ArticleNature communications2024
Host cell CRISPR genomics and modelling reveal shared metabolic vulnerabilities in the intracellular development of Plasmodium falciparum and related hemoparasites.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Peptide-Enabled Nanoplatforms for Malaria and Leishmaniasis: From Intracellular Targeting to Translational Diagnostic Perspectives.ChemMedChem · 2026Review
- Targeting metabolism to combat anticancer and antibacterial drug resistance.Trends in pharmacological sciences · 2026Review
- Epigenetic landscape of the H3K27me3 mark in macrophages transformed by Theileria annulata.Communications biology · 2026Article
- The Dawn of High-Throughput and Genome-Scale Kinetic Modeling: Recent Advances and Future Directions.ACS synthetic biology · 2025Review
- Adversarial regularized autoencoder graph neural network for microbe-disease associations prediction.Briefings in bioinformatics · 2024Article
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Authors and funding
14 authors.
Funding
Abstract
Parasitic diseases, particularly malaria (caused by Plasmodium falciparum) and theileriosis (caused by Theileria spp.), profoundly impact global health and the socioeconomic well-being of lower-income countries. Despite recent advances, identifying host metabolic proteins essential for these auxotrophic pathogens remains challenging. Here, we generate a novel metabolic model of human hepatocytes infected with P. falciparum and integrate it with a genome-wide CRISPR knockout screen targeting Theileria-infected cells to pinpoint shared vulnerabilities. We identify key host metabolic enzymes critical for the intracellular survival of both of these lethal hemoparasites. Remarkably, among the metabolic proteins identified by our synergistic approach, we find that host purine and heme biosynthetic enzymes are essential for the intracellular survival of P. falciparum and Theileria, while other host enzymes are only essential under certain metabolic conditions, highlighting P. falciparum's adaptability and ability to scavenge nutrients selectively. Unexpectedly, host porphyrins emerge as being essential for both parasites. The shared vulnerabilities open new avenues for developing more effective therapies against these debilitating diseases, with the potential for broader applicability in combating apicomplexan infections.
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