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Last Updated: 02/08/2024
Interdisciplinary research aimed at elucidating the molecular basis responsible for liver infection specificity of malaria parasites
Objectives
*Original title and text were machine translated from Japanese.
This study aims to identify host-side receptor molecules that bind to P36 or P52 and host-side molecules that interact with LISP2 using a proximal-dependent biotin labeling method. Next, the molecular mechanism underlying malaria parasite liver infection specificity will be elucidated by analyzing the role of the identified host molecules in parasite infection and the parasite-side cellular responses caused by ligand-receptor interactions. Furthermore, a virtual human liver chip will be used to conduct verification in a model more similar to human liver infection.
Malaria is one of the world’s three major infectious diseases, causing approximately 200 million infections and 600,000 deaths annually. Plasmodium sporozoites first infect the human liver, rapidly multiply in a short period of time, and then migrate into the bloodstream, causing various pathological conditions. The question of why sporozoites of malaria parasites infect only liver cells in the body has not yet been answered. Until now, P36 and P52 have been identified as ligand molecules involved in hepatocyte invasion, and LISP2 has been identified as a molecule that is transported to the hepatocyte side after hepatocyte invasion, but the host molecules that interact with these are unknown. The nature of the subsequent cell responses on the protozoan and host sides is also unknown.
Apr 2023 — Mar 2026
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