Department of Medical Parasitology and Infection Biology, Swiss Tropical and Public Health Institute, Basel, Switzerland.
University of Basel, Basel, Switzerland.
Microbiol Mol Biol Rev. 2019 Sep 4;83(4). doi: 10.1128/MMBR.00013-19. Print 2019 Nov 20.
The asexual intraerythrocytic development of , causing the most severe form of human malaria, is marked by extensive host cell remodeling. Throughout the processes of invasion, intracellular development, and egress, the erythrocyte membrane skeleton is remodeled by the parasite as required for each specific developmental stage. The remodeling is facilitated by a plethora of exported parasite proteins, and the erythrocyte membrane skeleton is the interface of most of the observed interactions between the parasite and host cell proteins. Host cell remodeling has been extensively described and there is a vast body of information on protein export or the description of parasite-induced structures such as Maurer's clefts or knobs on the host cell surface. Here we specifically review the molecular level of each host cell-remodeling step at each stage of the intraerythrocytic development of We describe key events, such as invasion, knob formation, and egress, and identify the interactions between exported parasite proteins and the host cell cytoskeleton. We discuss each remodeling step with respect to time and specific requirement of the developing parasite to explain host cell remodeling in a stage-specific manner. Thus, we highlight the interaction with the host membrane skeleton as a key event in parasite survival.
疟原虫的无性红细胞内发育会导致最严重的人类疟疾，其特点是宿主细胞的广泛重塑。在入侵、细胞内发育和逸出的过程中，疟原虫会根据每个特定发育阶段的需要重塑红细胞膜骨架。这种重塑是由大量输出的寄生虫蛋白促成的，而红细胞膜骨架是观察到的寄生虫与宿主细胞蛋白之间大多数相互作用的接口。宿主细胞重塑已被广泛描述，并且有大量关于蛋白输出或寄生虫诱导结构（如 Maurer 裂隙或宿主细胞表面的小结）描述的信息。在这里，我们专门回顾疟原虫红细胞内发育各个阶段每个宿主细胞重塑步骤的分子水平。我们描述了关键事件，如入侵、小结形成和逸出，并确定了输出的寄生虫蛋白与宿主细胞细胞骨架之间的相互作用。我们根据时间和发育中寄生虫的特定要求讨论每个重塑步骤，以特定于阶段的方式解释宿主细胞的重塑。因此，我们强调与宿主膜骨架的相互作用是寄生虫生存的关键事件。
