CUET UG Biology Booster Test 2-Medical Applications

The passage explicitly states that insulin consists of two short polypeptide chains, chain A and chain B. It also notes that the C peptide is an "extra stretch" that must be processed out before it becomes a fully mature, functional hormone. Thus, a mature molecule lacks the C peptide.

Mature insulin is held together by disulphide bridges between its two polypeptide chains. Applying a chemical agent that breaks these specific bonds will release the linkage, causing chain A and chain B to dissociate (separate) from one another.

The logical flow begins with the implementation of recombinant DNA technology (III). This technology enables mass industrial-scale production (I), which yields safer and more effective products (IV), ultimately leading to an overall increase in the availability of these treatments in healthcare (II).

Non-human sources (like pigs) are biologically distinct, and the human immune system recognizes them as foreign, triggering an immunological response (allergy). Recombinant human insulin is identical to the insulin naturally produced by the human body, thus avoiding these "unwanted immunological responses."

The statistics are as follows: Globally approved therapeutics (1-ii) number about 30; Indian marketed drugs (2-i) number 12; The first gene therapy (3-iii) occurred in 1990 as a singular landmark event; Indian drugs (12) compared to global (30) is less than half (iv).

Given that 30 therapeutics are approved globally and 12 are marketed in India, the fraction is 12/30, which simplifies to 2/5 or 0.4. Since 0.4 is less than 0.5, "less than half" is the mathematically correct descriptor.

Pro-hormone processing involves the cleavage/removal of portions (like the C-peptide) to yield a mature protein, which is biologically analogous to activating a pro-enzyme (I). It is essential for maturation (III). Statement II is incorrect as it implies adding chains, whereas maturation involves removing them.

The C-peptide is present in pro-insulin but is removed as part of the maturation process. Mature insulin lacks the C-peptide entirely; the A and B chains are instead held together by disulphide bridges.

The involved isolating the specific DNA sequences for the A and B chains, inserting them into plasmids, and using E. coli as a host to produce the protein chains independently. These chains were later extracted and joined via disulfide bonds.

The sequence is: (III) Plasmid insertion > (IV) Bacterial production of separate A/B chains > (I) Extraction of the chains > (II) Chemical bonding (disulphide bridges) to create the mature insulin product.

The purpose of delivering a functional, "normal" gene into cells is to allow that gene to express the necessary protein. By doing so, the normal gene supplements or "takes over" the biological function that the defective gene could not perform, thereby compensating for the deficit.

The goal of gene therapy is to provide a functional, healthy gene to rectify a deficiency. Amplifying the already "defective" gene (C) would only increase the amount of dysfunctional or absent protein, which serves no therapeutic purpose.

ADA deficiency causes severe combined immunodeficiency (I) and was the target of the first gene therapy in 1990 (II). Statement III is the opposite of the truth, as the condition is defined by a lack (deficiency) of the enzyme, not an overproduction.

ADA deficiency is a hereditary disease caused by the deletion of the gene that encodes for the adenosine deaminase enzyme. Without the gene, the body cannot produce the enzyme required for immune system health.

While enzyme replacement therapy provides the missing enzyme, it does not fix the patient's genetics. As the injected enzyme eventually breaks down or is used up, the patient requires regular, repeated infusions to maintain enzyme levels, making it a management rather than a permanent cure.

Treatments are matched by their operational mechanism or limitation: Bone marrow transplantation is a cellular transplant that is often not fully curative (1-iii); Enzyme replacement involves injecting the functional protein (2-i); Retroviral gene therapy uses vectors to introduce functional cDNA (3-ii); Early embryonic therapy offers the best hope for a permanent cure (4-iv).

The standard methodology for ADA gene therapy involves using a retroviral vector as a biological delivery vehicle. This vector integrates the functional ADA cDNA into the genome of the patient's lymphocytes, allowing those cells to begin producing the enzyme.

Statement C is false because the gene therapy performed on adult lymphocytes is a "somatic" treatment—it does not affect the patient's germline DNA. The reason for repeated treatment is simply that the engineered cells have a limited lifespan and are not immortal (A, B, D).

To design a permanent treatment, the functional gene must be isolated from its natural biological source in the body—the cells that would normally produce the enzyme, such as bone marrow/stem cells. Once isolated, this gene is introduced early in development for a permanent effect.

A "permanent cure" implies that the genetic defect has been corrected for life, rendering periodic treatments like lymphocyte infusions unnecessary. Statement C describes a limitation of temporary adult gene therapy, not a requirement for a permanent embryonic cure.