Problem 1
When crossing plants of one of the pumpkin varieties with white and yellow fruits, all F 1 offspring had white fruits. When these offspring were crossed with each other in their F 2 offspring, the following was obtained:
207 plants with white fruits,
54 plants with yellow fruits,
18 plants with green fruits.
Determine possible genotypes of parents and offspring.
Solution:
1. The 204:53:17 split corresponds to approximately a 12:3:1 ratio, indicating the phenomenon of epistatic gene interaction (when one dominant gene, such as A, dominates another dominant gene, such as B). Hence, the white color of the fruit is determined by the presence of the dominant gene A or the presence of dominant genes of two AB alleles in the genotype; The yellow color of the fruit is determined by the B gene, and the green color of the fruit by the aabv genotype. Consequently, the original plant with yellow fruit color had the genotype aaBB, and the white-fruited one had the genotype AAbb. When they were crossed, the hybrid plants had the genotype AaBb (white fruits).

First crossing scheme:

2. When self-pollinating plants with white fruits, the following were obtained: 9 white-fruited plants (genotype A!B!),
3 - white-fruited (genotype A!bb),
3 - yellow-fruited (genotype aaB!),
1 - green-fruited (genotype aabb).
The phenotypic ratio is 12:3:1. This corresponds to the conditions of the problem.

Second crossing scheme:

Answer:
The genotypes of the parents are AABB and aabb, the genotypes of the F 1 offspring are AaBb.

Problem 2
In Leghorn chickens, feather color is determined by the presence of the dominant gene A. If it is in a recessive state, the color does not develop. The action of this gene is influenced by gene B, which in a dominant state suppresses the development of the trait controlled by gene B. Determine the probability of the birth of a colored chicken from crossing chickens with the genotypes AABb and aaBb.
Solution:
A - a gene that determines the formation of color;
a - a gene that does not determine the formation of color;
B - a gene that suppresses color formation;
b - a gene that does not affect the formation of color.

aaBB, aaBb, aabb – white color (allele A is absent in the genotype),
AAbb, Aabb – colored plumage (allele A is present in the genotype and allele B is absent),
AABB, AABb, AaBB, AaBb – white color (the genotype contains allele B, which suppresses the manifestation of allele A).

The presence of dominant alleles of gene A and gene I in the genotype of one of the parents gives them white plumage, the presence of two recessive alleles a gives the other parent also white plumage. When crossing chickens with the AABb and aaBb genotypes, it is possible to obtain chickens with colored plumage in the offspring, since individuals form two types of gametes, when fused, the formation of a zygote with both dominant genes A and B is possible.

Crossing scheme:

Thus, with this crossing, the probability of obtaining white chickens in the offspring is 75% (genotypes: AaBB, AaBb and AaBb), and colored ones - 25% (genotype Aabb).
Answer:
The probability of birth of a colored chick (Aabb) is 25%.

Problem 3
When pure lines of brown and white dogs were crossed, all the offspring were white. Among the offspring of the resulting hybrids there were 118 white, 32 black, 10 brown dogs. Define types of inheritance.
Solution:
A - a gene that determines the formation of black coloring;
a - a gene that causes the formation of brown coloring;
J - gene that suppresses color formation;
j is a gene that does not affect the formation of color.

1. The offspring of F 1 are uniform. This indicates that the parents were homozygous and the white color trait is dominant.
2. Hybrids of the first generation F 1 are heterozygous (obtained from parents with different genotypes and have a split in F 2).
3. In the second generation there are three classes of phenotypes, but the segregation is different from that of codominance (1:2:1) or complementary inheritance (9:6:1, 9:3:4, 9:7 or 9:3:3 :1).
4. Suppose that a trait is determined by the opposite action of two pairs of genes, and individuals in which both pairs of genes are in a recessive state (aajj) differ in phenotype from individuals in which the action of the gene is not suppressed. The 12:3:1 split in the progeny confirms this assumption.

First crossing scheme:

Second crossing scheme:

Answer:
The genotypes of the parents are aajj and AAJJ, the genotypes of the F1 offspring are AaJj. An example of dominant epistasis.

