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Red cell membrane protein distribution during malarial invasion
A R Dluzewski1, P R Fryer, S Griffiths
1Medical Research Council Cell Biophysics Unit, King's College, London, UK.
Abstract:
Immuno-gold labelling electron microscopy of thin sections was used to determine the distribution of red cell membrane and membrane skeleton proteins in the vicinity of internalized malaria parasites. When examined immediately after invasion (young ring-stage parasites), the parasitophorous vacuole membranes of both Plasmodium falciparum and P. knowlesi were found to be characterized by the essentially complete absence of spectrin, ankyrin and the most abundant transmembrane protein, band 3. P. knowlesi merozoites were trapped in the attached but not internalized state by pretreatment with cytochalasin B. In this merozoite-red cell complex antibody labelling showed that band 3 had been eliminated from the region of the host cell membrane in contact with the parasite. Internal vesicles, originating apparently from the site of attachment, were often observed in the red cell. Opposite the attached parasite a cavity was also sometimes seen in the host cell, presumably representing an incipient internal vesicle. The membrane was intact, as judged by the absence of protein (haemoglobin) in the cavity, and, like the membranes surrounding the internal vesicles, was devoid of membrane proteins. A large multilamellar body was sometimes seen in the merozoite close to its point of attachment. The lamellar spacing was about 50 nm. The electron microscope images suggest a diffusion of electron-dense material from the lamellar body into the cavity in the host cell.
Insights
Malaria parasites disrupt red blood cell membranes, removing key proteins like spectrin and band 3 during invasion. This study reveals how Plasmodium parasites alter host cell structure for survival.
Area of Science:
- Cell Biology
- Parasitology
- Biochemistry
Background:
- Red blood cell membrane integrity is crucial for oxygen transport.
- Malaria parasites, such as Plasmodium falciparum and Plasmodium knowlesi, invade red blood cells to replicate.
- Understanding host-parasite interactions at the molecular level is key to developing new treatments.
Purpose of the Study:
- To investigate the distribution of red blood cell membrane and skeleton proteins around malaria parasites.
- To elucidate the molecular mechanisms by which malaria parasites alter host cell membranes.
Main Methods:
- Immuno-gold labelling electron microscopy was employed to visualize protein localization.
- Thin sections of infected red blood cells were analyzed.
- Cytochalasin B was used to trap merozoites in an attached, non-internalized state.
Main Results:
- Spectrin, ankyrin, and band 3 proteins were absent from parasitophorous vacuole membranes of young ring-stage parasites.
- Band 3 protein was eliminated from the host cell membrane region contacting the parasite.
- Internal vesicles and cavities devoid of host membrane proteins were observed in the red blood cell.
- A multilamellar body within the merozoite appeared to release material into the host cell cavity.
Conclusions:
- Malaria parasites actively remodel the red blood cell membrane during invasion.
- The removal of key membrane proteins suggests a mechanism for parasite survival and immune evasion.
- Parasite-derived structures may contribute to the observed membrane alterations.