BLOOD GROUP SEROLOGY

Presenters; 1.Salehe Kijangwa(MMED 1 SURGERY).

2. Dominic Peter (MMED 1 SURGERY).

Facilitator; Dr. Charles G Massambu: DDS, Mmed (Anat Path), MSc

(Biomed Sci), FCP (COPECSA)
President - APT, Consultant Pathologists, Senior Lecturer-UDOM

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 CONTENTS
1. Introduction
2. Blood cell production
3. Blood group system
4. ABO blood group system
5. Rhesus factor system (Rh system)
6. Other blood group system
7. ABO incompatibility
8. Blood groups and disease association
9. Haemolytic disease of new born
10. Serological detection of ABO and Rh antigens and antibodies
11. Inheritance of Rhesus antigen
12. Importance of blood group
13. References
14. Article review
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 1. Introduction
Definition of terms
• Blood is a body fluid in the circulatory system
of humans and other vertebrates that delivers
necessary substances such as nutrients and oxygen to
the cells, and transports metabolic waste products
away from those same cells.(Wikipedia)
• Serology is the scientific study of serum and
other body fluids. In practice, the term usually refers
to the diagnostic identification of antibodies in the
serum (Wikipedia)
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 Introduction cont..
• Blood group serology is the study of the
antigens and antibodies of the blood cells, i.e.
immunohematology.
• A blood group system is a group of antigens
encoded by alleles at a single locus.

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 2. Blood Cell Production (Hemopoiesis)
• Red bone marrow produces RBCs, WBCs and platelets
• stem cells called hemocytoblasts multiply
continually & are pluripotent (capable of
differentiating into multiple cell lines)
• committed cells are destined to continue down
one specific cell line
• Stimulated by erythropoietin, thrombopoietin &
colony-stimulating factors (CSFs)

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Hemopoiesis

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 2.Blood cell production cont.…
• Erythropoiesis produces 2.5 million
RBCs/second from stem cells (hemocytoblasts)
in bone marrow
• First committed cell is proerythroblast
– has receptors for erythropoietin (EPO) from
kidneys
• Erythroblasts multiply & synthesize
hemoglobin

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 Cont…

• Normoblasts discard their nucleus to form a

reticulocyte
– named for fine network of endoplasmic reticulum
– enters bloodstream as 0.5 to 1.5% of circulating RBCs
• Development takes 3-5 days & involves
– reduction in cell size, increase in cell number,
synthesis of hemoglobin & loss of nucleus
– blood loss speeds up the process increasing
reticulocyte count
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 3.Blood group systems
• To date, 23 blood group systems are defined.
• Clinically important
– ABO or ABH
– Rhesus
• Others are less important or uncommon, e.g.
H, Lewis (Le), MNSs, Kell (K), Duffy (Fy), Kidd
(Jk), Lutheran (Lu).

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 4. ABO blood group system
• The ABO blood group was discovered in 1900
by Austrian scientist, Karl Landsteiner.
• The ABO blood group system consists of four
antigens (A, B, O and AB).
• These antigens are known as oligosaccharide
antigens, and widely expressed on the
membranes of red cell and tissue cells as well
as, in the saliva and body fluid.

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 ABO phenotypes

• The immune system forms antibodies against whichever

ABO blood group antigens are not found on the
individual's RBCs.
• Thus, a group A individual will have anti-B antibodies
and a group B individual will have anti-A antibodies.
• Blood group O is common, and individuals with this
blood type will have both anti-A and anti-B in their
serum.
• Blood group AB is the least common, and these
individuals will have neither anti-A nor anti-B in their
serum.
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• In contrast to protein-based blood groups, the
antigens of the ABO system are carbohydrate antigens.
• The determinant carbohydrate structures are
synthesized stepwise by the action of
glycosyltransferases which transfer single
monosaccharide residues onto an appropriate
precursor substance.
• The genes responsible for the formation of the
antigens of the ABO system each encode single
glycosyltransferases.

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• The ABO locus has three main allelic forms: A, B, and O.
• The A allele encodes a glycosyltransferase that produces
the A antigen (N-acetylgalactosamine is its
immunodominant sugar), and
• The B allele encodes a glycosyltransferase that creates
the B antigen (D-galactose is its immunodominant
sugar).
• The O allele encodes an enzyme with no function, and
therefore neither A or B antigen is produced, leaving the
underlying precursor (the H antigen) unchanged.

