Abstract

Malaria is a complex disease afflicting more than 250 million people and almost 600 000 avoidable deaths per year. The Plasmodium falciparum parasites responsible for the disease have the ability to develop resistance to antimalarial drugs through rapid mutations on the var2 gene resulting in altered protein sequences. To date antimalarial vaccines are showing limited success due to protein alteration.

The recognition and attachment of the merozoite stage of the parasite to an uninfected erythrocyte potentially also uses numerous alternative pathways to ensure rapid infection rates.

During invasion a complex sequence of binding, reorientation, formation of a tight junction and internalisation accompanied by the release of surface proteins takes place. During the late trophozoite stage the erythrocyte exposes several parasite proteins responsible for the adhesion of infected cells in the microvasculature.

Modification of erythrocyte surface proteins and drug treatments that alter the expressed parasite proteins coupled with invasion assay data provide a platform to investigate the potential target proteins using both classical and new proteomic techniques.

SDS PAGE and nLC-MS/MS techniques have identified two possibly overlooked proteins affecting invasion success and a truncated form of an adhesion protein has been identified. Some potential shortcomings of the approach will be highlighted