Problem 4
The coloring of mice is determined by two pairs of non-allelic genes. The dominant gene of one pair causes gray color, its recessive allele causes black color. The dominant allele of the other pair promotes the manifestation of color, while its recessive allele suppresses color. When gray mice were crossed with white mice, all the offspring were obtained gray. When crossing F 1 offspring with each other, 58 gray, 19 black and 14 white mice were obtained. Determine the genotypes of parents and offspring, as well as the type of inheritance of traits.
Solution:
A - a gene that causes the formation of gray coloring;
a - a gene that determines the formation of black coloring;
J - gene that contributes to the formation of color;
j is a gene that suppresses the formation of color.

1. The offspring of F 1 are uniform. This indicates that the parents were homozygous and the gray color trait is dominant over the black color.
2. Hybrids of the first generation F 1 are heterozygous (obtained from parents with different genotypes and have a split in F 2). Cleavage 9: 3: 4 (58: 19: 14), indicates the type of inheritance - single recessive epistasis.

First crossing scheme:

Second crossing scheme:

3. In the F 2 offspring, a 9: 4: 3 split is observed, characteristic of single recessive epistasis.
Answer:
The original organisms had genotypes AAJJ and aajj. The uniform offspring of F 1 carried the genotype AaJj; in the F 2 offspring, a 12: 4: 3 split was observed, characteristic of single recessive epistasis.

Problem 5
The so-called Bombay phenomenon is that in a family where the father had I (0) blood group and the mother III (B), a girl was born with I (0) blood group. She married a man with blood group II (A), and they had two girls with group IV (AB) and group I (0). The appearance of a girl with group IV (AB) from a mother with group I (0) caused bewilderment. Scientists explain this by the action of a rare recessive epistatic gene that suppresses blood groups A and B.
a) Determine the genotype of the indicated parents.
b) Determine the probability of the birth of children with group I (0) from a daughter with group IV (AB) from a man with the same genotype.
c) Determine the probable blood types of children from the marriage of a daughter with I (0) blood group, if the man is with IV (AB) group, heterozygous for the epistatic gene.
Solution:

In this case, the blood type will be determined in this way

a) A recessive epistatic gene manifests its effect in a homozygous state. The parents are heterozygous for this gene, since they had a daughter with blood group I (0), who, from a marriage with a man with group II (A), gave birth to a girl with blood group IV (AB). This means that she is a carrier of the IB gene, which is suppressed in her by the recessive epistatic gene w.

Diagram showing the crossing of parents:

Diagram showing the crossing of a daughter:

Answer:
The mother's genotype is IBIBWw, the father's genotype is I0I0Ww, the daughter's genotype is IBI0ww and her husband is I0I0Ww.

Diagram showing the crossing of a daughter from group IV (AB) and a man with the same genotype:

Answer:
Probability of having children with I (0) gr. equal to 25%.

Diagram showing the crossing of a daughter from group I (0) and a man from group IV (AB), heterozygous for the epistatic gene:

Answer:
Probability of having children with I (0) gr. equal to 50%, with II (B) gr. - 25% and from II (A) gr. - 25%.

) is a type of non-allelic interaction (recessive epistasis) of a gene h with genes responsible for the synthesis of blood group agglutinogens of the AB0 system on the surface of erythrocytes. This phenotype was first discovered by Dr. Y. M. Bhende in 1952 in the Indian city of Bombay, who gave the name to this phenomenon.

Opening

The discovery was made during research related to cases of mass malaria, after three people were found to lack the necessary antigens, which are usually used to determine whether blood belongs to a particular group. There is an assumption that the emergence of such a phenomenon is associated with frequent consanguineous marriages, which are traditional in this part of the globe. Perhaps it is for this reason that in India the number of people with this blood type is 1 case per 7,600 people, with an average for the world population of 1:250,000.

Description

In people who have this gene in a recessive homozygous state hh, agglutinogens are not synthesized on the erythrocyte membrane. Accordingly, agglutinogens are not formed on such red blood cells A And B, since there is no basis for their formation. This leads to the fact that carriers of this blood type are universal donors - their blood can be transfused to any person who needs it (naturally, taking into account the Rh factor), but at the same time, they themselves can only be transfused with the blood of people with the same "phenomenon".

Spreading

The number of people with this phenotype is approximately 0.0004% of the total population, but in some areas, particularly in Mumbai (formerly Bombay), their number is 0.01%. Considering the exceptional rarity of this type of blood, its carriers are forced to create their own blood bank, since in case of need for an emergency transfusion they can receive required material there will be practically nowhere.

