Parasite life cycles may be more flexible than traditionally thought, potentially allowing single-cell infections of insect vectors and transmission between hosts even at very low parasite densities.

The structure of the trypanosome haptoglobin-haemoglobin receptor bound to its ligand reveals the molecular basis for ligand recognition in innate immunity and identifies molecular determinants that aid efficient uptake.

The transparent zebrafish reveals the reality of trypanosomes swimming in a vertebrate host, and their adaptations to an extremely heterogenic environment.

The endosomal apparatus of African trypanosomes consists a continuous membrane system with functional subdomains rather than distinct compartments for early, late, and recycling endosomes.

The kinetoplastid parasite Trypanosoma brucei employs a unique mechanism to target the conserved Aurora B kinase to kinetochores and the central spindle.

Mapping DNA replication timing, allied to genetic analysis of a RecQ repair helicase, reveals that antigenic variation in the African trypanosome may be initiated by locus-specific, replication-derived sequence instability.

The information for mRNAs expression level is set by codon choice in trypanosomes and requires translation to be interpreted into a turnover rate.

A structure derived from cryogenic electron microscopy shows how ISG65, an African trypanosome receptor that aids virulence, binds C3b and suggests mechanisms through which ISG65 might aid complement resistance.

The ligand specificity and expression profile of the haptoglobin-haemoglobin receptor has diversified throughout the evolution of trypanosomes.

Ferroptosis is an evolutionary ancient process that is counterbalanced by distant peroxidases, GPx4 in mammals and tryparedoxin peroxidases in trypanosomes, and can be induced at distinct subcellular membranes depending on the individual cell type.