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Plasmodium falciparum strains spontaneously switch invasion phenotype in suspension culture.*

Posted by on in 2018
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Awandare GA1,2Nyarko PB3Aniweh Y3Ayivor-Djanie R3,4Stoute JA5Sci Rep. 2018 Apr 10;8(1):5782. doi: 10.1038/s41598-018-24218-0.

1
West African Centre for Cell Biology of Infectious Pathogens, University of Ghana, Legon, Ghana. gawandare@ug.edu.gh.
2
Department of Biochemistry, Cell and Molecular Biology, University of Ghana, Legon, Ghana. gawandare@ug.edu.gh.
3
West African Centre for Cell Biology of Infectious Pathogens, University of Ghana, Legon, Ghana.
4
Department of Biomedical Sciences, University of Health and Allied Sciences, Ho, Ghana.
5
Department of Medicine, Pennsylvania State University College of Medicine, Hershey, PA, USA.

Abstract

The extensive redundancy in the use of invasion ligands by Plasmodium falciparum, and its unique ability to switch between invasion pathways have hampered vaccine development. P. falciparum strains Dd2 and W2mef have been shown to change from sialic acid (SA)-dependent to SA-independent phenotypes when selected on neuraminidase-treated erythrocytes. Following an observation of increasing ability of Dd2 to invade neuraminidase-treated cells when cultured for several weeks, we systematically investigated this phenomenon by comparing invasion phenotypes of Dd2, W2mef and 3D7 strains of P. falciparum that were cultured with gentle shaking (Suspended) or under static (Static) conditions. While Static Dd2 and W2mef remained SA-dependent for the entire duration of the investigation, Suspended parasites spontaneously and progressively switched to SA-independent phenotype from week 2 onwards. Furthermore, returning Suspended cultures to Static conditions led to a gradual reversal to SA-dependent phenotype. The switch to SA-independent phenotype was accompanied by upregulation of the key invasion ligand, reticulocyte-binding homologue 4 (RH4), and the increased invasion was inhibited by antibodies to the RH4 receptor, CR1. Our data demonstrates a novel mechanism for inducing the switching of invasion pathways in P. falciparum parasites and may provide clues for understanding the mechanisms involved.

Normal Chicken IgY antibodies used in this publication were produced by Gallus Immunotech Inc.

PMID:
 
29636510
 
PMCID:
 
PMC5893586
 
DOI:
 
10.1038/s41598-018-24218-0
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