The uptake of glucose into human erythrocytes infected with Plasmodium falciparum was investigated using a number of different glucose analogues. In short time-courses with cells suspended in media containing 5 mM glucose, 2-deoxy-D-glucose equilibrated rapidly between the intracellular and extracellular compartments. Its transport into the infected cell was primarily via the host cell (cytochalasin B-sensitive) transporter. 2-Deoxy-D-glucose did permeate the broad-specificity pathway that is induced in infected cells by the intracellular parasite. However, this pathway made little contribution to the total uptake of 2-deoxy-D-glucose under physiological conditions. In parasitised cells incubated with [14C]2-deoxy-D-glucose for prolonged periods the intracellular concentration of radiolabel increased to values higher than that in the external medium; it reached a maximum value three to six times higher than the extracellular concentration before falling back to a concentration similar to that outside the cells. This transient intracellular accumulation of radiolabel was due entirely to the phosphorylation of the [14C]2-deoxy-D-glucose and its consequent trapping within the cell. The specific characteristics of the 2-deoxy-D-glucose uptake time courses measured under different conditions were accounted for by the kinetics of the phosphorylation process and the energy status of the cell. The data indicate that 2-deoxy-D-glucose (as well as the non-phosphorylated compounds 3-O-methyl-D-glucose and L-glucose) enter the intracellular parasite via a passive (i.e. equilibrative) rather than an active (i.e. concentrative) transport process.