Abstract
After a successful invasion, malaria parasite Plasmodium falciparum extensively remodels the infected erythrocyte cellular architecture, conferring cytoadhesive properties to the infected erythrocytes. Cytoadherence plays a central role in the parasite's immune-escape mechanism, at the same time contributing to the pathogenesis of severe falciparum malaria. In this review, we discuss the cytoadhesive interactions between P. falciparum infected erythrocytes and various host cell types, and how these events are linked to malaria pathogenesis. We also highlight the limitations faced by studies attempting to correlate diversity in parasite ligands and host receptors with the development of severe malaria.
Highlights
Malaria continues to be a significant healthcare problem to many human populations, despite efforts to eliminate this debilitating and potentially fatal tropical disease
If the cytoadhesive phenotypes of IRBCs collected from the peripheral circulation are essentially similar to the sequestering late stage-IRBCs, the findings from in vitro rosetting studies may not imply the actual situation in vivo since the recruited IRBCs are not given an equal exposure to URBCs and endothelial cells in rosetting assays, which raises doubts if rosetting ever happens in vivo
Rosetting rates obtained from such samples may reflect the relative endothelial cytoadhesion propensity of the IRBCs, which is associated with the severe malaria development
Summary
Malaria continues to be a significant healthcare problem to many human populations, despite efforts to eliminate this debilitating and potentially fatal tropical disease. While it has been suggested that rosetting may aggravate the vasculature occlusion initiated by endothelial-cytoadhered IRBCs [162,163,164], its importance to pathogenesis of falciparum malaria is still debated.
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