scholarly journals The Survival Strategies of Malaria Parasite in the Red Blood Cell and Host Cell Polymorphisms

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Gunanidhi Dhangadamajhi ◽  
Shantanu Kumar Kar ◽  
Manoranjan Ranjit
Keyword(s):  
Natural Selection ◽  
Blood Cell ◽  
Host Cell ◽  
Red Blood Cell ◽  
Malaria Parasite ◽  
Parasite Growth ◽  
Survival Strategies ◽  
Genes Encoding ◽  
Extracellular Environment ◽  
Selection Of

Parasite growth within the erythrocyte causes dramatic alterations of host cell which on one hand facilitates nutrients acquisition from extracellular environment and on other hand contributes to the symptoms of severe malaria. The current paper focuses on interactions between the Plasmodium parasite and its metabolically highly reduced host cell, the natural selection of numerous polymorphisms in the genes encoding hemoglobin and other erythrocyte proteins.

scholarly journals Author response: Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion

2018 ◽  
Author(s):  
May M Paing ◽  
Nichole D Salinas ◽  
Yvonne Adams ◽  
Anna Oksman ◽  
Anja TR Jensen ◽  
...  
Keyword(s):  
Blood Cell ◽  
Immune Evasion ◽  
Red Blood Cell ◽  
Malaria Parasite ◽  
Parasite Growth ◽  
Author Response ◽  
Cell Clustering

The RhopH complex is transferred to the host cell cytoplasm following red blood cell invasion by Plasmodium falciparum

2008 ◽  
Vol 160 (2) ◽  
pp. 81-89 ◽  
Author(s):  
Laetitia Vincensini ◽  
Gamou Fall ◽  
Laurence Berry ◽  
Thierry Blisnick ◽  
Catherine Braun Breton
Keyword(s):  
Plasmodium Falciparum ◽  
Blood Cell ◽  
Host Cell ◽  
Cell Invasion ◽  
Red Blood Cell ◽  
Cell Cytoplasm ◽  
Host Cell Cytoplasm

scholarly journals Accounting for red blood cell accessibility reveals distinct invasion strategies inPlasmodium falciparumstrains

2019 ◽  
Author(s):  
Francisco Cai ◽  
Tiffany M. DeSimone ◽  
Elsa Hansen ◽  
Cameron V. Jennings ◽  
Amy K. Bei ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Cell Structure ◽  
Clinical Manifestations ◽  
Parasite Growth ◽  
Invasion Pathways ◽  
Invasion Rate

AbstractThe growth of the malaria parasitePlasmodium falciparumin human blood causes all clinical manifestations of malaria, a process that begins with the invasion of red blood cells. Parasites enter red blood cells using distinct pairs of parasite ligands and host receptors that define particular invasion pathways. Parasite strains have the capacity to switch between invasion pathways. This flexibility is thought to facilitate immune evasion against particular parasite ligands, but may also reflect the fact that red blood cell surfaces are dynamic and composed of heterogeneous invasion targets. Different host genetic backgrounds affecting red blood cell structure have long been recognized to impact parasite growthin vivo, but even within a host, red blood cells undergo dramatic changes in morphology and receptor density as they age. The consequences of these heterogeneities for parasite growthin vivoremain unclear. Here, we measured the ability of laboratory strains ofP. falciparumrelying on distinct invasion pathways to enter red blood cells of different ages. We estimated invasion efficiency while accounting for the fact that even if the red blood cells display the appropriate receptors, not all are physically accessible to invading parasites. This approach revealed a tradeoff made by parasites between the fraction of susceptible cells and their invasion rate into them. We were able to distinguish between “specialist” strains exhibiting high invasion rate in fewer cells versus “generalist” strains invading less efficiently into a larger fraction of cells. We developed a mathematical model to predict that infection with a generalist strain would lead to higher peak parasitemiasin vivowhen compared with a specialist strain with similar overall proliferation rate. Thus, the heterogeneous ecology of red blood cells may play a key role in determining the rate of parasite proliferation between different strains ofP. falciparum.

