Attenuating candidate live virus vaccines by incorporating unfavoured codon pairs to reduce translation efficiency is actually mediated though changes in frequencies of CpG and UpA dinucleotides, which make viruses more visible to the innate immune system.

RNA virus replication is attenuated by an intrinsic restriction mechanism after introducing CpG/UpA dinucleotides into both non-translated and coding regions of viral genomes, which may be exploited in the design of attenuated virus vaccines.

KHNYN, a putative endoribonuclease, interacts with the zinc-finger antiviral protein (ZAP) and is required for the inhibition of HIV replication and RNA abundance by CpG dinucleotides.

Mutants of influenza A virus with increased CpG dinucleotide frequencies show restricted replication and reduced or absent pathogenicity, and powerful host innate and adaptive responses to infection that confer immunity to re-infection.

A protein that can recognize regions of DNA with a high proportion of unmethylated CpG dinucleotides, and then recruit polycomb group proteins to these CpG islands, has been identified.

The quiescence-driven mutational landscape reveals replication-independent mutagenesis as a novel evolutionary force.

Genomic landmarks, known generically as ‘CpG islands’, program chromatin structure via their richness in the dinucleotide CG and their skewed composition of DNA bases.

Variably methylated retrotransposons have an underlying sequence that allows them to escape KAP1-mediated silencing and recruit ZF-CxxC proteins.

Islands of non-methylated DNA are shown to perform a similar epigenetic role in many different vertebrate species.

Different types of epigenetic DNA modifications affect the likelihood of cytosine mutations in cancer.