Who doesn’t know that people have four main blood groups. The first, second and third are quite common, the fourth is not so widespread. This classification is based on the content of so-called agglutinogens in the blood - antigens responsible for the formation of antibodies.

Blood type is most often determined by heredity, for example, if the parents have the second and third groups, the child can have any of the four, if the father and mother have the first group, their children will also have the first, and if, say, the parents have the fourth and the first, the child will have either the second or the third.

However, in some cases, children are born with a blood type that, according to the rules of inheritance, they cannot have - this phenomenon is called the Bombay phenomenon, or bombay blood.

Within the ABO/Rhesus blood group systems that are used to classify most blood types, there are several rare blood types. The rarest is AB-, this blood type is observed in less than one percent of the world's population. Types B- and O- are also very rare, each accounting for less than 5% of the world's population. However, in addition to these two main ones, there are more than 30 generally accepted blood typing systems, including many rare types, some of which are observed in a very small group of people.

Blood type is determined by the presence in the blood certain antigens. Antigens A and B are very common, making it easier to classify people based on which antigen they have, whereas people with type O blood have neither antigen. Positive or negative sign after the group means the presence or absence of the Rh factor. At the same time, in addition to antigens A and B, other antigens may be present, and these antigens may react with the blood of certain donors. For example, someone may have blood type A+ and lack another antigen in their blood, indicating the likelihood of an adverse reaction with donated blood group A+ containing this antigen.

Bombay blood does not have antigens A and B, so it is often confused with the first group, but it also does not contain antigen H, which can become a problem, for example, when determining paternity - after all, the child does not have a single antigen in his blood that he has. him from his parents.

A rare blood type does not cause its owner any problems, except for one thing - if he suddenly needs a blood transfusion, then only the same Bombay blood can be used, and this blood can be transfused to a person with any group without any consequences.

The first information about this phenomenon appeared in 1952, when the Indian doctor Vhend, conducting blood tests in a family of patients, received an unexpected result: the father had blood group 1, the mother had blood group II, and the son had blood group III. He described this case in the largest medical journal, The Lancet. Subsequently, some doctors encountered similar cases, but could not explain them. And only at the end of the 20th century the answer was found: it turned out that in such cases the body of one of the parents mimics (fake) one blood group, while in fact it has another; two genes are involved in the formation of the blood group: one determines the group blood, the second encodes the production of an enzyme that allows this group to be realized. This scheme works for most people, but in rare cases the second gene is missing, and therefore the enzyme is missing. Then the following picture is observed: a person has, for example. Blood group III, but it cannot be realized, and the analysis reveals II. Such a parent passes on his genes to the child - hence the “inexplicable” blood type in the child. There are few carriers of such mimicry - less than 1% of the Earth's population.

The Bombay phenomenon was discovered in India, where, according to statistics, 0.01% of the population have “special” blood; in Europe, Bombay blood is even less common - approximately 0.0001% of the population.

And now a little more detail:

There are three types of genes responsible for blood group - A, B, and 0 (three alleles).

Every person has two blood type genes - one received from the mother (A, B, or 0), and one received from the father (A, B, or 0).

There are 6 possible combinations:

How it works (from the point of view of cell biochemistry)

On the surface of our red blood cells there are carbohydrates - “H antigens”, also known as “0 antigens”. (On the surface of red blood cells there are glycoproteins that have antigenic properties. They are called agglutinogens.)

Gene A encodes an enzyme that converts some of the H antigens into A antigens. (Gene A encodes a specific glycosyltransferase that adds an N-acetyl-D-galactosamine residue to an agglutinogen, resulting in agglutinogen A).

Gene B encodes an enzyme that converts some of the H antigens into B antigens (Gene B encodes a specific glycosyltransferase that adds a D-galactose residue to the agglutinogen, resulting in agglutinogen B).

Gene 0 does not code for any enzyme.

Depending on the genotype, carbohydrate vegetation on the surface of red blood cells will look like this:

For example, let’s cross parents with groups 1 and 4 and see why they cannot have a child with group 1.

(Because a child with type 1 (00) should receive a 0 from each parent, but a parent with blood type 4 (AB) does not have a 0.)

Bombay phenomenon

It occurs when a person does not produce the “original” antigen H on his red blood cells. In this case, the person will have neither antigens A nor antigens B, even if the necessary enzymes are present. Well, great and powerful enzymes will come to convert H into A... oops! but there’s nothing to transform, there’s no one!

