Maps defining environmental risk of the leishmaniases provide insights into the ecology of these diseases and identify regions to target public health measures and inform future burden estimates.

Genomic data for the parasites that cause visceral leishmaniasis provides the first global picture of the diversity and evolution of the pathogen and the epidemiology of this fatal tropical disease.

Biological and pharmacokinetic studies indicate that the anti-tubercular drug, delamanid, could be repurposed for the treatment of visceral leishmaniasis.

LeishBASEedit enables gene editing in Leishmania without requiring DNA double-strand breaks, homologous recombination, or donor DNA, thereby facilitating loss-of-function screens via delivery of plasmid libraries and regardless of limitations due to gene copy number variations and/or lack of RNAi components.

A conceptual and unifying framework with a critical appraisal of lipid hijacking by microbes cycling between an arthropod vector and a mammalian host is explored.

High-speed holographic microscopy shows that Leishmania parasites modify their swimming behaviour to target human macrophages.

Following exposure of Leishmania culture promastigotes to DNA stress, single-cell RNA sequencing reveals discrete clusters of cells associated with efficient generation of hybrids between different species and strains in vitro marked by expression of the ancestral gamete fusogen HAP2.

Detailed analysis of the sequence of monocyte differentiation into distinct gut tissue macrophages provides insights into monocyte biology and can serve as a platform for the design of cell therapies.