Erythrocyte invasion is a process essential to the survival of malaria parasites. An understanding of the mechanism of erythrocyte invasion by malarial merozoites is important, since interruption of any of these events . would halt the parasites asexual cycle and prevent disease. Much work has focused on the human malaria Plasmodium falciparum, however it is expensive to maintain in the laboratory. The research described here concentrates on the rodent malaria Plasmodium berghei, which in many ways is similar to P. falciparum, but is more convenient to obtain, cheaper to maintain and remains relatively uninvestigated. A percoll density gradient centrifugation step was developed to purify mature parasite-infected erythrocytes from other infected and uninfected erythrocytes. This purification step allowed the development of in vitro invasion assays and erythrocyte receptor binding assays for P. berghei. The invasion assays confirmed in vitro, the invasion specificities observed in vivo for P. berghei, in particular the preference of P. berghei merozoites for invasion of immature erythrocytes, the reticulocytes. The binding assays identified a 130 kDa P. berghei molecule that bound exclusively to murine erythrocytes, and which undoubtedly has a role in merozoite invasion of erythrocytes. Polyclonal antisera was raised to various protein preparations of P. berghei, and these were used to screen a cDNA expression library of P. berghei constructed in gt11. This cDNA library was also screened with radiolabelled oligonucleotide probes corresponding to fragments of a gene encoding an erythrocyte binding protein of the human malaria Plasmodium falciparum. A cDNA library constructed in gt11 from the sexual stages of P. falciparum was screened with an antisera specific for sexual stage antigens. Isolated clones were characterised and (3-galactosidase fusion proteins prepared. Antisera was raised to these fusion proteins.