Paper No. : 13 Research Methods and Fieldwork Module : 30 Blood Groups: ABO, Rh and MN systems

Development Team

Principal Investigator Prof. Anup Kumar Kapoor Department of Anthropology, University of Delhi

Dr. P. Venkatramana Paper Coordinator Faculty of Anthropology, School of Social Sciences, IGNOU, Delhi

Dr. SAA Latheef and Dr. P. Venkatramana Content Writer School of Life Sciences,

Hyderabad University, Hyderabad

Dr. Rashmi Sinha Content Reviewer Faculty of Anthropology, School of Social Sciences, IGNOU, Delhi 1

Blood Groups: ABO, Rh and MN systems Anthropology

Description of Module

Subject Name Anthropology

Paper Name Research Methods and Field work

Module Name/Title Blood Groups: ABO, Rh and MN systems Module Id 30

Glossary: • ABO blood group system was discovered by Karl Landsteiner in 1901 and was awarded Nobel Prize for his seminal contribution in 1930. The AB blood group was described by von Decastelo and Sturli in 1902. • ABO is a histo-blood group expressed in lymphocytes, platelets, tissue cells, endothelial cells, epithelial cells, sensory neurons, mucins secreted by exocrine glands, bone marrow and kidney. • Soluble form of ABO antigens are found in all body fluids except cerebrospinal fluid. • ABO antigen could be detected in 5-6 weeks of fetal life and adult level reach within 2-4 years. • ABO blood groups are divided into four groups i.e A, B, AB and O based on the presence and absence of antigen on RBC. ABO antigens are oligosaccharides expressed on RBC as glycoproteins and glycolipids. • Blood group A has antigen A and antibody anti-B, B blood group has antigen B and antibody anti-A, AB blood has antigens A and B and no antibodies, whereas O blood group has no antigens but contains antibodies anti-A and anti-B. • Antibodies of ABO are called natural antibodies (immunoglobulins produced by B lymphocytes of B1 type without stimulation. • Antibodies are produced in the gut after contact with bacteria and virus carrying A-like and B like antigens. • The natural antibodies belong to the class of IgM,IgG3 and IgA immunoglobulins.

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Blood Groups: ABO, Rh and MN systems Anthropology

• ABO antibodies are detected by three months and reach adult levels by 5-10 years. • Bombay blood group (oh group) named after the city in which it was first discovered by Bhende and co-workers in 1952. Bombay blood group has no antigens but has anti-A, anti-B and anti- H antibodies (IgM an IgG type). • ParaBombay blood group is characterized by weak expression of A,B, H antigens on red cells, weak reaction to antisera to A,B,H, presence of H antigen in serum and secretions. Presence of it detected at 4°C, by adsorption and elution or by anti-H lectin. Presence of it detected at 4°C, by adsorption and elution or by anti-H lectin. • ABO blood group system has six genotypes: A(AA,AO),B(BB,BO), AB and OO(Zhang et al., 2015). Bombay blood group genotype is hh (Das et al., 2011) whereas paraBombay blood group is (H), Se/Se or Se/se, or se/se. • Variations in ABO antigens were observed and were termed as subtypes.Antigen Subtypes in various blood group antigens as follows: A(A1,A2, A3,Ax,Afinn,Aend, Abantu, Am, Aw, Ay), B(B1,B2,B4, B3,BX,Bv,Bel,Bw), and O(O1, OIV ,O2, O3,O4, O5,O6 ., AB(A1B,A2B) and variants of ABO blood group system include cis-AB and B(A). • A and B in A/O and B/O are dominant, A and B in AB are codominant, O in A/O and B/O are autosomal recessive. • ABO gene (alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase) is located on q arm of chromosome 9 at position 34.2. It has seven exons and 6 introns. Exons span over 18kb of genomic DNA. The size of exons ranges from 28 to 688 bp, whereas, size of introns ranges from 554 to 12982. Of the exons such as exon 6 and 7 cover most of the coding sequence. • The ABO has three alleles A,B and O. A and B allele encode alpha 1-3-N- Acetylgalactosaminyltransferase (A-transferase) and alpha 1-3-Galactosyltransferase (designated B- transferase). • A transferase catalyze the transfer of N-acetylgalactose amine from the donor substrate uridine diphosphate N-acetyl-D-galactosamine to the fucosylated galactosyl residue of H antigen and form A antigen. B transferase catalyze the transfer of UDP-galactose to the fucosylated galactose of H antigen and form B antigen. O allele do not encode transferase for the formation of antigen due to deletion of

