Shared host, distinct invaders: metabolomic footprints of plasmodium and babesia in host red cells.

PURPOSE OF REVIEW

Malaria and babesiosis are important transfusion-transmitted diseases, therefore, it is important to report novel insights into the complex interactions the causative parasites share with their common host RBCs. Metabolomics is an important tool that can be used to reveal an in-depth analysis of parasite infections in the context of the host. Similarities and differences in the biochemical fingerprints between malaria and babesia infected RBCs are reviewed with potential reasons for these differences and implications for the host.

RECENT FINDINGS

Recent results from Babesia-infected RBCs offer an opportunity to develop comparative models of pathogenesis for both infections. Perturbation in the levels of key biomolecules including sugars, amino-acids and lipids, along with redox homeostasis, and heme utilization, are hallmarks of both diseases. Key similarities include enhanced glycolytic rate in both infected RBCs together with lipid scavenging from RBC membranes. Differences relate to hemoglobin breakdown and the use of resultant amino acids for propagation.

SUMMARY

Altered metabolic profiles reflect the unique lifecycles of Plasmodium and Babesia, pointing to how they carve out a niche for successful proliferation. A comprehensive understanding of the metabolic similarities and differences between the two parasites will aid in identifying new biomarkers as well as specific, effective targeted therapies.