ArticlePLoS computational biology2009
The homeostasis of Plasmodium falciparum-infected red blood cells.
Article in PLoS computational biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 94 citations in OpenAlex.
- Contact Dynamics of CytoadheringACS infectious diseases · 2025Article
- Aspartyl protease inhibition interferes with Plasmodium falciparum asexual blood-stage and early gametocyte development.Malaria journal · 2025Article
- Progeny counter mechanism in malaria parasites is linked to extracellular resources.PLoS pathogens · 2023Article
- pH-dependence of the Plasmodium falciparum chloroquine resistance transporter is linked to the transport cycle.Nature communications · 2023Article
- The circulatory dynamics of human red blood cell homeostasis: Oxy-deoxy and PIEZO1-triggered changes.Biophysical journal · 2023Article
- 2,3-Diphosphoglycerate and the Protective Effect of Pyruvate Kinase Deficiency against Malaria Infection-Exploring the Role of the Red Blood Cell Membrane.International journal of molecular sciences · 2023Article
- Biophysical Tools and Concepts Enable Understanding of Asexual Blood Stage Malaria.Frontiers in cellular and infection microbiology · 2022Review
- PIEZO1 and the mechanism of the long circulatory longevity of human red blood cells.PLoS computational biology · 2021Article
- Cation-Chloride Cotransporters, Na/K Pump, and Channels in Cell Water and Ion Regulation:Frontiers in cell and developmental biology · 2021Article
- Syk Kinase Inhibitors Synergize with Artemisinins by Enhancing Oxidative Stress inAntioxidants (Basel, Switzerland) · 2020Article
- The natural function of the malaria parasite's chloroquine resistance transporter.Nature communications · 2020Article
- Delayed death in the malaria parasite Plasmodium falciparum is caused by disruption of prenylation-dependent intracellular trafficking.PLoS biology · 2019Article
- The logic of ionic homeostasis: Cations are for voltage, but not for volume.PLoS computational biology · 2019Article
- Hemoglobin S and C affect biomechanical membrane properties ofCommunications biology · 2019Article
- Quantitative Model for Ion Transport and Cytoplasm Conductivity of Chinese Hamster Ovary Cells.Scientific reports · 2018Article
- Fitness Loss under Amino Acid Starvation in Artemisinin-Resistant Plasmodium falciparum Isolates from Cambodia.Scientific reports · 2018Article
- Evidence against a Role of Elevated Intracellular CaBiophysical journal · 2018Article
- Unexpected Connections between Humidity and Ion Transport Discovered Using a Model to Bridge Guard Cell-to-Leaf Scales.The Plant cell · 2017Article
- Rolling Adhesion of Schizont Stage Malaria-Infected Red Blood Cells in Shear Flow.Biophysical journal · 2017Article
- Differential time-dependent volumetric and surface area changes and delayed induction of new permeation pathways in P. falciparum-infected hemoglobinopathic erythrocytes.Cellular microbiology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
The asexual reproduction cycle of Plasmodium falciparum, the parasite responsible for severe malaria, occurs within red blood cells. A merozoite invades a red cell in the circulation, develops and multiplies, and after about 48 hours ruptures the host cell, releasing 15-32 merozoites ready to invade new red blood cells. During this cycle, the parasite increases the host cell permeability so much that when similar permeabilization was simulated on uninfected red cells, lysis occurred before approximately 48 h. So how could infected cells, with a growing parasite inside, prevent lysis before the parasite has completed its developmental cycle? A mathematical model of the homeostasis of infected red cells suggested that it is the wasteful consumption of host cell hemoglobin that prevents early lysis by the progressive reduction in the colloid-osmotic pressure within the host (the colloid-osmotic hypothesis). However, two critical model predictions, that infected cells would swell to near prelytic sphericity and that the hemoglobin concentration would become progressively reduced, remained controversial. In this paper, we are able for the first time to correlate model predictions with recent experimental data in the literature and explore the fine details of the homeostasis of infected red blood cells during five model-defined periods of parasite development. The conclusions suggest that infected red cells do reach proximity to lytic rupture regardless of their actual volume, thus requiring a progressive reduction in their hemoglobin concentration to prevent premature lysis.
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