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.

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.

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.

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

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.

Mycobacterium tuberculosis exploits an IFN/IL6/CEBP axis linked to monocyte expansion in humans.

Ancient protein domains remain shaped by amino acid availability during early life, while young animal proteins are shaped by a need for high intrinsic structural disorder.