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The genetic defect-Adenosine Deaminase d...

The genetic defect-Adenosine Deaminase deficiency may be cured permanently by

A

periodic infusion of genetically engineered lymphocytes having functional ADA C-DNA

B

administering adenosine deaminase activators

C

introducing bone marrow cells producing ADA into cells at early embryonic stages

D

enzyme replacement therapy

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### Step-by-Step Solution 1. **Understanding Adenosine Deaminase Deficiency**: - Adenosine deaminase (ADA) is an enzyme produced by the ADA gene. - This enzyme plays a crucial role in the immune system, particularly in lymphocytes, which are produced in the bone marrow. 2. **Identifying the Genetic Disorder**: - The deficiency of the ADA enzyme leads to a genetic disorder known as Severe Combined Immunodeficiency (SCID). - SCID is characterized by a life-threatening syndrome of recurrent infections due to a compromised immune system. 3. **Exploring Treatment Options**: - The question asks how this deficiency can be cured permanently. - Several treatment options can be considered, including periodic infusion of genetically engineered lymphocytes, enzyme replacement therapy, and bone marrow transplantation. 4. **Evaluating Treatment Options**: - **Option A**: Periodic infusion of genetically engineered lymphocytes – This method requires ongoing treatment and is not a permanent solution. - **Option B**: Administering adenosine deaminase activators – This does not address the root cause of the deficiency and is not a permanent cure. - **Option C**: Introducing bone marrow cells producing ADA into cells at early embryonic stages – This option is a permanent solution as it targets the root cause by ensuring the production of functional ADA from the start. - **Option D**: Enzyme replacement therapy – Similar to option A, this is not a permanent solution as it requires continuous administration. 5. **Conclusion**: - The best option for permanently curing adenosine deaminase deficiency is **Option C: Introducing the bone marrow cells producing the ADA into cells at early embryonic stages**. This method ensures that the ADA enzyme is produced effectively, addressing the deficiency at its source.
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