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Blood Groups: ABO, Rh and MN systems Anthropology

guanine at position 258 in the coding region near N- terminus of the protein, resulting frameshift generating a translational stop signal at codon 117 and this allele encodes a truncated protein lacking catalytic activity. • Fucosyl transferase 1(H gene) and 2(Secretor) genes(two variant transcripts of the geneFUT1,FUT2) are located on q arm of chromosome 19 at position 13.33, encodes proteins involved in the formation of H antigen and soluble H antigen which are required for the formation of A,B antigens and it soluble forms. These two forms vary in substrate specificity. • Non-sectors have nonsense mutation in FUT2 converting the codon for Trp143 to a translation stop codon. Mutations in FUT1 is responsible for Bombay blood group. Secretors of Bomabay phenotypes have traces of H,A or B on their RBC • A transferase sequence is referred as reference sequence and compared with B transferases or blood group subtypes. Coding sequence of O(O1) is identical to A sequence. • Rh is a largest and complex blood group system in humans with 51 antigens and 493 alleles. This blood group system was discovered by Landsteiner and Weiner in 1940. • Antigens of Rh blood group are proteins and are encoded by genes RHD and RHCE located closely on the p arm of the chromosome 1 at position 36.1. • Both RHD and RHCE genes have 10 exons, spread over 75kb DNA sequence, similar in 97% of sequence and considered to be evolved by gene duplications. RHD encode D antigen, whereas RHCE encode CE antigens in different combinations (ce, Ce, cE or CE)and also Cw(RH8),Cx(RH9) and VS(RH20) . • RhD and RhCE proteins vary in 32-35 amino acids sequence. Each protein has 12 transmembrane protein segments with internal termini and six loops extending outside RBC membrane. • D antigen is considered as more immunogenic and its absence is considered as Rh negative. • Rh associated glycoprotein(RHAG) present in RBC are essential for targeting of RhCE and RhD proteins to the membrane and mutations in RHAG cause loss of Rh antigens. • RHAG analogues such as RhBG and RhCG are found in liver, kidney, brain and skin.

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Blood Groups: ABO, Rh and MN systems Anthropology

• RHAG gene is located on p arm of chromosome 6 at position 12.3, has 10 exons and share 30% of sequence of RHD/RHCE genes. • Rh Proposed roles of RhD and RhCE proteins includes membrane integrity, transport of CO2 , whereas RhAG in ammonia transport, gas exchange across the plasma membrane and in mutated form in hereditary stomatocytosis. • For description of Rh blood group, three classifications described by Fisher and Race, Wiener and International society of blood transfusion are in usage, which are based on the assumptions of the aforementioned researchers on the inheritance of antigens. • In RHD gene more than 200 alleles were reported which are due to single nucleotide polymorphism or hybridization of RHD/RCHE. • Phylogenetically RHD alleles are categorized into four clusters namely Eurasian D cluster and African clusters: DIVa, DAU and weak D type 4 based on the allele that differ from consensus RHD allele. • Based on the phenotypic correlation with molecular variations, RHD alleles have been categorized into partial D, weak D type, DEL and non-functional alleles. • Except in some weak D types (1-3, 4/4.115,4.2(DAR),7) the risk of anti-D immunization is weak. • In partial D type some D epitopes are missing, carriers of partial D antigen produce anti-D upon exposure to normal D antigen R. RBC type as D positive. Of the six categories, DII-VII, DII and DVII are the result of extracellular amino acid substitutions, whereas, DIII-DVI are the products of RHD- CE-D hybrid alleles. • In carriers of weak D, epitopes are expressed weakly and RBC reacts with anti-D after an extended testing period in indirect antiglobulin test. • Weak expression of epitopes is due to amino acid substitutions in transmembrane or intracellular segments and cause problems in integration of protein to the RBC membrane. As of now, 80 weak D types including subtypes are found. • Except in some weak D types (1-3, 4/4.115,4.2(DAR),7) the risk of anti-D immunization is weak

