesis.
Filbin et al. (2011) studied Hepatitis C virus (HCV) translation initiation. HCV IRES domain IIb mutation vs. Wild-type HCV IRES was evaluated on Translation initiation efficiency and RNA configuration in the 40S decoding groove. Mutation of the HCV IRES domain IIb alters the configuration of the viral RNA in the 40S subunit decoding groove and decreases translation initiation efficiency by approximately 50% compared to wild-type.
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