scholarly journals Antimalarial Activity of Cupredoxins

2013 ◽  
Vol 288 (29) ◽  
pp. 20896-20907 ◽  
Author(s):  
Isabel Cruz-Gallardo ◽  
Irene Díaz-Moreno ◽  
Antonio Díaz-Quintana ◽  
Antonio Donaire ◽  
Adrián Velázquez-Campoy ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Antimalarial Activity ◽  
Surface Protein ◽  
Merozoite Surface Protein ◽  
Food Vacuole ◽  
Parasite Growth ◽  
Titration Calorimetry ◽  
Erythrocyte Invasion ◽  
Promising Target

The discovery of effective new antimalarial agents is urgently needed. One of the most frequently studied molecules anchored to the parasite surface is the merozoite surface protein-1 (MSP1). At red blood cell invasion MSP1 is proteolytically processed, and the 19-kDa C-terminal fragment (MSP119) remains on the surface and is taken into the red blood cell, where it is transferred to the food vacuole and persists until the end of the intracellular cycle. Because a number of specific antibodies inhibit erythrocyte invasion and parasite growth, MSP119 is therefore a promising target against malaria. Given the structural homology of cupredoxins with the Fab domain of monoclonal antibodies, an approach combining NMR and isothermal titration calorimetry (ITC) measurements with docking calculations based on BiGGER is employed on MSP119-cupredoxin complexes. Among the cupredoxins tested, rusticyanin forms a well defined complex with MSP119 at a site that overlaps with the surface recognized by the inhibitory antibodies. The addition of holo-rusticyanin to infected cells results in parasitemia inhibition, but negligible effects on parasite growth can be observed for apo-rusticyanin and other proteins of the cupredoxin family. These findings point to rusticyanin as an excellent therapeutic tool for malaria treatment and provide valuable information for drug design.

scholarly journals Plasmodium falciparum erythrocyte-binding antigen 175 triggers a biophysical change in the red blood cell that facilitates invasion

2017 ◽  
Vol 114 (16) ◽  
pp. 4225-4230 ◽  
Author(s):  
Marion Koch ◽  
Katherine E. Wright ◽  
Oliver Otto ◽  
Maik Herbig ◽  
Nichole D. Salinas ◽  
...  
Keyword(s):  
Cell Surface ◽  
Blood Cell ◽  
Signaling Pathways ◽  
Red Blood Cell ◽  
Malaria Parasite ◽  
Red Cell ◽  
Biophysical Properties ◽  
Parasite Invasion ◽  
Bending Modulus ◽  
Erythrocyte Binding

Invasion of the red blood cell (RBC) by the Plasmodium parasite defines the start of malaria disease pathogenesis. To date, experimental investigations into invasion have focused predominantly on the role of parasite adhesins or signaling pathways and the identity of binding receptors on the red cell surface. A potential role for signaling pathways within the erythrocyte, which might alter red cell biophysical properties to facilitate invasion, has largely been ignored. The parasite erythrocyte-binding antigen 175 (EBA175), a protein required for entry in most parasite strains, plays a key role by binding to glycophorin A (GPA) on the red cell surface, although the function of this binding interaction is unknown. Here, using real-time deformability cytometry and flicker spectroscopy to define biophysical properties of the erythrocyte, we show that EBA175 binding to GPA leads to an increase in the cytoskeletal tension of the red cell and a reduction in the bending modulus of the cell’s membrane. We isolate the changes in the cytoskeleton and membrane and show that reduction in the bending modulus is directly correlated with parasite invasion efficiency. These data strongly imply that the malaria parasite primes the erythrocyte surface through its binding antigens, altering the biophysical nature of the target cell and thus reducing a critical energy barrier to invasion. This finding would constitute a major change in our concept of malaria parasite invasion, suggesting it is, in fact, a balance between parasite and host cell physical forces working together to facilitate entry.

scholarly journals A multifunctional serine protease primes the malaria parasite for red blood cell invasion

2009 ◽  
Vol 28 (6) ◽  
pp. 725-735 ◽  
Author(s):  
Konstantinos Koussis ◽  
Chrislaine Withers-Martinez ◽  
Sharon Yeoh ◽  
Matthew Child ◽  
Fiona Hackett ◽  
...  
Keyword(s):  
Blood Cell ◽  
Serine Protease ◽  
Cell Invasion ◽  
Red Blood Cell ◽  
Malaria Parasite
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