Pasvol G, Carlsson J, Clough B
Department of Infectious Diseases and Tropical Medicine, St Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, Northwick Park Hospital, Harrow, Middlesex, UK.
Baillieres Clin Haematol. 1993 Jun;6(2):513-34. doi: 10.1016/s0950-3536(05)80157-x.
The red cell membrane with its bilipid layer, integral membrane proteins (especially the GPs and band 3), and the red cell skeleton pose a formidable barrier for the malarial parasite to overcome during invasion. Invasion is an ordered and sequential process, indicating a highly complex and specific process involving numerous molecular interactions. For P. vivax and P. knowlesi infections the Duffy glycoprotein seems to be a specific requirement in invasion. For P. falciparum the GPs, and especially the N-acetyl neuraminic acid linked in an alpha 2-3 configuration on them, appear to act as specific ligands although some strains of P. falciparum may use alternate ligands for invasion. The parasite enters the red cells within an invagination continuous with the red cell bilipid layer, the parasitophorous vacuole membrane, and recent evidence would indicate that this membrane is largely of parasite origin. The numerous occasions in which the red cell needs to deform during invasion indicates that membrane deformability could be an important factor in determining invasion, but the dissociation of invasion and deformability as induced by a number of reagents would not support this contention. Instead it is suggested that reagents which modify invasion may be acting via alterations in red cell or parasite protein phosphorylation or dephosphorylation.
具有双脂层、整合膜蛋白(特别是糖蛋白和带3蛋白)以及红细胞骨架的红细胞膜,对疟原虫在入侵过程中构成了巨大的障碍。入侵是一个有序且连续的过程,这表明它是一个涉及众多分子相互作用的高度复杂且特定的过程。对于间日疟原虫和诺氏疟原虫感染,达菲糖蛋白似乎是入侵的特定必需物质。对于恶性疟原虫,糖蛋白,尤其是其上以α2-3构型连接的N-乙酰神经氨酸,似乎充当特定配体,尽管一些恶性疟原虫菌株可能使用替代配体进行入侵。疟原虫通过与红细胞双脂层连续的内陷进入红细胞,即寄生泡膜,最近的证据表明该膜在很大程度上源自疟原虫。红细胞在入侵过程中需要多次变形,这表明膜的可变形性可能是决定入侵的一个重要因素,但许多试剂诱导的入侵与可变形性的分离并不支持这一观点。相反,有人认为改变入侵的试剂可能是通过改变红细胞或疟原虫蛋白的磷酸化或去磷酸化来起作用的。