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14
.The first step in the bio-synthesis of ABO
antigens is the addition of a L -
fucose in α1-2 linkage on terminal galactose
(Gal) of a common precursor attached to lipids
or proteins by α1,2 - fucosyltransferase (H
transferase),resulting in the H antigen.

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16
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• The A and B alleles encode glycosyltransferase (α1,3 - N
acetylgalacto-
saminyltransferase (A transferase) and α1,3 - ga-
lactosyltransferase (B transferase)), which catalyze the
addition of specific sugars, N acetylgalactosamine
(GalNAc) and galactose (Gal) residue, respectively, in a
α1-3 linkage on terminal Gal of H antigen
• Since O allele encodes proteins without
glycosyltransferase (Otransferase) function, H antigen is
the only ABO structure present
in blood type O
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19
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 Structure of the ABO gene locus
• Human ABO genes are located in chromosome
9q34.1 - q34.2(6 - 9) and consists of 7 exons
distributed over 18 kb of genomic DNA.
• Exon 7 contains most of the largest coding
sequence.
• Exon 6 contains the deletion found in most O
alleles.

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• The ABO locus has three main allele forms, A,B,
and O.
• A and B alleles have seven nucleotide substitutions
(297A>G, 526C>G, 657C>T, 703G>A, 796C>A,
803G>C and 930G>A).
• Four nucleotide substitutions (526C>G, 703G>A,
796C>A and
803G>C) are translated into different amino acid
substitutions (Arg526Gly, Gly703Ser, Leu796Met
and Gly803Ala)
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• These substitutions determine the specificities of
glycosyltransferases.
• The A allele encodes A transferase catalyzing the addition
of GalNAc (N-acetylgalactosamine)residue, and the B allele
encodes B transferase catalyzing the addition of Gal
residue, respectively, in a α1-3 linkage on terminal Gal of
the H antigen.
• On the other hand, the O allele differs from the A allele by
a single nucleotide deletion of guanine (G) at position 261.
• This deletion causes a frameshift and results in a loss of
transferases activity
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 ABO sub group.
• Blood group A contain about 20 subgroups of which A1 and A2
are most common (over 99%).
• A1 makes up of about 80% of all A-type blood, with A2 making
up all of the rest.
• These subgroup are not always interchangeable as far as
transfusion is concerned, as some A2 individuals produce
antibodies against A1 antigen.
• With the development of DNA sequencing it has been possible
to identify a much larger numbers of alleles at the ABO locus,
each of which can categorized as A, B, O in terms of reaction to
transfusion, but which can be distinguished by variation in the
DNA sequences.
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Table 1:Frequency of Blood Types

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 5.Rhesus factor system(Rh System)
• Its another important system which
considered to cause agglutinations.
• This was first delivered from the horse and
protein in nature.
• There are 6 types of inherited antigen which
are; C, c, D, d, E and e.
• The most antigenic and dominant is D .

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 CONT..
• Then it is known as Rhesus Positive, without
it is Rhesus Negative.
• Distribution accordingly to races are in
Whites Rh Positive 85 % and Rh Negative
15% .In Black American, Rh-positives is 95%.

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Rh ANTIGENS

Makes the blood Type

“positive” or “Negative”
Figure 1: shows Rh in red
blood cell(google)
• Agglutination with RhD =
Positive

• No Agglutination with RhD =

Negative

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6. Other blood groups system..1/6
• H-antigen
• H-antigen is the precursor to the ABO blood group
antigens. Apparently present in all people except
with the Bombay blood phenotype which do not
express H Antigen, the antigen which is present in
group O. As H-antigen acts as precursor, its
absence means the absence of antigen A and B.
However, the individuals produce isoantibodies to
H-antigen as well as to antigens A and B.

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 6.Other blood groups system 2/6
• MNS antigen system
• MNS antigen system, first described by
Landsteiner and Levine in 1927 is based on two
genes: Glycophorin A and Glycophorin B.
• The blood group is under control of an autosomal
locus on chromosome 4 and also under control of
a pair of co-dominant alleles LM and LN. Anti-M
and anti-N antibodies are usually IgM types and
rarely, associated with transfusion reactions.
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 6.Other blood groups system 3/6
Lutheran system
• Lutheran system comprised of four pairs of
allelic antigens representing single amino acid
substitution in the Lutheran glycoprotein at
chromosome 19. Antibodies against this blood
group are rare and generally not considered
clinically significant.