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Blood Groups: ABO, Rh and MN systems Anthropology

• In Del type D, epitopes are expressed very weakly and found only when anti-D is adsorbed and eluted from RBC. This is due to RHD (K406K) allele containing C1225 nucleotide substitution in exon 9 which caluse missplicing of RNA that result in minor form of transcript for translation. • D negative haplotype is due to deletion of RHD gene. • Rhnull phenotype is due to inheritance of non-functional RHCE and RHD alleles. D an CE antigens are not expressed. Alterations in RHAG can also cause the loss of Rhd and RhCE proteins. • Cardinal features of carriers of Rhnull phenotypes are stomatocytosis, spherocytosis, increased osmotic fragility, altered phospholipid asymmetry, altered cell volume, defective cation flexes, elevated Na+/K+ ATPase activity, shortened survival of RBC in vivo and mild compensated hemolytic anemia. • On the basis of pattern of inheritance, Rhnull is of two types i.e. amorph and regulator. • C and c antigens are distinguished by four amino acids and the change from serine to proline occurs at position 103. Change from proline to alanine at position 226 differentiate E and e antigens. • C and c and E and e antigens are antithetical antigens (if one antigen present other antigen is absent). E is less frequent than e antigen in populations. • RHCE encode Cw and Cx both differ by single amino acid change and RBC typed as C+. Haplotype (C)ces encode altered C and e antigen and RBC type as C+, e+. Carriers of this phenotype produce anti-C, anti-e or anti-Ce and these multiple antibody specificities are called anti-hrB. Homo or heterozygous (C)ces with altered Rh haplotype on other chromosome is termed as hrB-. • Expression of e antigen is affected by amino acid change such as presence of valine than leucine at position 245, cystein than tryptophan at position 16 and deletion of arginine at position 229. Amino acid substitution of valine than leucine at position 245 causes the simultaneous presence of both VS and V antigens. • G antigen is encoded by exon 2 of RHD and RCHE genes, RBC type as D+ and C+ and also positive for G antigen. • Loss of Rh antigens was observed in patients with myeloid leukemia, change from D positive to negative was also found.

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Blood Groups: ABO, Rh and MN systems Anthropology

• After ABO, MNS system is oldest blood group system discovered. After Rh blood group system, it is a complex system containing 46 antigens. • MNS was first blood group for which molecular basis both at the protein and gene level was attempted. It is the blood group system in which most of the variants are immunogenic. • MNS blood group system is one of the nine blood group systems which are clinically significant because of their role in haemolytic transfusion reactions and haemolytic disease of newborn. • In 1927, Landsteiner and Levine discovered MN antigens. MN blood group was named after second and fifth letter of the word ‘immune’. • S antigen was discovered in 1947 in the serum of patient from Sydney city and antithetical antigen ‘s’ discovered in 1950. • Another antigen ‘U’ was discovered 1953 and named U due to its universal distribution. Other antigens were named after the person in whom antigen was discovered. • Low prevalent antigen which were under miltenberger series or system were found to be expressed by hybrid alleles of glycophorin involved in MNS system and merged with MNS system. • A convention was started to name glycophorin as GP and genes as GYP. • MN antigens are found on glycophorin A, whereas Ss antigens are born by glycophorin B. • Glycophorin is a type 1 glycoprotein composed of 131 amino acids (aa). It is associated with anion exchange protein1 of the AE1. It has amino terminal extracellular domain (72 aa), single transmembrane domain and cytoplasmic domain (36 aa) and densely glycosylated with one N glycon and 15 O glycans. • Glycophorin B is composed of 72 aa. It has extracellular domain (44 aa) and 11 O-glycon sites. Glycophorin B is a component of AE1/band 3-ankyrin macrocomplex. • O glycan residues constitute 60% of sialic acid on RBC and responsible for negative charge of RBC. Both M and N antigens differ at two amino acids positions of 1 and 5. • GPA and GPB provide a glycan coat to the RBC, act as receptor for complement, cytokines, bacteria, viruses and may regulate the integrity of the RBC membrane.

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Blood Groups: ABO, Rh and MN systems Anthropology

• Glychophorin A(GYPA), B(GYPB) and E(GYPE) genes occur as a cluster(A-B-E) spanning 330kb on long arm(q) of chromosome 4. • Glycophorin A is encoded by exon by exonA2-A7, whereas, mature glycophorin B is encoded by exon B2 and B4-6. GYPE gene participate in gene arrangements forming variant alleles. GYPE has six exons (3 and 4 pseudo exons). • Difference between S and s is due to single amino acid substitutions (Met29Thr). • Cells lacking glycophorin A and glycophorin B have reduced sialic acid levels and En(a-) and S-s-U- phenotypes. The former phenotype is due to recombination between exons A2 and B2 and deletion of exons A3 to A7. The later phenotype result from recombination and deletion of exons B2 and B4/B5. • Recombination between GYPA and GYPE and resultant loss of expression of GYPA and GYPB form Mk phenotype(M-N- S-s-U-). • MN variants result from single nucleotide substitutions, unequal crossover, gene coversion and formation of hybrid alleles. • Glycophorin variants can be detected by enzyme treatment, immunotyping,immunoblotting, SDSPAGE, PCR based assays, cloning, sequencing inhibition studies with synthetic peptides and analysis of trypsin digested products of GPA , GPB and epitopes. • Antibodies to low prevalence MNs antigens such as anti-Mia, -Vw, -Hil, -Hut and -Mur have been implicated in haemolytic disease of the foetus and newborn and delayed type of haemolytic transfusion reactions. • Alloantibodies to high prevalence antigens such as MNS antigens(Wrb) lacking in individuals carrying phenotypes such as GP.Mur, GP.Bun, GP.HF, GP.Hop, GP.Hil and GP.JL, cause haemolytic transfusion reactions. • Blood group phenotyping is carried out using glass slide or porcelain tile, test tube an microplate. Each method has its own merits and demerits. ABO,Rh and MNS antigens present on RBC are detected by anti sera(anti-A,anti-B, anti-AB, anti-D, anti-C, anti-c, anti-E and anti-e, anti-M, anti- N, anti-S and anti-s) using 3% RBC suspension prepared in normal saline and ABH antigens in body fluids are detected by absorption-inhibition test.

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Blood Groups: ABO, Rh and MN systems Anthropology

• Allele frequencies of A,B,O, D,d, M and N are calculated using Hardy-weinberg method.

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 Singh IP, Bhasin MK. A manual of biological Anthropology, Kamal Raj Enterprises,2004.

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Blood Groups: ABO, Rh and MN systems Anthropology

Web links  Alexander Weiner. Available at http://www.scienceheroes.com/index.php?option=com_content&view=article&id=195&Itemid =195, http://www.faqs.org/health/bios/77/Alexander-Wiener.html.

 Answers----population genetics problem. Available http://science.kennesaw.edu/~rmatson/Biol%203380/ANSWERS.html.

 Anti-S(monoclonal),Anti-s(monoclonal).ImmucorInc. www.fda.gov/.../BiologicsBloodVaccines/BloodBloodProducts/.../BloodDonorScreeni

 Blood group antigen gene mutation database.Available at: https://www.ncbi.nlm.nih.gov/gv/rbc/xslcgi.fcgi?cmd=bgmut/systems_info&system=abo.

 Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Chapter 4, Hemolytic disease of the newborn. Available from: https://www.ncbi.nlm.nih.gov/books/NBK2266/.

 FUT1 gene. https://ghr.nlm.nih.gov/gene/FUT1#synonyms

 FUT2 gene. Available at https://ghr.nlm.nih.gov/gene/FUT2

 Karl Landsteiner.Available at https://www.nobelprize.org/nobel_prizes/medicine/laureates/1930/landsteiner-bio.html

 Kruzel TA. Serotyping technique. www.dadamo.com/pdf/Kruzel-Serotype.pdf.

 Lamaba DS, Kaur R, Basu S. Clinically significant minor blood group antigens amongst north Indian donor population. Advances in hematology 2013.Available at http://dx.doi.org/10.1155/2013/215454.

 Macaca mulatta. Available at http://www.iucnredlist.org/details/12554/0.

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Blood Groups: ABO, Rh and MN systems Anthropology

 MNS blood group system.Available at: https://www.ncbi.nlm.nih.gov/projects/gv/rbc/xslcgi.fcgi?cmd=bgmut/systems_info&system= mns.

 National institute of biological(NIB).Guidance manual on ABO and Rh blood grouping.Ministry of Health and Family welfare, Government of India,2013. http://nib.gov.in/guidance.../Guidance_manucal_QC_ABO_Rh_blood_grouping_26_03_20.

 Rh blood group sytem. Blood group antigen gene mutation database. Available at https://www.ncbi.nlm.nih.gov/projects/gv/rbc/xslcgi.fcgi?cmd=bgmut/systems_info&system=r h.

 Westhoof CM.Online source. Rhttp://downloads.lww.com/wolterskluwer_vitalstream_com/sample- content/9780781782043_Quinley/samples/Chapter10.pdf.

Know more Karl Landsteiner: K Landsteiner was born on14th June,1868 in Vienna. He graduated in Medicine in 1891.Lansteiner published first paper on the effect of diet on the composition of blood ash. From 1898 to 1908, he worked as assistant in department of pathological anatomy and in 1911 he became Professor in the same department of University of Vienna. Due hard condition prevalent at Vienna, Landsteiner moved to Hague to work as procsecutor in Roman Catholic hospital, later appointed as Emeritus Professor at Rockfeller Institute, NewYork and died in the year 1943. He was awarded Nobel prize for Physiology or Medicine in 1930 .Apart from his discover of ABO blood groups, other seminal contributions include immunology of Syphilis, knowledge on Wassermann reaction, discovery of hapten, knowledge on paroxysmal hemoglobinuria, immunology of poliomyelitis and serological specificity of hemoglobins. Alexander Wiener: He was born on 13th March, 1907 in Brooklyn to Russian immigrants to United States of America . He studied maths at Cornell University and also majored in Biology. In 1930 he

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Blood Groups: ABO, Rh and MN systems Anthropology

obtained doctor of Medicine(MD) from Long Island College of Medicine. From 1930 to 1932, weiner worked as Intern and later, head of genetics and biometrics from 1932 to 52. In 1952, he became Professor in Forensic Medicine of New York University School of Medicine. Wiener was awarded with Lasker Award of American Public Health Association and Passano Founation award in 1951. Wiener discovered Rh factor.In collaboration with Karl Landsteiner, Wiener discovered MN and P blood groups. Wiener died in the year 1976. Rhesus monkey (Macca mulatta): This species is listed as least concern by International union of conservation of nature. Widely found in south, southeast and east Asia. It is commensal with humans. Live in group of average size of 12. Species is diurnal, omnivorous, arboreal and terrestrial. Species can be found different habitats. Major threats to this species include hunting for laboratory testing and loss of habitat. This species is included in part 1 in wildlife protection act of India and also mentioned amended act made in 2002.

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Blood Groups: ABO, Rh and MN systems Anthropology