New Nucleoside Transport Pathways Induced in the Host Erythrocyte Membrane of Malaria and Babesia Infected Cells

Abstract

Within hours after the human malarial parasite Plasmodium falciparum invades the host erythrocyte, new permeability pathways appear in the host cell membrane¹. We have demonstrated that the intraerythrocytic malarial parasite appears to induce an additional component of nucleoside transport in the host erythrocyte membrane and this comprises about 40% of the total transport in the infected cells. It is stage specific; it occurs mainly at the trophozoite stage of the malarial parasite development. This induced component is insensitive to the classical inhibitors of mammalian nucleoside transport, nitrobenzylthioinosine (NBMPR), nitrobenzylthioguanosine (NBTGR), dilazep and dipyridamole, indicating that the properties of the induced transporter are significently different to that of the host erythrocyte^2,3. Similarly, nucleoside transport, which is inoperative in normal bovine erythrocytes, is induced upon infection of the bovine erythrocyte with Babesia bovis. In a manner similar to transport in malaria infected cells, transport inhibitors, such as NBMPR, showed significantly less inhibition⁴.