Metabolic changes of the malaria parasite during the transition from the human to the mosquito host.

Plasmodium falciparum is an obligate human parasite that is the causative agent of the most lethal form of human malaria. Transmission of P. falciparum to a new human host requires a mosquito vector within which sexual replication occurs. P. falciparum replicates as an intracellular parasite in man and as an extracellular parasite in the mosquito, and it undergoes multiple developmental changes in both hosts. Changes in the environment and the activities of parasites in these various life-cycle stages are likely to be reflected in changes in the metabolic needs and capabilities of the parasite. Most of our knowledge of the metabolic capabilities of P. falciparum is derived from studies of the asexual erythrocytic cycle of the parasite, the portion of the parasite life cycle found in infected humans that is responsible for malarial symptoms. Efforts to control transmission and to understand the sometimes unique biology of this parasite have led to information about the metabolic capabilities of sexual and/or sporogonic stages of these parasites. This review focuses on comparing and contrasting the carbohydrate, nucleic acid, and protein synthetic capabilities of asexual erythrocytic stages and sexual stages of P. falciparum.