The machinery underlying malaria parasite virulence is conserved between rodent and human malaria parasites

Mariana De Niz, Ann-Katrin Ullrich, Arlett Heiber, Alexandra Blancke Soares, Christian Pick, Ruth Lyck, Derya Keller, Gesine Kaiser, Monica Prado, Sven Flemming, Hernando del Portillo, Chris J. Janse, Volker Heussler () and Tobias Spielmann ()
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Mariana De Niz: Institute of Cell Biology, University of Bern
Ann-Katrin Ullrich: Bernhard Nocht Institute for Tropical Medicine, Parasitology Section
Arlett Heiber: Bernhard Nocht Institute for Tropical Medicine, Parasitology Section
Alexandra Blancke Soares: Bernhard Nocht Institute for Tropical Medicine, Parasitology Section
Christian Pick: Institute of Zoology, Universtity of Hamburg
Ruth Lyck: Theodor Kocher Institute, University of Bern
Derya Keller: Institute of Cell Biology, University of Bern
Gesine Kaiser: Institute of Cell Biology, University of Bern
Monica Prado: Bernhard Nocht Institute for Tropical Medicine, Parasitology Section
Sven Flemming: Bernhard Nocht Institute for Tropical Medicine, Parasitology Section
Hernando del Portillo: ICREA at ISGlobal, Barcelona Ctr. Int. Health Res. (CRESIB), Hospital Clínic—Universitat de Barcelona and Institut d’Investigació Germans Trias i Pujol (IGTP). Ctra. de Can Ruti. Camí de les Escoles, s/n
Chris J. Janse: Leiden Malaria Research Group, Leiden University Medical Center
Volker Heussler: Institute of Cell Biology, University of Bern
Tobias Spielmann: Bernhard Nocht Institute for Tropical Medicine, Parasitology Section

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract Sequestration of red blood cells infected with the human malaria parasite Plasmodium falciparum in organs such as the brain is considered important for pathogenicity. A similar phenomenon has been observed in mouse models of malaria, using the rodent parasite Plasmodium berghei, but it is unclear whether the P. falciparum proteins known to be involved in this process are conserved in the rodent parasite. Here we identify the P. berghei orthologues of two such key factors of P. falciparum, SBP1 and MAHRP1. Red blood cells infected with P. berghei parasites lacking SBP1 or MAHRP1a fail to bind the endothelial receptor CD36 and show reduced sequestration and virulence in mice. Complementation of the mutant P. berghei parasites with the respective P. falciparum SBP1 and MAHRP1 orthologues restores sequestration and virulence. These findings reveal evolutionary conservation of the machinery underlying sequestration of divergent malaria parasites and support the notion that the P. berghei rodent model is an adequate tool for research on malaria virulence.

Date: 2016
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DOI: 10.1038/ncomms11659

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