Key result
Analysis of massively recoded poliovirus variants does not support the hypothesis that loosely conserved hairpins determine assembly specificity, suggesting instead a two-step cocondensation process.
The study proposes a two-step model for +ssRNA virus assembly involving specificity and cocondensation, challenging the hypothesis that loosely conserved hairpins determine assembly specificity.
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Challenges hairpin model of poliovirus assembly; leaves open two-step cocondensation mechanism for validation in +ssRNA viruses.
Significance We constructed viable poliovirus (PV) variants carrying up to 2,104 synonymous mutations in the ORF. We studied proliferation phenotypes, particularly the specific infectivity ( si ) that defines the probability of a single virion to initiate a single cell infection. A recent hypothesis proposes that dozens of loosely conserved hairpins, formed within the viral genome, determine assembly specificity of +ssRNA viruses. Our analysis of recoded PVs does not support this hypothesis. We propose that the progression of +ssRNA virus assembly follows two steps. ( i ) Specificity: recognition between either ( a ) replication protein and capsid precursor or ( b ) single RNA packaging signal and cognate capsid precursor. ( ii ) Cocondensation, occurring between single genome/single capsid precursor complex and multiple cognate capsids aided by multiple genome-specific hairpins.
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Song et al. (2017) studied Poliovirus infection. Massively recoded poliovirus genomes was evaluated on Proliferation phenotypes and specific infectivity. Analysis of massively recoded poliovirus variants does not support the hypothesis that loosely conserved hairpins determine assembly specificity, suggesting instead a two-step cocondensation process.
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