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Plasmodium spp.
Published in Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward, Case Studies in Infectious Disease, 2010
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward
These invade and destroy erythrocytes giving rise to symptoms (see complications later). The entry of the merozoites into erythrocytes is achieved through attachment of a number of surface molecules (merozoite surface proteins, MSPs) to structures on the erythrocyte, for example band 3 protein for P. falciparum. P. vivax has a specific reticular binding protein to enable it to attach and invade reticulocytes. In addition, P. vivax has surface molecules (Duffy binding proteins – DBPs) that bind to Duffy blood group antigens on the erythrocytes. The lack of this antigen in some human populations, mostly West Africans, explains their resistance to P. vivax.
Contribution of Plasmodium immunomics: potential impact for serological testing and surveillance of malaria
Published in Expert Review of Proteomics, 2019
Kokouvi Kassegne, Eniola Michael Abe, Yan-Bing Cui, Shen-Bo Chen, Bin Xu, Wang-Ping Deng, Hai-Mo Shen, Yue Wang, Jun-Hu Chen, Xiao-Nong Zhou
The release of the whole-genome sequence of Pf, Pv, and Pk, enabled major advances in malaria post-genomic research. Important differences among gene families found in these three species should be reflected in differences in biology, pathogenicity and clinical features. For example, unlike falciparum, Pv and Pk Duffy-binding proteins (DBPs) use the Duffy blood group antigens as receptors on the surface of red blood cells (RBCs) to selectively invade reticulocytes (young RBCs) [21–23]; even if it was thought that Pv or Pk merozoites are able to interact with Duffy-negative human RBCs, studies showed only normal apical orientation but no invasion since a junction does not take place [21,24]. In addition, the deletion of gene encoding PkDBP results in the complete inability of Pk merozoites to invade Duffy-positive human RBCs [23], showing that DBP is crucial for invasion during the asexual blood stage of Pv and Pk. More so, parasite sequestration and parasite-mediated rosetting of uninfected RBCs are unique characteristics of a phenomenon central to the pathogenesis of severe falciparum malaria [14]. Pf-infected RBCs together with the parasite’s VSA ligands – RIFINs and STEVORs – adhere to the vascular endothelium and cause multiorgan failures, making them major factors of virulence and severity of falciparum malaria. Similarly, this phenomenon is also observed with both Pv and Pk VSA families – VIRs and SICAs, respectively. There have been revelations that VIR proteins are expressed on or near the surface of infected RBCs and therefore mediate rosetting and cytoadherence of Pv-infected reticulocytes, especially to the ICAM-1 (intracellular adhesion molecule-1) endothelial cell receptor [25–27]. Thus, rosetting is a frequent cytoadhesive phenotype in Pv infections that may contribute to the development of anemia. SICA antigens, encoded by Pk SICAvar gene family, are also associated with parasite virulence [8]. Infected RBCs with Pk are able to bind to the inducible endothelial receptors – ICAM-1 and VCAM (vascular cell adhesion molecule) – although in a variable manner, but none bound to CD36 receptor [28]. This suggests the possibility of cytoadherence to ICAM-1 if this receptor is upregulated on brain endothelium, but further studies are needed to better understand the pathophysiology of severe knowlesi malaria.