ArticleParasitology research1991
Ultrastructure of erythrocytes from Aotus trivirgatus and Saimiri sciureus monkeys infected by Plasmodium vivax.
Article in Parasitology research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- 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
- Long-term in vitro culture of Plasmodium vivax isolates from Madagascar maintained in Saimiri boliviensis blood.Malaria journal · 2017Article
- Merozoite release from Plasmodium falciparum-infected erythrocytes involves the transfer of DiIC₁₆ from infected cell membrane to Maurer's clefts.Parasitology research · 2011Article
- Prolonged in vitro cultivation of Plasmodium vivax using Trager's continuous-flow method.Parasitology research · 1992Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Erythrocytes from Aotus and Saimiri monkeys parasitized by Plasmodium vivax show dramatic changes starting during the early stages of parasite development. Invaginations of the erythrocyte membrane, caveolae, are found during all parasite development stages. Up to six vesicles can be fused with one caveola, forming a caveola-vesicle complex. As the parasite grows, large accumulations of these vesicles can be seen within the erythrocyte cytoplasm. In addition to these caveolae-vesicle complexes, knob-like structures appear on the erythrocyte surface that are similar to those seen on the host-cell surface of P. falciparum-infected red cells. Extensive membrane-bound clefts spread throughout the erythrocytic cytoplasm, sometimes forming stacks or large whorls. The density of the red cell cytoplasm begins to decrease at an early stage of parasite development. All of these changes may be responsible for an increased fragility of the P. vivax-infected red cell from Aotus or Saimiri monkeys. Moreover, the large amount of parasite material that is released during rupture of the red cell may account for the high fever paroxysms that are characteristic of P. vivax malaria infection.
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Registered trials
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