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Methods to Investigate the Regulatory Role of Small RNAs and Ribosomal Occupancy of Plasmodium falciparum
Published on: December 4, 2015
Malaria and human red blood cells
1Red Cell Physiology Laboratory, New York Blood Center, New York, NY 10065, USA. MNarla@NYBloodcenter.org
Abstract:
Invasion by the malaria parasite, Plasmodium falciparum, brings about extensive changes in the host red cells. These include loss of the normal discoid shape, increased rigidity of the membrane, elevated permeability to a wide variety of ionic and other species and increased adhesiveness, most notably to endothelial surfaces. These effects facilitate survival of the parasite within the host cell and tend to increase the virulence of disease that includes cerebral malaria and anemia. Numerous proteins secreted by the internalized parasite and interacting with red cell membrane proteins are responsible for the changes occurring to the host cell. Anemia, a serious clinical manifestation of malaria, is due to increased destruction of both infected and uninfected red cells due to membrane alterations, as well as ineffective erythropoiesis. There is very good evidence that various red cell disorders including hemoglobinopathies and hereditary ovalocytosis decrease the virulence of disease following parasite infection. A number of mechanism(s) are likely responsible for the protective effect of various red cell abnormalities including decreased invasion, impaired intraerythrocytic development of the parasites and altered interaction between exported parasite proteins and the red cell membrane skeleton.
Insights
Malaria parasite Plasmodium falciparum invasion alters red blood cells, increasing disease severity. Red blood cell disorders like hemoglobinopathies offer protection against severe malaria outcomes.
Area of Science:
- Hematology
- Infectious Diseases
- Cell Biology
Background:
- The malaria parasite Plasmodium falciparum invades red blood cells, causing significant host cell alterations.
- These changes include loss of cell shape, increased membrane rigidity, altered permeability, and enhanced adhesion, contributing to severe malaria manifestations like cerebral malaria and anemia.
- Parasite-secreted proteins interacting with red cell membrane proteins mediate these detrimental host cell modifications.
Purpose of the Study:
- To investigate the mechanisms by which Plasmodium falciparum infection alters host red blood cells.
- To understand how red blood cell disorders influence malaria virulence and disease outcomes.
Main Methods:
- The study reviews existing evidence on red blood cell changes induced by Plasmodium falciparum.
- It examines the impact of genetic red blood cell disorders on malaria severity.
Main Results:
- Plasmodium falciparum infection leads to red cell shape loss, rigidity, permeability changes, and adhesion.
- These alterations facilitate parasite survival and increase disease virulence, causing anemia through increased red cell destruction and ineffective erythropoiesis.
- Red cell disorders such as hemoglobinopathies and hereditary ovalocytosis are associated with decreased malaria virulence.
Conclusions:
- Parasite-induced red blood cell modifications are key to malaria pathogenesis and virulence.
- Red blood cell abnormalities confer protection against severe malaria by potentially reducing parasite invasion, impairing parasite development, or altering host-parasite protein interactions.
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