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 6.Other blood groups system 4/6
Kell system
• These erythrocyte antigens are the third most potent
immunogenic antigen after ABO and Rh system, and
are defined by an immune antibody, anti-K.
• It was first noticed in the serum of Mrs. Kellacher. She
reacted to the erythrocytes of her newborn infant
resulting in hemolytic reactions. Since then 25 Kell
antigens have been discovered. Anti-K antibody causes
severe hemolytic disease of the fetus and newborn
(HDFN) and haemolytic transfusion reactions (HTR).

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6.Other blood groups system… 5/6
Duffy system
• Duffy-antigen was first isolated in a patient called
Duffy who had haemophilia. It is also known as Fy
glycoprotein and is present in the surface of RBCs. It
is a nonspecific receptor for several chemokines and
acts as a receptor for human malarial parasite,
Plamodium vivax. Antigens Fya and Fyb on the Duffy
glycoprotein can result in four possible phenotypes,
namely Fy(a+b−), Fy(a+b+), Fy(a−b+), and Fy(a−b−).
The antibodies are IgG subtypes and can cause HTR.
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 6.Other blood groups system…6/6
Kidd system
• Kidd antigen (known as Jk antigen) is a glycoprotein,
present on the membrane of RBCs and acts as a urea
transporter in RBCs and renal endothelial cells.
• Kidd antibodies are rare but can cause severe transfusion
reactions. These antigens are defined by reactions to an
antibody designated as anti-Jka, discovered in the serum of
Mrs. Kidd who delivered a baby with HDFN.
• Jka was the first antigen to be discovered by Kidd blood
group system, subsequently, two other antigens Jkb and
Jk3 were found.
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 7. Blood groups and disease association

• No diseases are known to result from the lack

of expression of ABO blood group antigens, but
the susceptibility to a number of diseases has
been linked with a person's ABO phenotype.
• Such correlations remain controversial and
include the observation that gastric cancer
appears to be more common in group A
individuals, whereas gastric and duodenal
ulcers occur more often in group O individuals
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 Blood groups and disease association
cont..
• A clear correlation has been established
between the ABO phenotype and the level of
two proteins involved in blood clotting; factor
VII (FVIII) and von Willebrand factor (vWF).
• Blood group O individuals have about 25% less
FVIII and vWF in their plasma.

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 Blood groups and disease association
cont..
• It is well established that low levels of FVIII and
vWF are a cause of excess bleeding, and
therefore it may also be the case that increased
levels make clotting more likely, increasing the
risk of both arterial (ischemic heart disease) and
venous (thromboembolic disease) problems.
• Indeed, non-group O individuals have been
shown to be at an increased risk of both arterial
and venous disease.
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 Blood groups and disease association
cont..
• Significant association of ABO groups with the
prevalence of preeclampsia has been reported,
where AB group was found to be associated with
an increased risk of 2.1-folds.
• Preliminary studies suggested an association of
ABO system with malignancies.
• A positive correlation has been shown between
blood group A with chronic hepatitis-B infection
and pancreatic cancer; and blood group B with
ovarian cancer.
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 Blood groups and disease association
cont..
• Protection against falciparum malaria can be
achieved with group O by reducing rosette
formation.
• Blood group O increases the severity of
infection in Vibrio cholerae strains (O1 El Tor
and O139).

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 8. ABO incompatibility
• The Antibodies produced against red
cell agglutinogens.
• Thus, type A individuals develop anti-B
antibodies, type B individuals develop
anti-A antibodies, type O individuals
develop both, and type AB individuals
develop neither.

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 .CONT..
• The agglutinins are produced in the bone
marrow and lymph gland cells.
• The agglutinins are gamma globulin
• The agglutinin have two binding sites
which are IgM and IgG.

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42
The Agglutination in ABO incompatibility

• Is the process of clump formation

following attachment of agglutinin to the
(RBC) Red Blood Cells.
• Blood typing is process of mixing an
individual's red blood cells with serum
containing the different agglutinins on a
slide and seeing whether agglutination
will occur.
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 Table 4:Acomparison of IgG & IgM Abs

IgG IgM
Optimal 37°c 4°c
reaction temp.
Molecular wt 150kDa 900kDa
Sedimentation 75 195
constant
Placental Yes No
transfer
Serological type “Incomplete” Saline
(Complete)
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 Cont...
• The hemolytic transfusion reactions occur when
blood is transfused into an individual with an
incompatible blood type; that is, an individual who
has agglutinins against the red cells in the
transfusion.
• When the recipient's plasma has agglutinins against
the donor's red cells, the cells agglutinate and
hemolyzed where by hemolysis is degradation of
RBC and hemoglobin released to the plasma after
phagocytosis.

