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Disorders of blood and immune function
Published in Angus Clarke, Alex Murray, Julian Sampson, Harper's Practical Genetic Counselling, 2019
A variety of disease associations have been described with the ABO blood group system but are too weak to be of use in genetic counselling. The Duffy blood group is associated with malaria susceptibility. Similarly, although blood groups have been useful genetic markers in the study of genetic linkage, it is rare to be able to apply this form of information in risk prediction. DNA markers have superseded blood group typing for such purposes.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
ABO blood groups are inherited in the following manner. Blood group O is recessive to both A and B, but A and B exhibit co-dominance. Thus, AO or AA = blood group A; BO or BB = blood group B; OO = blood group O; AB = blood group AB. Blood group O is the most common blood group in the UK population. There is no known evolutionary advantage of being one ABO blood group over another, although people with blood group O are more susceptible to duodenal ulceration than other blood groups, and patients with blood group A are at higher risk of developing gastric carcinoma. Duffy blood group–negative individuals are resistant to Plasmodium vivax, since the Duffy antigen acts as a receptor for invasion by the human parasite.
Malaria
Published in F. Y. Liew, Vaccination Strategies of Tropical Diseases, 2017
Michael J. Lockyer, Anthony A. Holder
The invasion of erythrocytes by malaria merozoites is initiated via surface receptors on the merozoite interacting with ligands on the erythrocyte surface.11 Blockade of receptor function by a vaccine against surface receptors represents a possibility for interrupting the progress of the disease. The presence of the Duffy blood group antigens is required for invasion of human erythrocytes by P. knowlesi merozoites, and the Duffy-negative phenotype correlates with resistance to P. vivax infection.11 Duffy antigens may be associated with a ligand required by merozoites of both species.
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.