
(a) Mention the cause and the body system affected by ADA deficiency in humans.
(b) Name the vector used for transferring ADA-DNA into recipient cells in humans. Name the recipient cells.
Answer
561.9k+ views
Hint:Adenosine deaminase deficiency (ADA deficiency) is a metabolic disorder that causes immunodeficiency. It is caused by alterations in the ADA gene.
Complete answer:
To answer this question, we have to know about the ADA deficiency. ADA deficiency is a hereditary situation that harms the immune system and is a usual reason for severe combined immunodeficiency (SCID). People with SCID due to ADA deficiency are unable to fight off most types of infections, including bacterial, viral and fungal infections. Most people with ADA deficiency develop symptoms before 6 months age. The first symptoms of ADA deficiency involve pneumonia, chronic diarrhea, widespread skin rashes and slowed development.
ADA deficiency is a result of mutation in ADA genes that code for Adenosine deaminase enzyme included in purine metabolism. It influences immune response and results in severe combined immunodeficiency.
The ex vivo initiation of functional ADA genes in bone marrow cells of the patient, suffering with SCID, is done through an engineered retrovirus containing a functional ADA gene. Recipient cells are lymphocytes/bone marrow cells.
Note:A few individuals with ADA deficiency will grow symptoms in life. ADA deficiency is caused by ADA gene alteration as we have mentioned above and it is also inherited in an autosomal acceptor order. Detection may be identified by newborn baby symptoms and verified by blood and genetic test results. Recently, the most functional treatment is transferring of blood producing stem cells found in the bone marrow of a sister or brother having a good health of the individual with ADA deficiency.
Complete answer:
To answer this question, we have to know about the ADA deficiency. ADA deficiency is a hereditary situation that harms the immune system and is a usual reason for severe combined immunodeficiency (SCID). People with SCID due to ADA deficiency are unable to fight off most types of infections, including bacterial, viral and fungal infections. Most people with ADA deficiency develop symptoms before 6 months age. The first symptoms of ADA deficiency involve pneumonia, chronic diarrhea, widespread skin rashes and slowed development.
ADA deficiency is a result of mutation in ADA genes that code for Adenosine deaminase enzyme included in purine metabolism. It influences immune response and results in severe combined immunodeficiency.
The ex vivo initiation of functional ADA genes in bone marrow cells of the patient, suffering with SCID, is done through an engineered retrovirus containing a functional ADA gene. Recipient cells are lymphocytes/bone marrow cells.
Note:A few individuals with ADA deficiency will grow symptoms in life. ADA deficiency is caused by ADA gene alteration as we have mentioned above and it is also inherited in an autosomal acceptor order. Detection may be identified by newborn baby symptoms and verified by blood and genetic test results. Recently, the most functional treatment is transferring of blood producing stem cells found in the bone marrow of a sister or brother having a good health of the individual with ADA deficiency.
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