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.

Genome sequencing reveals the evolution and epidemiology of Leishmania donovani in the Indian subcontinent, where epidemics have caused up to 30,000 deaths per year.

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

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.

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.

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.

An optimized cytosine base editing system for Leishmania species improves editing efficiency, reduces toxicity, and ensures stable guide expression, enabling scalable loss-of-function screening and efficient creation of functional mutants.

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

Why does protein kinase A respond to purine nucleosides in certain pathogens, but not to the cyclic nucleotides that activate this kinase in most other organisms?