Abstract

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.

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