Appendix 26. ABO Polymorphism & Infectious Disease Susceptibility



ABO Polymorphism & Disease Susceptibility

Infectious Diseases (1)

Genetic polymorphisms may have played a critical role in defending humans against pathogen invasion. A classical example on how variability is of such importance is the major histo-compatility complex (MHC) genes, which encode for the proteins that present peptide-antigens to T-cells.  Another example is the ABO polymorphism which specifies the end product of specific oligosaccharide antigens. Because ABH antigens are expressed on the surface of various types of cells and are also secreted, differential interactions with infectious pathogens have been suggested, in the past, by association studies and by binding experiments in recent years. Pathogens may have carbohydrate-binding proteins, glycosyltransferases, and/or glycosidases that recognize and bind to ABH antigens, and the host’s ABO phenotype may potentially affect the pathogen adhesion and invasion.  It may also change the constituency of resident bacterial flora in the intestine, and modify the immune response of the host. Additionally, blood group-like antigens are present on some bacteria, and they may interact with host proteins with carbohydrate-binding capacity, such as selectins, galectins, and siglecs.  They may also interact with naturally occurring antibodies.

A.E. Mourant summarized previous results of association studies of diseases, including infectious diseases, with ABO blood group polymorphism in the Oxford Monographs on Medical Genetics (Blood Groups and Diseases: A study of associations of diseases with blood groups and other polymorphisms).

Higher incidences of infection with malaria parasites (in A individuals), plague (O), and smallpox (A) were mentioned in the article.

Relatively recently, differential susceptibility towards Noroviruses has been reported among individuals with different ABO phenotypes. Noroviruses are the leading cause of relatively mild nonbacterial, acute gastroenteritis among adults and are responsible for numerous outbreaks. Noroviruses bind type-1 H antigens, and individuals with O phenotype are more likely to be infected by the viruses, whereas those with B phenotype have decreased risk of infection although different strains exhibit different binding patterns and susceptibility.

Another well-characterized example is Helicobacter pylori. This bacterium can bind to the Lewis b (Leb) oligosaccharide structure, and therefore, infects more readily individuals with certain Lewis and ABO phenotypes. However, it should be mentioned that various strains of H. pylori also use certain sialoglycoconjugates that are unrelated to Lewis or ABO antigens, as receptors when they bind host cells. The routes of infection are not as simple as they were first imagined.

Appendix 27. ABO Polymorphism & Infectious Disease Susceptibility-2

Molecular genetic basis of the blood group ABO system


Keywords

Histo-blood group ABO system, blood group ABO system, ABO system, AB0 system, ABO blood groups, AB0 blood groups, ABO blood types, AB0 blood types, ABO genetic locus, ABO genes, ABO, AB0, A glycosyltransferases, B glycosyltransferases, glycosyltransferases, A transferase, B transferase, cell surface antigens, carbohydrate antigens, oligosaccharide antigens, oligosaccharides, complex carbohydrate antigens, complex carbohydrates, A antigen, B antigen, H antigen, red blood cell antigens, A/B antigens, ABH antigens, glycolipid, glycosphingolipids, glycoproteins, oligo sugars, red blood cells, RBC, blood transfusion, transfusion medicine, cell/tissue/organ transplantation, transplantation medicine, immunohematology, immunohaematology, immuno-hematology, immunology, ABO genotyping, forensic sciences, legal medicine, human genetics, population genetics, evolution, enzymology, glycobiology, glycosciences, human genes, primate genes, mouse gene, pig genes, alpha 1,3-Gal(NAc) transferases, a1,3-galactosyl transferase, a1,3-GalNAc transferase, structural basis, molecular genetic basis of ABO, ABO polymorphism, single nucleotide polymorphism, SNP, A, B, AB, O, A2, A3, Ax, B3, alleles, weak subgroups, homo sapiens, pig AO genes, cis-AB, B(A), mouse cis-AB gene, ABO genotype, ABO phenotype, DNA methylation, transcription, alternative splicing, Golgi apparatus, transferase chimeras, GBGT1, GGTA1, A3GALT2, monoclonal antibody, sera, plant lectins, Fumi-ichiro Yamamoto, Fumiichiro Yamamoto, F. Yamamoto, Landsteiner, enzyme, kinetics, sugar specificity, acceptor substrate specificity, acceptors, donors, sugars, nucleotide-sugars, genetic engineering, differential susceptibility to infectious diseases, differential cancer susceptibility, alterations in glycosylation in cancer, pancreatic cancer, diets, Peter D'Adamo, Blood type diets, neurobiology, Masahiko Nomi, personality, Burnham Institute, Burnham Institute for Medical Research, Biomembrane Institute, IMPPC, IMPPC Institute of Predictive and Personalized Medicine of Cancer, Institut de Medicina Predictiva i Personalitzada del Càncer,  AABB, ISBT, dbRBC - Blood Group Antigen Gene Mutation Database

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