Malaria remains a major global health burden, with Plasmodium vivax and Plasmodium falciparum being the parasites that mostly infect humans. Even though P. falciparum can cause more severe diseases, P. vivax is more widespread, and its eradication is particularly challenging due to its ability to form dormant liver stages and to persist in poorly understood tissue reservoirs. Recent evidence indicates that the bone marrow serves as a key niche for P. vivax, where the parasite shows a strong tropism for newly formed reticulocytes expressing CD71 receptor. This selective invasion suggests a close relationship between P. vivax infection and erythropoiesis within the bone marrow microenvironment. We aim thus at deciphering the interactions between P. vivax and bone marrow cells during red blood cells development. To achieve this, we will use a humanized mouse model developed in our laboratory that supports human erythropoiesis and P. vivax infection. By combining this model with single-cell RNA sequencing of bone marrow cells, we will characterize parasite–host interactions at high resolution. This work will provide new insights into P. vivax biology within the bone marrow and may uncover novel targets for intervention strategies aimed at malaria elimination.
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