Key result
Deoptimized codons influence cotranslational folding in the capsids of poliovirus and hepatitis A virus, emphasizing the role of codon frequency in determining viral phenotype.
Experimental molecular evolution highlights the role of codon usage and deoptimized codons in the cotranslational folding of viral capsids.
Codon deoptimization may inform viral attenuation strategies; leaves open broader applicability beyond these models.
Codon bias is common to all organisms and is the result of mutation, drift, and selection. Selection for the efficiency and accuracy of translation is well recognized as a factor shaping the codon usage. In contrast, fewer studies report the control of the rate of translation as an additional selective pressure influencing the codon usage of an organism. Experimental molecular evolution using RNA virus populations is a powerful tool for the identification of mechanisms underlying the codon bias. Indeed, the role of deoptimized codons on the cotranslational folding has been proven in the capsids of two fecal-orally transmitted picornaviruses, poliovirus, and the hepatitis A virus, emphasizing the role of the frequency of codons in determining the phenotype. However, most studies on virus codon usage rely only on computational analyses, and experimental studies should be encouraged to clearly define the role of selection on codon evolution.
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Pintó et al. (2021) conducted a review in RNA virus populations. Deoptimized codons was evaluated. Deoptimized codons influence cotranslational folding in the capsids of poliovirus and hepatitis A virus, emphasizing the role of codon frequency in determining viral phenotype.
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