The same host–virus interactions can evolve multiple times in nature, due to the high effective mutation rate of viruses, and provide interesting systems of study.

Integrated multi-scale, multi-tool approach to design novel 'evolution drugs' which can delay the emergence of antibiotic resistance by constraining bacterial evolutionary escape strategies.

A viral protein hijacks the key effector of transcriptional gene silencing, Su(var)3-9, to evade host plant surveillance.

In the setting of CNS infection, meningeal lymphatic drainage promotes dendritic cell and T cell responses in the deep cervical lymph nodes but is not necessary for maintaining control of parasite in the brain.

A unique, widely distributed gut bacterial enzyme selectively metabolizes plant-derived cardiac glycoside drugs.

Graph genotyping of structural variation in diverse human populations reveals functional associations and signatures of local adaptation within poorly resolved regions of the genome.

Irradiation of normal human fibroblasts and mice in conditions mimicking standard external X-ray radiotherapy protocols highlights that noncancerous cells surrounding the planning target volume accumulate DNA single-strand breaks but almost no double-strand breaks, putting them in a pre-cancerous senescent state.

A generalizable approach to understanding the logic of molecular recognition reveals the contributions of individual residues to the specificity of protein-protein interactions.

A peptide derived from BK and JC polyomavirus protein VP2/3 inhibits viral infection by targeting a binding site in the pore of polyomavirus VP1 pentamers, enabling future VP1-targeted therapeutic strategies.