ArticleJournal of structural biology2008
The avian malaria parasite Plasmodium gallinaceum causes marked structural changes on the surface of its host erythrocyte.
Article in Journal of structural biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 23 citations in OpenAlex.
- Seasonal Dynamics of Symptomatic and Asymptomatic Plasmodium falciparum and Plasmodium vivax Infections in Coendemic Low-Transmission Settings, South Ethiopia.The American journal of tropical medicine and hygiene · 2024Article
- A member of the tryptophan-rich protein family is required for efficient sequestration of Plasmodium berghei schizonts.PLoS pathogens · 2022Article
- Physicochemical Aspects of the Plasmodium chabaudi-Infected Erythrocyte.BioMed research international · 2015Article
- Identification and expression of maebl, an erythrocyte-binding gene, in Plasmodium gallinaceum.Parasitology research · 2013Article
- Neuroimmunological blood brain barrier opening in experimental cerebral malaria.PLoS pathogens · 2012Article
- The density of knobs on Plasmodium falciparum-infected erythrocytes depends on developmental age and varies among isolates.PloS one · 2012Article
- Is there a direct role for erythrocytes in the immune response?Veterinary research · 2011Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Using a combination of atomic force, scanning and transmission electron microscopy, we found that avian erythrocytes infected with the avian malaria parasite Plasmodium gallinaceum develop approximately 60 nm wide and approximately 430 nm long furrow-like structures on the surface. Furrows begin to appear during the early trophozoite stage of the parasite's development. They remain constant in size and density during the course of parasite maturation and are uniformly distributed in random orientations over the erythrocyte surface. In addition, the density of furrows is directly proportional to the number of parasites contained within the erythrocyte. These findings suggest that parasite-induced intraerythrocytic processes are involved in modifying the surface of host erythrocytes. These processes may be analogous to those of the human malaria parasite P. falciparum, which induces knob-like protrusions that mediate the pathogenic adherence of parasitized erythrocytes to microvessels. Although P. gallinaceum-infected erythrocytes do not seem to adhere to microvessels in the host chicken, the furrows might be involved in the pathogenesis of P. gallinaceum infections by some other mechanism involving host-pathogen interactions.
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