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Two stages involved in antibody and antigen reaction :
• Stage 1 :the antibody bind to its red cell antigen as
soon as it contact with it . This does not cause
agglutionation of cell, but simply coats or sensitizes
the cell.
• Stage 2 :A lattice is formed , producing the clumps
or agglutination. This is a continuation of stage 1 in
which ,providing the conditions are suitable ,the
antibody can cause physical agglutination of cells.

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• IgM antibodies are large and have 10 antigen-
combining sites. They can both sensitize and
agglutinate cells directly .

figure2: Reaction of red cell with igM leading to agglutination of

cell(from WHO GPA-CNP)

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• IgG antibodies are smaller and do not directtly
agglutinate cell .Instead they coat or sensitize
the cell .

Figure3:Red cell sensitized with IgG(WHO GPA-CNP)

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• Haemolysis of red cell is caused by some of
IgM antibodies and a few IgG .After antibody
bind to the antigen the complement pathway
C3 can be activated and this lead to the red
cells being ruptured and lysing .
• Some cells coated with C3 will be removed as
they pass through the liver, but other remain
in circulation and detected when a direct
antiglobulin test is performed.
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9.Hemolytic disease of new born
• Fetal erythroblastosis Is the fetal disease which
occurs during pregnancy or short time after
delivery. It is also known as Rhesus incompatibility,
Rhesus disease RhD and Hemolytic Disease of the
Newborn.
• This occurred when the Female with Rhesus
Negative(Rh –ve) gets pregnant to Rhesus Positive
(Rh +ve ) fetus
• Pregnant mother are sensitized to Rh antigen and
develop antibodies, which will cross through the
placenta and cause hemolysis of fetal red blood
cells. 50
.

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 Pathophysiology
• Usually due to Rhesus incompatibility.
• Other alloimmune antibody (Kell, Duffy,
Kidd) can also cause hemolytic disease of
the newborn.
• Rh gene complex consists of 3 genetic loci
each with 2 major alleles.

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 CONT..
• They code for 6 major antigens denoted by
letters, C, c, E, e, and D,d
• Rh antigen is not expressed on RBC progenitor.
• The exposure of the Rh-negative mother to
Rh-positive red cells occurs as a result of
asymptomatic feto-maternal hemorrhage
during pregnancy.

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 CONT..
• Fetomaternal hemorrhage has been
documented in:
• 7% in the first trimester.
• 16% in the second trimester
• 29% in the third trimester

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 CONT…
• Risk of fetomaternal hemorrhage is
increased in abruption placenta,
threatened abortion, after cesarean
section, ectopic pregnancy,
amniocentesis, intrauterine fetal
transfusion.
• And it occur during normal delivery

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 CONT..
• After sensitization, maternal anti-D antibodies
cross the placenta into fetal circulation---
leading to hemolysis of fetal red blood cells &
fetal anemia ( HB < 11 gm/dl).

• If fetal hemoglobin is less than 4 gm/dl---

hydrops fetalis occur, fetal pleural effusion,
fetal ascites generalized edema, &
polyhydramnios.
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 CONT…
• Hyperbilirubinemia becomes apparent
only in the delivered newborn because
the placenta effectively metabolizes
bilirubin .

• Hyperbilirubinemia in the newborn lead

to Kernicterus, can cross BBB

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 CONT..
• hemolysis (less than 1%) 1% of all
pregnant women developed Rh
alloimmunization.
• less than 10% requiring intrauterine
transfusion.
• Anti-D is the most common antibodies
found in pregnant women followed by
anti-K, anti-c, and anti-E
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 CONT..
• The first baby is normal

• The second baby is anemic

• The third baby on-ward will be hydrpoic

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Figure 5:Shows Rh antigen and antibody across placenta (google)

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Figure 6:Shows Rh antigen and antibody across placenta (google)

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 CONT..
• Screening of all pregnant mothers to Rh D
antigen and antibody screening for Rh D –ve
mothers.

