Fiche publication
Date publication
mai 2017
Journal
eLife
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas
Tous les auteurs :
Manzoni G, Marinach C, Topçu S, Briquet S, Grand M, Tolle M, Gransagne M, Lescar J, Andolina C, Franetich JF, Zeisel MB, Huby T, Rubinstein E, Snounou G, Mazier D, Nosten F, Baumert TF, Silvie O
Lien Pubmed
Résumé
sporozoites, the mosquito-transmitted forms of the malaria parasite, first infect the liver for an initial round of replication before the emergence of pathogenic blood stages. Sporozoites represent attractive targets for antimalarial preventive strategies, yet the mechanisms of parasite entry into hepatocytes remain poorly understood. Here we show that the two main species causing malaria in humans, and , rely on two distinct host cell surface proteins, CD81 and the Scavenger Receptor BI (SR-BI), respectively, to infect hepatocytes. By contrast, CD81 and SR-BI fulfil redundant functions during infection by the rodent parasite . Genetic analysis of sporozoite factors reveals the 6-cysteine domain protein P36 as a major parasite determinant of host cell receptor usage. Our data provide molecular insights into the invasion pathways used by different malaria parasites to infect hepatocytes, and establish a functional link between a sporozoite putative ligand and host cell receptors.
Mots clés
Animals, Cell Line, Endocytosis, Hepatocytes, parasitology, Host-Pathogen Interactions, Humans, Membrane Proteins, metabolism, Plasmodium berghei, growth & development, Plasmodium falciparum, growth & development, Plasmodium vivax, growth & development, Protozoan Proteins, metabolism, Rodentia, Scavenger Receptors, Class B, metabolism, Sporozoites, growth & development, Tetraspanin 28, metabolism
Référence
Elife. 2017 05 16;6:
