Department of Infectious Diseases, Parasitology, Heidelberg University, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany.
Trends Parasitol. 2012 Nov;28(11):479-85. doi: 10.1016/j.pt.2012.08.003. Epub 2012 Sep 11.
Many intracellular pathogens remodel the actin of their host cells, and the human malaria parasite Plasmodium falciparum is no exception to this rule. The surprising finding is that several hemoglobinopathies that protect carriers from severe malaria may do so by interfering with host actin reorganization. Here we discuss our current understanding of actin remodeling in P. falciparum-infected erythrocytes, how hemoglobinopathies interfere with this process, and how impaired host actin remodeling affects the virulence of P. falciparum.
许多细胞内病原体重塑宿主细胞的肌动蛋白，人类疟原虫恶性疟原虫也不例外。令人惊讶的是，几种可保护携带者免受严重疟疾的血红蛋白病可能通过干扰宿主肌动蛋白重组来实现这一点。在这里，我们讨论我们目前对恶性疟原虫感染红细胞中肌动蛋白重塑的理解，血红蛋白病如何干扰这一过程，以及宿主肌动蛋白重塑受损如何影响恶性疟原虫的毒力。