• -Prophylactic anti D immunoglobulin

( Rhogam) to all Rh –ve mothers after delivery
if the fetus is Rh +ve or( at 28, 36 weeks of
pregnancy) and after abortion, amniocentesis,
abruption
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 CONT..
• The standard dose of anti D is 0.3 mg —will eradicate
15 ml of fetal red blood cells (routine for all Rh –ve
pregnancies) within 3 days of delivery.
• If more feto-maternal bleeding is suspected as in
abruption or ante partum hemorrhage---Do
Kleihauer –Betke test to estimate the amount of fetal
red cells in maternal circulation and re-calculate the
dose of the anti-D

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 CONT..
• Ant –D inhibits antigen-induced antibody
production in the expectant mother
• Eliminates Rh+ve RBC in circulation of
mother
• Attaches to D antigen site on Rh +ve fetal
RBC that may cross the placenta and
enters the circulation of the expectant
mother-prevent immunization
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10.Serological detection of ABO
& Rh antigens and antibodies

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 To detect unknown ABO antigens on red
cells
• This is called cell or forward grouping
• Use serum with known ABO antibodies:
– Anti-A will agglutinate or haemolyse red cells with
A antigen
– Anti-B will agglutinate or haemolyse red cells with
B antigen
– Anti-H will agglutinate or haemolyse red cells with
H antigen
• Technique: saline at room temperature

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 To detect unknown ABO antibodies in
serum
• This is called serum or reverse grouping
• Use red cells with known ABO antigens:
– A cells will agglutinate or haemolyse with anti-A serum.
– B cell will agglutinate or haemolyse with anti-B serum.
– O cells will NOT agglutinate or haemolyse with neither
anti-A nor with anti-B serum.
– O cells will agglutinate or haemolyse with anti-H serum
most strongly than B and A cells.
• Technique: saline at room temperature

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To detect unknown Rh antigens on red cells

• This is called cell or forward grouping

• Use serum with known Rh antibodies:
– Anti-D will agglutinate cells with D antigen
– Anti-C will agglutinate cells with C antigen
– Anti-c will agglutinate cells with c antigen
– Anti-E will agglutinate cells with E antigen
– Anti-e will agglutinate cells with e antigen
• Techniques:
– Indirect antiglobulin test

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 To detect irregular or unexpected Rh
antibodies in serum
• This is done only in antibody screening
• Use red cells with known Rh antigens:
– D cells will agglutinate with anti-D serum
– C cells will agglutinate with anti-C serum
– c cells will agglutinate with anti-c serum
– E cells will agglutinate with anti-E serum
– e cells will agglutinate with anti-e serum
• Technique: Indirect antiglobulin test

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 Antiglobulin test(Coombs test)
• Technique for detecting presence of IgG
antibodies on red cell surface
• Two methods are used:
– Direct antiglobulin test
– Indirect antiglobulin test

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 Direct antiglobulin test (DAT)
• Method of detecting in vivo sensitization of
red cells with IgG antibodies
• Red cells are washed with saline 4 times to
remove free IgG which will neutralize anti-IgG
• Anti-IgG is then added to the washed cells
– Agglutination = sensitization of red cells
– No agglutination = no sensitization

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Causes of in vivo red cell sensitization
• Autoimmune haemolytic anaemia
• Haemolytic transfusion reaction
• Haemolytic disease of the newborn

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 Indirect antiglobulin test (IAT)
• Method of detecting in vitro sensitization of
red cells with IgG antibodies
• Red cells are incubated for 90 minutes with a
test serum suspected to contain an offending
IgG antibody.
• After incubation, follow the same procedure
as for DAT above.

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 11. INHERITANCE OF Rh ANTIGEN

– Rhesus factor is an inherited dominant factor. It

may be homozygous Rhesus positive with DD or
heterozygous Rhesus positive with Dd .
– Rhesus negative occurs only with complete
absence of D (i.e. with homozygous dd).

