Review highlights metabolic strategies of apicomplexan and trypanosomatid parasites in host cells.
Apicomplexan and trypanosomatid parasites cause important human diseases, including malaria, toxoplasmosis, Chagas disease, and human leishmaniasis. The mammalian-infective stages of these parasites colonize nutrient-rich, intracellular niches in a range of different host cells. These niches include specialized vacuoles (Plasmodium spp., Toxoplasma gondii), the mature lysosome of phagocytic cells (Leishmania), and the cytoplasm of nucleated host cells (Trypanosoma cruzi). Here, we review the different growth and metabolic strategies utilized by each of these protists to survive in these niches. Although all stages utilize sugars as preferred carbon sources, different species or developmental stages vary markedly in their dependence on aerobic fermentation versus respiratory metabolism and their co-utilization of other carbon sources. Stage-specific differences in glycolytic and mitochondrial respiratory capacity may be a hardwired feature of each stage and reflect the trade-off of achieving high growth rates at the expense of host range adaptability and establishing long-lived persistent infections.
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McConville et al. (2025) studied this question.
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