Codon usage can also be strongly influenced by underlying biases in dinucleotide frequency, which differs greatly among organisms. Specifically, after accounting for dinucleotide biases, the proportion of codon usage bias explained by mutation pressure often increases, as seen in human RNA viruses [25] . Our study revealed that CpG and the eight CpG-containing codons are notably deficient in ORFs of 48 poliovirus genomes. The explanation for the CpG deficiency is immunologic escape. A high CpG content may be detrimental to small DNA (or RNA) viruses, as unmethylated CpGs are recognized by the host's innate immune system (Toll-like receptor 9) as a pathogen signature [32] . As with vertebrate genomes, methylated viral genomes would face a high chance of mutation at CpGs, that would result in a reduction of this dinucleotide [9, 33] . We found that DVPVs and live attenuated virus of genotype 1 have lower frequencies of CpG dinucleotide compare with wild viruses of polioviruses genotype 1. The most popular explanation for lower frequencies of CpG in ORFs of DVPV genomes is that when OPV viruses turning into VDPV genotype 1, a lower frequencies of CpG dinucleotide maybe help VDPV out of the host immunity.