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Fig7:Inheritence Rh Antigen (Google)

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Fig 8:Inheritence Rh Antigen (Google)

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Fig 9:Inheritence Rh Antigen (Google)

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 12. IMPORTANCE OF KNOWING
BLOOD GROUP
1. Medically, it is important during blood transfusions and in
tissue transplants.
2. Socially, one should know his or her own blood group and
become a member of the Blood Donor’s Club so that he or
she can be approached for blood donation during
emergency conditions.
3. It general among the couples, knowledge of blood groups
helps to prevent the complications due to Rh incompatibility
and save the child from the disorders like erythroblastosis
fetalis.
4. Judicially, it is helpful in medico-legal cases to sort out
parental disputes.
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 13.Refference;
1. Ganong Medical Physiology - 21 Edition
2. Guyton & Hall Textbook Of Medical Physiology 13th_Edition
3. Robins Basic Pathology 10th Edition
4. WHO_GPA_CNP_93.2D_Mod3.pdf
5. www.pubmed.com
6. Matzhold EM, Berghold A, Bemelmans MKB, et al. Lewis
and ABO histo-blood types and the secretor status of
patients hospitalized with COVID-19 implicate a role for
ABO antibodies in susceptibility to infection with SARS-CoV-
2. Transfusion. 2021;61: 2736–2745.
https://doi.org/10.1111/trf.16567
79
14.ARTICLE REVIEW

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• Abstract :Severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) targets the respiratory
and gastric epithelium, causing coronavirus disease
2019 (COVID-19).
• Tissue antigen expression variations influence host
susceptibility to many infections.
• This study aimed to investigate the closely linked
Lewis (FUT3) and ABO histo-blood types, including
secretor (FUT2) status, to infections with SARS-CoV-
2 and the corresponding severity of COVID-19.
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 Introduction
• The severe acute respiratory syndrome coronavirus2 (SARS-
CoV-2) targets the respiratory mucosa, and it can infect and
replicate in the gastric and intestinal epithelium, causing
coronavirus disease 2019 (COVID-19).
• This emerging infectious disease is usually characterized by an
acute respiratory infection, with symptoms varying from mild
to severe, including pneumonia, respiratory failure,
coagulopathy, multiple organ failure, and death.
• COVID-19 is a complex and multifactorial disease, where
inherited predispositions together with existing comorbidities
and acquired risk factors are likely to influence the severity of
the disease.
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 Introduction cont..
• Differences in blood group antigen expression can increase
or decrease host susceptibility to many infections.
• Pathogens including viruses, bacteria, and eukaryotic
parasites carry lectins on their surfaces, which can bind to
glycan structures such as blood group antigens on the host
cell surface as a first step in the infection process.
• Blood group antigen structures may be involved in the
binding of their toxins, facilitating invasion and
colonization or evasion of host clearance mechanisms.
They can also serve as false receptors, preventing
pathogen binding to target tissues.
83
 Introduction cont…
• The carbohydrate histo-blood group antigens Lewis
and ABO are widely expressed in many tissues,
including respiratory and gastric mucosa,
endothelium, kidney, and heart.8
• The Lewis enzyme (fucosyltransferase 3), encoded
by FUT3, is responsible for the last step in the
biosynthesis of Lewis antigens.
• The immunodominant glycan structures defining
the ABO antigens are synthesized by
glycosyltransferases, encoded by the ABO gene.
84
 Introduction cont..
• The expression of soluble ABO(H) antigens in
secretory epithelium is regulated by
Fucosyltransferse 2 (Fut 2), encoded by the
FUT2 gene.
• The activity of fucosyltransferase 2 (Fut 2) is
also required for the production of Lewis b (Le
b) antigen, and reflected by the Le (a-b+)
phenotype. In contrast, the Le (a+b-) is found
in ABH nonsecretors (18%–22%)
85
 Conclusion
• Findings suggest that Lewis antigens
contribute to infection with SARS-CoV-2.
Further more confirm, ABO blood group O,
with obligatory anti-A and anti-B antibodies
present, to be protective against COVID-19.

86
 Conclusion cont…
• The blood type AB, lacking those isoagglutinins, is
suggested to increase the risk of infection.
• There are therefore strong indications that ABO
antibodies affect susceptibility to COVID-19, and
should be the subject of further research.
• Sophisticated in vitro studies investigating the
mechanism of virus–host cell interactions should
be included

87
 Study limitations
• Sample size was restricted to patients hospitalized with
COVID-19. Future studies should take into account the
whole cohort of individuals tested positive for SARS-CoV-2
to investigate the relationship between the disease and
blood group types.
• The sample size of 338 patients is relatively small.
• This is a retrospective observational study, can not rule
out the fact that unmeasured confounding factors may
have influenced the outcome. For the future study to use
another study design to eliminate confounding factor eg.
cohort prospective
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THANK YOU FOR LISTENING

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