A comprehensive description of gene expression and organisation in the cells that constitute the blood fluke larvae responsible for finding and invading its intermediate host.

Interactions among parasites in snails create cascading effects on their transmission and highlight that biodiversity has complex, context-dependent and important effects on human schistosomiasis transmission dynamics.

Cells that give rise to the infectious form of parasitic flatworms called schistosomes show similar patterns of gene expression to stem cells in free-living flatworms.

Gene knock-out of the omega-1 ribonuclease of Schistosoma mansoni eggs resulted in immunologically impaired phenotype, showcasing the novel application of CRISPR/Cas9 genome editing and utility for functional genomics in schistosomes.

Distinct stem cell populations drive larval, somatic, and germline development of the human parasitic flatworm, Schistosoma mansoni.

Genomic approaches can be integrated with epidemiological and ecological studies to provide high-resolution answers to open questions about schistosomiasis transmission dynamics, offering a level of precision that is actionable, such that schistosomiasis-control programming can be tailored to regional contexts.

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.

A coordinated humoral immune response that includes recognition, effector and cytotoxic factors engages the cell-mediated immune response to defend a snail against infection by schistosome parasites.

Engagement of both host and parasite signaling pathways proves a novel approach for developing improved anti-parasitic therapies.