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.

Stable isotope labeling reveals that NAD crosses the inner membrane of mammalian mitochondria via an unknown transporter.

Differential eIF4E binding to transcription initiation nucleotides and alternative promoter usage of eIF1A, PABP and other genes are involved in the response of the translation machinery to energy stress.

A family of fluorescent biosensors for nicotinamide adenine dinucleotides allows quantification of these cofactors in live cells with spatio-temporal resolution.

A method enabling identification of more than 100 RNA modifications in single ribosomal RNA molecules uncovers new classes of modified ribosomes.

Dinucleases, specialized enzymes that catalyze the final step in RNA degradation, have evolved independently and repeatedly to fulfill essential roles in cell growth.

RNA degradation is completed through specific intermediates, such as diribonucleotides, which must be removed from the cells by a specific enzyme.