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Plasmodium vivax  is the most widely distributed human malaria parasite. Previous studies have shown that circulating microparticles during  P. vivax  acute attacks are indirectly associated with severity. Extracellular vesicles (EVs) are therefore major components of circulating plasma holding insights into pathological processes. Here, we demonstrate that plasma-derived EVs from  Plasmodium vivax  patients ( Pv EVs) are preferentially uptaken by human spleen fibroblasts ( h SFs) as compared to the uptake of EVs from healthy individuals. Moreover, this uptake induces specific upregulation of ICAM-1 associated with the translocation of NF-kB to the nucleus. After this uptake,  P. vivax -infected reticulocytes obtained from patients show specific adhesion properties to  h SFs, reversed by inhibiting NF-kB translocation to the nucleus. Together, these data provide physiological EV-based insights into the mechanisms of human malaria pathology and support the existence of  P. vivax -adherent parasite subpopulations in the microvasculature of the human spleen.

Plasma-derived extracellular vesicles from Plasmodium vivax patients signal spleen fibroblasts via NF-kB facilitating parasite cytoadherence