Current malaria vaccines provide suboptimal, waning protection. Dacon et al. identify a protective post-translationally modified epitope on Plasmodium sporozoites that is absent from current vaccines. This discovery deepens our understanding of Plasmodium biology and may inform the development of improved vaccines and complementary prophylactic monoclonal antibodies.
Malaria mortality remains above 500 000 people annually, demonstrating the need for new and innovative control approaches. Using a genome-scale, functional screen of Plasmodium sexual replication, Sayers et al. identified over 300 genes essential for malaria transmission through the mosquito, providing many new candidates for drug and vaccine development.
Hybridization and introgression between host species or between parasite species are emerging challenges for human, plant, and animal health, especially as global trends like climate change and urbanization increase overlap of species ranges. This creates opportunities for heterospecific crosses between diverged taxa that could generate novel host and parasite genotypes with unique traits (e.g., transmission rate, virulence, susceptibility, and resistance) compared with their parental taxa. However, there seems to be slow appreciation of this biological phenomenon in empirical and theoretical approaches to host-parasite interactions. This limits our understanding of the effects of hybridization on epidemiology, ecology, and evolution. Here, we address some pressing questions regarding the emergence and relevance of eukaryotic hybrid genotypes for disease dynamics.
Parasitic infections can profoundly impact brain function through inflammation within the central nervous system (CNS). Once viewed as an immune-privileged site, the CNS is now recognized as vulnerable to immune disruptions from both local and systemic infections. Recent studies reveal that certain parasites, such as Toxoplasma gondii and Plasmodium falciparum, can invade the CNS or influence it indirectly by triggering neuroinflammation. These processes may disrupt brain homeostasis, influence neurotransmission, and lead to significant behavioral or cognitive changes. This review discusses the pathways by which parasites disrupt CNS function and highlights systemic inflammation as a critical link between peripheral infections and neuroinflammatory conditions, advancing understanding of parasite-associated neurological complications.
In Plasmodium falciparum malaria, infected cells accumulate in blood vessels of organs, including the brain. Recently, Reyes et al. identified monoclonal antibodies that stop infected cells from binding to the endothelial protein C receptor (EPCR) in a model of brain blood vessels. EPCR-blocking monoclonals could form the basis of new treatments for severe malaria.
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