A novel DNA/RNA modifying enzyme catalyzing a previously unknown 5-carbamoyloxymethylcytosine modification has been discovered using a novel framework called Metagenomics Genome-Phenome Association.

Accumulation of mutations in some cancers is correlated with an aberration of DNA repair and access of a DNA deaminase to normal genomic DNA.

Combining in vitro and in vivo assays demonstrates that the cytidine deaminase APOBEC3A can inhibit LINE-1 retrotransposition by deaminating transiently exposed single-strand DNA that arises during the process of LINE-1 integration.

Enzymes that remove amine groups from cytosine bases in DNA are likely involved in generating the clusters of mutations (kataegis) seen in breast cancer.

APOBEC3G, an anti-viral protein with the capability to inhibit HiV-1 infectivity, binds single stranded DNA in multiple physical conformations, enabling complex interactions that allow APOBEC3G to perform multiple diverse functions.

Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.

Genomes take advantage of the gene-duplicating ability of retroelements to birth novel innate immune defense genes.

Transcribed promoters are highly susceptible to mutation by cytidine deaminases, implicating stable exposure of single stranded DNA structures, rather than cofactors, in localising mutation during tumourigenesis and antibody maturation.

The birth of the antiviral gene APOBEC3B in ancient primates is linked to the evolution of a potent counterdefense by herpesviruses, a host-pathogen interaction maintained to present day.

Innate antiviral factors do not always perfectly distinguish between self and foreign, and potential adverse effects of antiviral defense mechanisms for the host have been discussed.