The original H antigen is encoded by a gene, which is unsurprisingly designated H.

H - gene encoding antigen H

h - recessive gene, H antigen is not formed

Example: a person with the AA genotype must have blood group 2. But if he is AAHh, then his blood type will be the first, because there is nothing to make antigen A from.

This mutation was first discovered in Bombay, hence the name. In India, it occurs in one person in 10,000, in Taiwan - in one in 8,000. In Europe, hh is very rare - in one person in two hundred thousand (0.0005%).

An example of the Bombay phenomenon No. 1: if one parent has the first blood group, and the other has the second, then the child cannot have the fourth group, because neither parent has the B gene necessary for group 4.

And now the Bombay phenomenon:

The trick is that the first parent, despite its BB genes, does not have B antigens, because there is nothing to make them from. Therefore, despite the genetic third group, from the point of view of blood transfusion, he has the first group.

An example of the Bombay phenomenon No. 2. If both parents have group 4, then they cannot have a child of group 1.

And now the Bombay phenomenon

As we see, with the Bombay phenomenon, parents with group 4 can still get a child with group 1.

Cis position A and B

In a person with blood type 4, during crossing over, an error (chromosomal mutation) may occur when both genes A and B appear on one chromosome, but nothing on the other chromosome. Accordingly, the gametes of such an AB will turn out strange: one will contain AB, and the other will have nothing.

Of course, chromosomes containing AB and chromosomes containing nothing at all will be rejected by natural selection, because they will have difficulty conjugating with normal, non-mutant chromosomes. In addition, AAV and ABB children may experience a gene imbalance (impaired viability, death of the embryo). The probability of encountering a cis-AB mutation is estimated at approximately 0.001% (0.012% cis-AB relative to all AB).

Example of cis-AV. If one parent has group 4, and the other has group 1, then they cannot have children of either group 1 or 4.

And now the mutation:

The probability of having children shaded in gray is, of course, less - 0.001%, as agreed, and the remaining 99.999% falls on groups 2 and 3. But still, these fractions of a percent “should be taken into account during genetic counseling and forensic medical examination.”

The everyday life of a person with unique blood does not differ from its other classifications, with the exception of several factors:
· transfusion is a serious problem; only the same blood can be used for these purposes, and it is universal donor and suits everyone;
· impossibility of establishing paternity; if it happens that DNA testing is necessary, it will not give results, since the child does not have the antigens that his parents have.

Interesting fact! In the USA, Massachusetts, there lives a family where two children have the Bombay phenomenon, only at the same time A-H type, such blood was diagnosed once in the Czech Republic in 1961. They cannot be donors to each other, since they have a different Rh factor, and transfusion of any other group is naturally impossible. The eldest child reached adulthood and became a donor for himself as a last resort, the same fate awaits his younger sister when she turns 18

And something else interesting on medical topics: here I talked in detail and here. Or maybe someone is interested or, for example, well-known to everyone

How does it work (from the point of view of cell biochemistry)…

On the surface of our red blood cells there are carbohydrates - “H antigens”, also known as “0 antigens”.(On the surface of red blood cells there are glycoproteins that have antigenic properties. They are called agglutinogens.)

Gene A encodes an enzyme that converts some H antigens into A antigens.(Gene A encodes a specific glycosyltransferase that adds the residueN-acetyl-D-galactosamineto an agglutinogen, resulting in agglutinogen A).

Gene B encodes an enzyme that converts some H antigens into B antigens. (Gene B encodes a specific glycosyltransferase that adds the residue D-galactose to agglutinogen, resulting in agglutinogen B).

Gene 0 does not code for any enzyme.

Inheritance of blood groups. Bombay phenomenon...

For example, let's cross parents with groups 1 and 4 and see why they havethere cannot be a child with 1

(Because a child with type 1 (00) should receive a 0 from each parent, but a parent with blood type 4 (AB) does not have a 0.)

Inheritance of blood groups. Bombay phenomenon...

Bombay phenomenon

It occurs when a person does not produce the “original” antigen H on his red blood cells. In this case, the person will have neither antigens A nor antigens B, even if the necessary enzymes are present.

Example: a person with the AA genotype must have blood group 2. But if he is AAHh, then his blood type will be the first, because there is nothing to make antigen A from.

This mutation was first discovered in Bombay, hence the name. In India, it occurs in one person in 10,000, in Taiwan - in one in 8,000. In Europe, hh is very rare - in one person in two hundred thousand (0.0005%).

