Abstract

Purpose of ReviewTo thrive and survive, intracellular pathogens actively remodel their host cells. The mechanisms developed by the asexual stages of the human malaria parasite Plasmodium falciparum to remodel their host erythrocyte have been extensively described. However, they are less characterized for the sexual stages, called gametocytes, which are responsible for parasite transmission.Recent FindingsGametocytes develop in erythrocytes and have recently been shown to mature in nucleated erythroid precursors as well. The sexual stages of the parasite affect erythroblastic differentiation; however, it is still unclear whether erythroblasts undergo the same remodeling as their mature counterparts. We explore how erythrocytes and erythroblasts may be impacted by parasite development.SummaryGametocytes deeply modify their erythrocyte host by exporting proteins to the host cell cytosol and membrane. These proteins induce dramatic changes in the morphology and physiology of the infected erythrocyte which acquires novel mechanical, adhesive, and serologic properties. Some of these modifications play a key role for gametocyte sequestration in the bone marrow, subsequent release in the bloodstream and ability to persist in blood circulation. The gametocytes development in erythroblasts and the potential-induced remodeling of the host cell may also contribute to anemia and have crucial implications for how to target gametocytes in drug- or vaccine-based strategies.

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