Predators may amplify multiple-host parasite spreading in systems with multiple transmission routes.

Plasmodium parasites use host-derived factors to form more rosettes and hamper phagocytosis, representing a new escape mechanism for the malaria parasites.

Genetic analysis identifies an enzyme of the malaria parasite that is required to seal its host red blood cell membrane upon invasion, a key requirement of this important intracellular pathogen.

Gene knockdowns reveal that the conserved RhopH protein complex functions in both host cell invasion and channel-mediated nutrient uptake in malaria.

A genetic screen in combination with biochemical approaches reveal hijacking of the host β-catenin destruction complex by the parasite T. gondii to reprogram immune gene expression.

A region of the Biomphalaria genome, containing highly divergent haplotypes with different combinations of transmembrane genes, strongly impacts whether these snails can transmit parasitic schistosomes.

Following initial invasion events, intracellular life stages of C. parvum rely upon an N-terminal host-targeting motif and proteolytic processing at a specific leucine residue to deliver proteins into the infected enterocyte.

The application of deep learning fills a major gap in host–pathogen research providing for unbiased, multi-module high-throughput image analysis.

Ecological and evolutionary perspectives are critical to understand, predict, prevent, and treat malaria parasites that may spread to humans from our close primate relatives.

The range of molecular forms adopted by L1 retrotransposons reflect a tapestry of lifecycle-permissive and -restrictive host-parasite interactions occurring within cells.