Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Mol Microbiol. 2021 May;115(5):891-900. doi: 10.1111/mmi.14652. Epub 2020 Dec 13.
Malaria is one of the most life-threatening infectious diseases worldwide, caused by infection of humans with parasites of the genus Plasmodium. The complex life cycle of Plasmodium parasites is shared between two hosts, with infection of multiple cell types, and the parasite needs to adapt for survival and transmission through significantly different metabolic environments. Within the blood-stage alone, parasites encounter changing levels of key nutrients, including sugars, amino acids, and lipids, due to differences in host dietary nutrition, cellular tropism, and pathogenesis. In this review, we consider the mechanisms that the most lethal of malaria parasites, Plasmodium falciparum, uses to sense nutrient levels and elicit changes in gene expression during blood-stage infections. These changes are brought about by several metabolic intermediates and their corresponding sensor proteins. Sensing of distinct nutritional signals can drive P. falciparum to alter the key blood-stage processes of proliferation, antigenic variation, and transmission.
疟疾是全球最致命的传染病之一，由人类感染疟原虫属寄生虫引起。疟原虫寄生虫的复杂生命周期在两个宿主之间共享，感染多种细胞类型，寄生虫需要适应不同的代谢环境以生存和传播。仅在血液阶段，寄生虫就会遇到关键营养素水平的变化，包括糖、氨基酸和脂质，这是由于宿主饮食营养、细胞嗜性和发病机制的差异。在这篇综述中，我们考虑了最致命的疟疾寄生虫疟原虫（Plasmodium falciparum）用来感知营养水平并在血液阶段感染期间引发基因表达变化的机制。这些变化是由几种代谢中间产物及其相应的传感器蛋白引起的。对不同营养信号的感知可以促使疟原虫改变增殖、抗原变异和传播等关键的血液阶段过程。