Inheritance of blood groups. Bombay phenomenon...

An example of the Bombay phenomenon at work:if one parent has the first blood group, and the other has the second, then the child can't have fourth group, because none of them

parents do not have the B gene required for group 4.

Polymerism…

Polymerism is the interaction of non-allelic multiple genes that unidirectionally influence the development of the same trait; The degree of manifestation of a trait depends on the number of genes. Polymer genes are designated by the same letters, and alleles of the same locus have the same subscript.

Polymer interaction of non-allelic genes can be

cumulative and non-cumulative.

With cumulative (accumulative) polymerization, the degree of manifestation of the trait depends on the total action of several genes. The more dominant gene alleles, the more pronounced a particular trait is. Segregation in F2 according to the phenotype during dihybrid crossing occurs in the ratio 1: 4: 6: 4: 1, and in general corresponds to the third, fifth (with dihybrid crossing), seventh (with trihybrid crossing), etc. lines in Pascal's triangle.

Polymerism…

With non-cumulative polymerization, the signmanifests itself in the presence of at least one of the dominant alleles of polymer genes. The number of dominant alleles does not affect the degree of expression of the trait. Segregation in F2 according to phenotype during dihybrid crossing is 15:1.

Polymer Example- inheritance of skin color in humans, which depends (to a first approximation) on four genes with a cumulative effect.

The human body is famous for its uniqueness. Due to various mutations that occur daily in our body, we become individual, since some of the characteristics that we acquire differ significantly from the same external and internal factors of other people. This also applies to blood type.

It is usually customary to divide it into 4 types. However, it is extremely rare, but it happens that a person who should have one (due to genetic characteristics parents) has a completely different, specific. This paradox is called the “Bombay phenomenon”.

What is it?

This term refers to a hereditary mutation. It is extremely rare - up to 1 case per ten million people. The Bombay phenomenon gets its name from the Indian city of Bombay.

In India, there is one settlement where people have a “chimeric” blood type quite often. This means that when determining erythrocyte antigens using standard methods, the result shows, for example, the second group, although in fact, due to a mutation in a person, the first.

This occurs due to the formation of a recessive pair of genes H in a person. Normally, if a person is heterozygous for this gene, then the trait does not appear; the recessive allele cannot perform its function. Due to the incorrect combination of parental chromosomes, a recessive pair of genes is formed, and the Bombay phenomenon occurs.

How does it develop?

History of the phenomenon

A similar phenomenon was described in many medical publications, but almost until the middle of the 20th century, no one had any idea why this was happening.

This paradox was discovered in India in 1952. The doctor, conducting a study, noticed that the parents had the same blood groups (the father had the first, and the mother the second), and the born child had the third.

Having become interested in this phenomenon, the doctor was able to determine that the father’s body had managed to somehow change, which made it possible to believe that he had the first group. The modification itself occurred due to the absence of an enzyme that allows the synthesis of the required protein, which would help determine the required antigen. However, since there was no enzyme, the group could not be determined correctly.

The phenomenon is quite rare among representatives. It is somewhat more common to find carriers of “Bombay blood” in India.

Theories of the origin of Bombay blood

One of the main theories for the emergence of a unique blood type is chromosomal mutation. For example, in a person with it is possible to recombine alleles on chromosomes. That is, during the formation of gametes, the genes responsible for can move as follows: genes A and B will end up in one gamete (the subsequent individual can receive any group except the first), and the other gamete will not carry the genes responsible for the blood type. In this case, inheritance of a gamete without antigens is possible.

The only obstacle to its spread is that many such gametes die without even entering embryogenesis. However, perhaps some survive, which subsequently contributes to the formation of Bombay blood.

It is also possible that gene distribution is disrupted at the zygote or embryonic stage (as a result of maternal malnutrition or excessive alcohol consumption).

The mechanism of development of this condition

As has been said, everything depends on genes.

A person’s genotype (the totality of all his genes) directly depends on the parent, or more precisely, on what characteristics were passed on from parents to children.

