Babesia divergens-infected red blood cells take up glutamate via an EAAT3 independent mechanism.

Human red blood cells infected with the malaria parasite Plasmodium falciparum show an increased permeability to a number of solutes. We have previously demonstrated that such infected cells take up glutamate via a member of the excitatory amino acid transporter protein family (EAAT), namely EAAT3. Babesia divergens is a parasite that also infects human erythrocytes, and also induces increased solute permeability, including for glutamate. Here we have investigated whether glutamate uptake in B. divergens infected human red blood cells is also dependent on EAAT3 activity. We find that, although B. divergens infected cells do take up glutamate, this uptake is independent on EAAT3. Thus, though infecting the same host cell, two related parasites have developed distinct pathways to obtain access to nutrients from the extracellular milieu.