Why Malaria Struggles with Sickle Cell: A Computational Study

Abstract

It is known that individuals with sickle cell anemia exhibit resistance to malaria but the molecular mechanism behind this protection is not fully understood. One factor is the interaction between malaria enzymes i.e., plasmepsin II and IV, and hemoglobin. This study examines how these enzymes bind to normal and sickle hemoglobin using docking simulations to analyze binding sites, binding affinities, amino acid interactions, and structural stability. Results suggest that sickle cell hemoglobin disrupts plasmepsin binding, hindering the parasite’s ability to degrade hemoglobin. Unlike genetic approaches, this study focuses on direct biochemical interactions, providing insights for antimalarial-drug development.