Hijacking the host: Red blood cell remodeling and extracellular vesicle release during Babesia infection.

The red blood cells (RBC) of various species serve as the host cells for the asexual stage of Babesia causing hemolysis and anemia, hallmark symptoms of parasitic infections that target RBCs. After Babesia invasion, RBCs are progressively modified by the parasite to suit their requirements of rapid proliferation and egress, while avoiding host immune consequences. This involves a complete morphological, biochemical and rheological overhaul of the RBC whereby the parasite confers on the host RBC, a new set of properties. Babesia infected RBCs exhibit increased membrane rigidity, reduced deformability, increased osmotic resistance, high vesiculation rates and in some species increased adhesiveness to the vascular endothelium. In this chapter we describe our current understanding of these changes in the Babesia-infected RBC that contribute to the modified RBC architecture. Further work must be directed to elucidate the structural and functional relationships of the pathogen-RBC networks at play in the infected cell, as these interactions may present targets for the development of novel therapeutics.