Plasmodium P36 determines host cell receptor usage during sporozoite invasion. Manzoni, G., Marinach, C., Topçu, S., Briquet, S., Grand, M., Tolle, M., Gransagne, M., Lescar, J., Andolina, C., Franetich, J., Zeisel, M. B., Huby, T., Rubinstein, E., Snounou, G., Mazier, D., Nosten, F., Baumert, T. F., & Silvie, O. eLife, May, 2017.
doi  abstract   bibtex   
Plasmodium 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, Plasmodium falciparum and Plasmodium vivax, 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 P. berghei. 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.
@article{manzoni_plasmodium_2017,
	title = {Plasmodium {P36} determines host cell receptor usage during sporozoite invasion},
	volume = {6},
	issn = {2050-084X},
	doi = {10.7554/eLife.25903},
	abstract = {Plasmodium 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, Plasmodium falciparum and Plasmodium vivax, 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 P. berghei. 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.},
	language = {eng},
	journal = {eLife},
	author = {Manzoni, Giulia and Marinach, Carine and Topçu, Selma and Briquet, Sylvie and Grand, Morgane and Tolle, Matthieu and Gransagne, Marion and Lescar, Julien and Andolina, Chiara and Franetich, Jean-François and Zeisel, Mirjam B. and Huby, Thierry and Rubinstein, Eric and Snounou, Georges and Mazier, Dominique and Nosten, François and Baumert, Thomas F. and Silvie, Olivier},
	month = may,
	year = {2017},
	pmid = {28506360},
	pmcid = {PMC5470872},
	keywords = {P. berghei, P. falciparum, P. vivax, P. yoelii, hepatocyte, human, infectious disease, malaria, microbiology, mouse, sporozoite},
}

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