If you study the composition of antigens more deeply, you will notice that the blood type is inherited from both parents. For example, if one of them has the first, and the other has the second, then the child will have only one of these groups. If the Bombay phenomenon develops, everything happens a little differently:

• The second blood group is controlled by the gene a, which is responsible for the synthesis of a special antigen - A. The first, or zero, has no specific genes.
• The synthesis of antigen A is due to the action of the section of chromosome H responsible for differentiation.
• If there is a malfunction in the system of this section of DNA, then the antigens cannot differentiate correctly, which is why the child can acquire antigen A from the parent, and the second allele in the genotype pair cannot be determined (conventionally it is called nn). This recessive pair suppresses the action of area A, as a result of which the child has the first group.

If we generalize everything, it turns out that the main process causing the Bombay phenomenon is recessive epistasis.

Non-allelic interaction

As was said, the development of the Bombay phenomenon is based on non-allelic interaction of genes - epistasis. This type of inheritance is distinguished by the fact that one gene suppresses the action of another, even if the suppressed allele is dominant.

The genetic basis for the development of the Bombay phenomenon is epistasis. The peculiarity of this type of inheritance is that the recessive epistatic gene is stronger than the hypostatic gene, but it determines the blood group. Therefore, the inhibitor gene that causes suppression is not capable of producing any trait. Because of this, a child is born with “no” blood type.

This interaction is determined genetically, so it is possible to identify the presence of a recessive allele in one of the parents. It is impossible to influence the development of such a blood group, much less change it. Therefore, for those who have the Bombay phenomenon, the pattern of everyday life dictates some rules, following which, such people will be able to live normally and not fear for their health.

Features of life of people with this mutation

In general, people who carry Bombay blood are no different from ordinary people. However, problems arise when a transfusion is required (major surgery, accident or disease of the blood system). Due to the peculiarity of the antigenic composition of these people, they cannot be transfused with blood other than Bombay. Such errors are especially common in extreme situations when there is no time to thoroughly study the analysis of the patient’s red blood cells.

The test will show, for example, the second group. When a patient is transfused with blood of this group, intravascular hemolysis may develop, which will lead to death. It is precisely because of this incompatibility of antigens that the patient needs only Bombay blood, always with the same Rh as his.

Such people are forced to preserve their own blood from the age of 18, so that later they will have something to transfuse if necessary. There are no other features in the body of these people. Thus, we can say that the Bombay phenomenon is a “way of life” and not a disease. You can live with him, you just have to remember your “uniqueness.”

Paternity issues

The Bombay phenomenon is the “thunderstorm of marriage”. The main problem is that when determining paternity, it is impossible to prove the existence of the phenomenon without special research.

If suddenly someone decides to clarify the relationship, then they should definitely be informed that such a mutation is possible. Genetic match test in such a case should be carried out more extensively, with the study of the antigenic composition of blood and red blood cells. Otherwise, the child’s mother risks being left alone, without a husband.

This phenomenon can only be proven using genetic tests and determining the type of inheritance of blood group. The study is quite expensive and is not currently widely used. Therefore, when a child is born with a different blood type, one should immediately suspect the Bombay phenomenon. The task is not easy, since only a few dozen people know about it.

Bombay blood and its occurrence today

As has been said, people with Bombay blood are rare. This type of blood is practically never found in representatives of the Caucasian race; Among Indians, this blood is more common (on average, among Europeans, the occurrence of this blood is one case per 10 million people). There is a theory that this phenomenon develops due to the national and religious characteristics of the Hindus.

Everyone knows that it is a sacred animal and its meat cannot be eaten. Perhaps because beef contains some antigens that can cause changes, Bombay blood appears more often. Many Europeans eat beef, which serves as a prerequisite for the emergence of the theory of antigenic suppression of a recessive epistatic gene.

Possibly they influence climatic conditions, however, this theory is not currently being studied, so there is no evidence to substantiate it.

The significance of Bombay blood

Unfortunately, few people have heard about Bombay blood these days. This phenomenon is known only to hematologists and scientists working in the field genetic engineering. Only they know about the Bombay phenomenon, what it is, how it manifests itself and what needs to be done when it is identified. However, the exact cause of this phenomenon has not yet been identified.

If we look at it from an evolutionary point of view, Bombay blood is an unfavorable factor. Many people sometimes require a transfusion or replacement to survive. In the presence of Bombay blood, the difficulty lies in the impossibility of replacing it with blood of another type. Because of this, deaths often occur in such people.

If we look at the problem from the other side, it is possible that Bombay blood is more advanced than blood with a standard antigenic composition. Its properties have not been fully studied, so it is impossible to say what the Bombay phenomenon is - a curse or a gift.