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Synonymous codon bias in the viral genome affects protein translation and gene expression, suggesting that the synonymous codon mutant plays an essential role in influencing virulence and evolution. However, how the recessive mutant form contributes to virus evolvability remains elusive. In this paper, we characterize how the Senecavirus A (SVA), a picornavirus, utilizes synonymous codon mutations to influence its evolution, resulting in the adaptive evolution of the virus to adverse environments. The phylogenetic tree and Median-joining (MJ)-Network of these SVA lineages worldwide were constructed to reveal SVA three-stage genetic development clusters. Furthermore, we analyzed the codon bias of the SVA genome of selected strains and found that SVA could increase the GC content of the third base of some amino acid synonymous codons to enhance the viral RNA adaptive evolution. Our results highlight the impact of recessive mutation of virus codon bias on the evolution of the SVA and uncover a previously underappreciated evolutionary strategy for SVA. They also underline the importance of understanding the genetic evolution of SVA and how SVA adapts to the adverse effects of external stress.

After a short-time surface mechanical attrition treatment process, a planar uneven structure was obtained on the surface of irons. The yield strength of the sample subjected to surface mechanical attrition treatment for 60 s is almost twice than that of the annealed sample, but the ductility is still well retained. The good combination of strength and ductility is mainly due to the extra strain hardening and the coexistence of soft and hard phases. The extra strain hardening delays the annihilation of dislocations and reduces the plastic instability, while the hard phase in the planar uneven structure suppresses the crack initiation, and the soft phase delays the crack propagation.