The asexual intraerythrocytic development of Plasmodium falciparum, 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 P. falciparum 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.

中文翻译：

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整个恶性疟原虫血液阶段的宿主细胞骨架重塑。

恶性疟原虫的无性红细胞内发育导致人类疟疾的最严重形式，其特征在于广泛的宿主细胞重塑。在整个入侵，细胞内发育和外出过程中，根据每个特定发育阶段的要求，寄生虫对红细胞膜骨架进行了重塑。大量出口的寄生虫蛋白促进了重塑，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界面。宿主细胞重塑已被广泛描述，关于蛋白质输出或寄生虫诱导的结构（例如宿主细胞表面上的毛勒氏c或瘤）的信息大量存在。在这里，我们专门审查恶性疟原虫的红细胞内发育的每个阶段的每个宿主细胞重塑步骤的分子水平。我们描述了关键事件，例如入侵，结节形成和外出，并确定了输出的寄生虫蛋白与细菌宿主细胞骨架。我们讨论有关时间和寄生虫发育的具体要求的每个重塑步骤，以阶段特定的方式解释宿主细胞重塑。因此，我们强调与宿主膜骨架的相互作用是寄生虫存活中的关键事件。我们讨论有关时间和寄生虫发育的具体要求的每个重塑步骤，以阶段特定的方式解释宿主细胞重塑。因此，我们强调与宿主膜骨架的相互作用是寄生虫存活中的关键事件。我们讨论有关时间和寄生虫发育的具体要求的每个重塑步骤，以阶段特定的方式解释宿主细胞重塑。因此，我们强调与宿主膜骨架的相互作用是寄生虫存活中的关键事件。