Red Cell Physiology Laboratory, New York Blood Center, New York, NY 10065, USA.
Med Microbiol Immunol. 2012 Nov;201(4):593-8. doi: 10.1007/s00430-012-0272-z. Epub 2012 Sep 11.
Invasion by the malaria parasite, Plasmodium falciparum, brings about extensive changes in the host red cells. These include loss of the normal discoid shape, increased rigidity of the membrane, elevated permeability to a wide variety of ionic and other species and increased adhesiveness, most notably to endothelial surfaces. These effects facilitate survival of the parasite within the host cell and tend to increase the virulence of disease that includes cerebral malaria and anemia. Numerous proteins secreted by the internalized parasite and interacting with red cell membrane proteins are responsible for the changes occurring to the host cell. Anemia, a serious clinical manifestation of malaria, is due to increased destruction of both infected and uninfected red cells due to membrane alterations, as well as ineffective erythropoiesis. There is very good evidence that various red cell disorders including hemoglobinopathies and hereditary ovalocytosis decrease the virulence of disease following parasite infection. A number of mechanism(s) are likely responsible for the protective effect of various red cell abnormalities including decreased invasion, impaired intraerythrocytic development of the parasites and altered interaction between exported parasite proteins and the red cell membrane skeleton.
疟原虫（Plasmodium falciparum）的入侵会导致宿主红细胞发生广泛变化。这些变化包括正常盘状形状的丧失、膜刚性增加、对各种离子和其他物质的通透性增加以及黏附性增加，尤其是与内皮表面的黏附性增加。这些效应有助于寄生虫在宿主细胞内的存活，并使包括脑疟疾和贫血在内的疾病的毒力增加。被内化的寄生虫分泌的许多与红细胞膜蛋白相互作用的蛋白质是导致宿主细胞发生变化的原因。贫血是疟疾的一种严重临床症状，是由于膜改变导致感染和未感染的红细胞破坏增加，以及无效的红细胞生成。有充分的证据表明，各种红细胞疾病，包括血红蛋白病和遗传性椭圆形红细胞增多症，会降低寄生虫感染后的疾病毒力。各种红细胞异常（包括入侵减少、寄生虫在红细胞内发育受损以及出口寄生虫蛋白与红细胞膜骨架之间相互作用改变）可能通过多种机制产生保护作用。
