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.

Understanding where future Ebola virus outbreaks may start and the changing nature of the populations living in these places is of critical importance in helping to prepare for future outbreaks.

Analysing a compilation of individual-level data gathered across the seven Ebola Virus Disease outbreaks in the Democratic Republic of the Congo reveals factors that contribute to the spread of the disease and mortality.

Cryo-electron tomography reveals the structure and arrangement of the VP40 matrix protein lattice that mediates the formation of Ebola and Marburg virus particles.

The pattern of past Ebola outbreaks is indicative of an effective reproductive ratio of less than 1, which can lead to the generation of a range of outbreak sizes consistent with the scale of the ongoing epidemic.

NPC1 is a genetic determinant of filovirus susceptibility in bats, and some variations in bat NPC1 may reflect host adaptations to reduce filovirus replication and virulence.

A new model describes how adaptive molecular evolution shapes phylogenetic trees and can be used to estimate the fitness effects of mutations from phylogenies.

A nanomolar inhibitor of cholesterol transport out of endosomes/lysosomes can be crosslinked to the “sterol-sensing domain” of NPC1, which implicates this domain in the transmembrane transport of cholesterol.

Bats' uniquely robust innate antiviral immune defenses select for faster transmitting viruses likely to generate extreme virulence upon spillover to secondary hosts with immune systems divergent from those of bat.

A combination of X-ray crystallography, molecular dynamics and small angle X-ray scattering shows that the transcription antiterminator M2-1 is a structurally dynamic homotetramer that undergoes large concerted conformational changes upon binding its target RNA.