ArticleCellular microbiology2019
Multimodal analysis of Plasmodium knowlesi-infected erythrocytes reveals large invaginations, swelling of the host cell, and rheological defects.
Article in Cellular microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 26 citations in OpenAlex.
- PfATG18 links V-ATPase assembly to endocytic membrane dynamics in malaria parasites.PLoS pathogens · 2026Article
- Caveola-vesicle complexes of Plasmodium vivax and Plasmodium cynomolgi: large-scale aggregation and structure of PHIST-positive vesicles in late schizont-infected red blood cells.Malaria journal · 2025Article
- Comparative 3D ultrastructure of Plasmodium falciparum gametocytes.Nature communications · 2025Article
- Effect of periostin (OSF-2) on phagocytosis ofFrontiers in microbiology · 2025Article
- The J Domain Proteins ofInternational journal of molecular sciences · 2024Review
- Proteomes of plasmodium knowlesi early and late ring-stage parasites and infected host erythrocytes.Journal of proteomics · 2024Article
- Effective cell membrane tension protects red blood cells against malaria invasion.PLoS computational biology · 2023Article
- Review
- In-depth biological analysis of alteration in Plasmodium knowlesi-infected red blood cells using a noninvasive optical imaging technique.Parasites & vectors · 2022Article
- Ultrastructural characterization of host-parasite interactions ofParasitology · 2022Article
- Budding pouches and associated bubbles: 3D visualization of exo-membrane structures inFrontiers in cellular and infection microbiology · 2022Article
- Article
- Zoonotic Malaria: Non-Pathogens (Basel, Switzerland) · 2021Review
- Plasmodium vivax infection compromises reticulocyte stability.Nature communications · 2021Article
- Cytoadherence Properties ofFrontiers in microbiology · 2021Article
- Surface area-to-volume ratio, not cellular viscoelasticity, is the major determinant of red blood cell traversal through small channels.Cellular microbiology · 2021Article
- Knowlesi malaria: Human risk factors, clinical spectrum, and pathophysiology.Advances in parasitology · 2021Article
- Three-dimensional ultrastructure of Plasmodium falciparum throughout cytokinesis.PLoS pathogens · 2020Article
- Functional genomics of simian malaria parasites and host-parasite interactions.Briefings in functional genomics · 2019Review
- Multimodal analysis of Plasmodium knowlesi-infected erythrocytes reveals large invaginations, swelling of the host cell, and rheological defects.Cellular microbiology · 2019Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The simian parasite Plasmodium knowlesi causes severe and fatal malaria infections in humans, but the process of host cell remodelling that underpins the pathology of this zoonotic parasite is only poorly understood. We have used serial block-face scanning electron microscopy to explore the topography of P. knowlesi-infected red blood cells (RBCs) at different stages of asexual development. The parasite elaborates large flattened cisternae (Sinton Mulligan's clefts) and tubular vesicles in the host cell cytoplasm, as well as parasitophorous vacuole membrane bulges and blebs, and caveolar structures at the RBC membrane. Large invaginations of host RBC cytoplasm are formed early in development, both from classical cytostomal structures and from larger stabilised pores. Although degradation of haemoglobin is observed in multiple disconnected digestive vacuoles, the persistence of large invaginations during development suggests inefficient consumption of the host cell cytoplasm. The parasite eventually occupies ~40% of the host RBC volume, inducing a 20% increase in volume of the host RBC and an 11% decrease in the surface area to volume ratio, which collectively decreases the ability of the P. knowlesi-infected RBCs to enter small capillaries of a human erythrocyte microchannel analyser. Ektacytometry reveals a markedly decreased deformability, whereas correlative light microscopy/scanning electron microscopy and python-based skeleton analysis (Skan) reveal modifications to the surface of infected RBCs that underpin these physical changes. We show that P. knowlesi-infected RBCs are refractory to treatment with sorbitol lysis but are hypersensitive to hypotonic lysis. The observed physical changes in the host RBCs may underpin the pathology observed in patients infected with P. knowlesi.
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