A series of selective events, each improving fitness relative to an immediate predecessor, can result in organisms that are less fit compared to a distant ancestor.

Experiments on yeast cells that are hosts to a killer virus confirm that natural selection can sometimes reduce fitness.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

Building on previous work (Pigott et al. 2014), estimates of areas of potential transmission of Ebola virus are revised and updated to provide a contemporary map for use by researchers and policymakers.

Bodo saltans virus defines the most abundant giant viruses in the ocean and highlights the genomic plasticity, rooted in evolutionary arms races, that gave rise to giant viruses.

Development of a generally adaptable conformational capture assay for use in-trans identifies the specific direct interaction sites between the parvovirus minute virus of mice and the cellular genome during infection as sites of cellular DNA damage.

HIV-1 viral protein u (Vpu) can stimulate novel versions of canonical interactions with the clathrin adaptor AP1 to counteract the host antiviral protein BST2.

The human cytomegalovirus US12 gene family work co-operatively to degrade large numbers of immune ligands and prevent recognition by natural killer cells.

Cryo electron microscopy and structure-based mutagenesis reveal that the bacteriophage BPP-1 contains two of the three major recognized viral folds, one of which exhibits a new topology.

The strongly coupled theoretical regime describes the function of mouse sensory and motor cortical areas.