Inlay

Babesia microti poses a significant threat to human health, underscoring the need for an improved in vitro culture system to reduce reliance on animal models and support drug and vaccine screening. Key challenges include the tropism of preferential host red blood cells (RBCs), parasite metabolic needs, culture medium formulation, and optimization of the microaerophilic environment (oxygenation).

Protist parasites cause devastating diseases worldwide, yet their complex metabolism remains poorly understood. Genome-scale metabolic models (GEMs) have emerged as powerful tools to systematically represent and simulate parasite metabolism, enabling the prediction of gene essentiality, metabolic vulnerabilities, and host–parasite interactions. This review examines the current landscape of GEMs for protist pathogens, focusing on the key modeling decisions (objective functions, constraints, and compartmentalization) that govern model behavior and predictive scope. We discuss how these choices shape biological interpretability and how inherited assumptions from early reconstructions propagate across successive models. Ongoing challenges in standardization and reusability highlight the need for consistent annotation, validation, and adherence to FAIR data principles to build interoperable and reproducible resources.

Parasites of dogs and cats are changing in ways that challenge our current understanding across many scientific fields. Factors such as climate change and increased global travel are reshaping parasite distributions, favoring their introduction and emergence in new foci. Some parasites appear to have emerged in new regions, while others have switched hosts or developed resistance. Other parasites may have long been overlooked because of limited diagnostic capacity. At the same time, genetic recombination and hybridization are producing variants with altered virulence and transmission patterns. Together, these trends suggest a future in which companion animal parasitology becomes more dynamic, unpredictable, and globally interconnected, demanding stronger surveillance, improved diagnostics, and closer integration between veterinary and public health efforts.

Myzozoa, a clade of alveolate protists including Apicomplexa, Chromerida, Perkinsozoa, and dinoflagellates, possesses the most reduced mitochondrial genomes among eukaryotes. Apicomplexan parasites, such as Toxoplasma gondii and Plasmodium spp., retain mitochondrial genomes encoding only three proteins and highly fragmented rRNAs. Despite this reduction, recent structural studies show that T. gondii mitoribosome incorporates lineage-specific RNA-binding proteins as integral components to maintain a functional complex composed of over 50 rRNA fragments. The conservation of rRNA fragmentation and protein repertoire observed among Apicomplexa suggests a shared evolution within the phylum. This radical divergence from all other currently investigated cytoplasmic and mitochondrial ribosomes highlights evolutionary plasticity and common ancestry, providing a model for studying mitochondrial evolution and potential antiparasitic drug discovery.

Parasites spread through shared environments, so observations from hosts sampled in the same environment are rarely independent. Ignoring shared environmental effects can lead to an underestimation of study outcome uncertainty and the potential to draw incorrect conclusions. Intraclass correlation coefficients help address this issue by quantifying cluster-level effects and adjusting sample sizes.

Vector-borne disease transmission is highly heterogeneous, yet existing models emphasize climate, host density, and pathogen load. We propose that host–vector microbiome similarity represents a previously unrecognized ecological axis in transmission biology. During blood feeding, vectors ingest host-derived immune effectors shaped by the host microbiota. When immune targeting depends on shared microbial features, microbiome similarity predicts the magnitude of immune-mediated disturbance within the vector gut, altering colonization resistance and influencing pathogen establishment. These effects are context-dependent and may enhance or suppress transmission. This framework generates testable predictions linking microbiome similarity, immune-mediated disturbance, and vector competence across systems. Incorporating microbiome similarity into transmission models may help explain heterogeneity and improve ecological understanding and intervention strategies.

Mosquitoes transmit a wide range of viruses and malaria parasites, posing a significant threat to global public health. Among recent advances in genetic pest control, gene drives have emerged as a powerful tool. Through super-Mendelian inheritance, gene drives ensure the biased transmission of specific traits to offspring, potentially enabling rapid propagation through wild populations. Gene drives can be utilized to alter or eliminate entire mosquito populations, potentially curbing vector-borne disease transmission in a sustainable manner. Additionally, several improved genetic control strategies provide temporally self-limiting and spatially confinable options for pest control. This review summarizes genetic control research in Anopheles, Aedes, and Culex mosquitoes, focusing on recent progress, major bottlenecks, and potential solutions.

Ochoa et al. identified a novel Plasmodium falciparum haplotype in ancient osteological remains of two notable members of the Medici family. The findings expand our current knowledge of historical P. falciparum genetic diversity and confirm its expansion in Europe.

Stanbery et al. show that tuft cells, previously defined as epithelial activators of innate type 2 immunity, are dispensable for memory T helper 2 (Th2) cell establishment but required for protective immunity during secondary helminth infection. This involves tuft cell secretion of interleukin-25 and leukotriene C4 to promote memory Th2 effector function.

Complex host–vector–virus interfaces can impose serious health challenges. Western honeybees have experienced high colony losses globally, mainly driven by the host-shifted, virus-vectoring ectoparasitic mites Varroa destructor and Tropilaelaps mercedesae. Host populations can survive mite infestations through natural selection, offering a long-term strategy for colony health. However, host–vector–virus coevolution requires local adaptations of this triad, which is poorly understood. We propose harnessing natural selection through a global approach focused on standardized monitoring of colony survival, mite infestation levels, and control of reproductives. Studying native and adapted mite hosts, host shifts, and comparing susceptible to surviving hosts will enhance understanding of this host–vector–virus system. This strategy promotes colony health in both managed and wild host populations and provides insights into other host–vector–virus interfaces.