Samacheer Kalvi 12th Biology Chapter 17 Exercise Solutions

Chapter 17 — Human Health and Diseases Exercise Solutions

This chapter has high board exam weightage. Immunity and infectious disease questions are common 5-mark topics.

How to Use This Page

1. Start with the Key Concepts table for a quick refresher of definitions and terminology. 2. Work through MCQs and Fill in the Blanks to test recall of facts and terminology. 3. Try True or False to catch common misconceptions — pay attention to the corrections. 4. Use Match the Following to reinforce pathogen–disease and antibody–function links. 5. Read Answer Briefly for concise 2-mark model answers you can replicate in the exam. 6. Study Answer in Detail for structured 5-mark responses — note the sub-point format examiners look for. 7. Review Common Mistakes to Avoid before the exam to prevent losing marks on subtle errors. 8. Check off items on the Exam Checklist to confirm you have covered every recurring board topic.

Key Concepts (Quick Recap)

Types of Immunity

Immunoglobulins (Antibodies)

I. Choose the Best Answer (MCQs)

1. Which of the following is a component of innate immunity? (a) B lymphocytes   (b) T lymphocytes   (c) Natural killer cells   (d) Plasma cells

II. Fill in the Blanks

1. The non-specific defence mechanism present from birth is called innate immunity. 2. IgA is the antibody found in secretions such as saliva, tears, and breast milk. 3. HIV uses the enzyme reverse transcriptase to convert its RNA genome into DNA. 4. The test used to confirm HIV infection after initial ELISA screening is the Western blot test. 5. A tumour that remains localised and does not invade other tissues is called a benign tumour. 6. The recombinant vaccine used against Hepatitis B is produced using yeast (Saccharomyces cerevisiae). 7. Colostrum, the first milk produced after childbirth, is rich in IgA and provides passive immunity to the infant. 8. The process by which cancer cells spread to distant body parts via blood or lymph is called metastasis. 9. Malarial parasite Plasmodium is transmitted by the bite of female Anopheles mosquito. 10. HAART stands for Highly Active Antiretroviral Therapy.

III. True or False (with corrections)

IV. Match the Following

V. Answer Briefly (2-mark)

1. Differentiate between active and passive immunity.

Active immunity is when the body produces its own antibodies after exposure to an antigen (through infection or vaccination). It develops slowly but provides long-lasting protection because memory cells are formed. Passive immunity is when ready-made antibodies are received from an external source (e.g., antiserum, colostrum). It provides immediate protection but is short-lived because no memory cells are created.

2. What is colostrum? Why is it important for a newborn?

Colostrum is the first milk secreted by the mammary glands after childbirth. It is rich in IgA antibodies, which provide passive immunity to the newborn. Since the infant's own immune system is immature, colostrum protects against enteric infections until the baby's own immune system becomes functional.

3. Name the causative agent of malaria and its vector.

Malaria is caused by Plasmodium, a protozoan parasite. The most severe form is caused by Plasmodium falciparum. The vector is the female Anopheles mosquito, which transmits the sporozoites into the human bloodstream during a blood meal.

4. Write a note on the role of T lymphocytes in cell-mediated immunity.

T lymphocytes mediate cell-mediated immunity (CMI). T-helper cells (Th) recognise antigen presented by MHC on antigen-presenting cells and secrete cytokines that activate other immune cells. Cytotoxic T cells (Tc) directly kill virus-infected cells and tumour cells by releasing perforin and granzymes. Memory T cells are formed for faster secondary responses.

5. What is an oncogene? How does it differ from a proto-oncogene?

A proto-oncogene is a normal gene that regulates cell growth and division. When a proto-oncogene mutates or is over-expressed due to carcinogen exposure or viral integration, it becomes an oncogene. Oncogenes drive uncontrolled cell proliferation, leading to cancer. The key difference: proto-oncogenes promote normal, regulated growth; oncogenes promote unregulated, excessive growth.

6. List two diagnostic tests for HIV with their principles.

ELISA (Enzyme-Linked Immunosorbent Assay): Detects anti-HIV antibodies in the patient's serum using enzyme-labelled antigens. It is the initial screening test. Western blot: Confirms HIV by separating viral proteins by electrophoresis, transferring to a membrane, and probing with the patient's serum to detect specific antibody–protein bands. It is the confirmatory test after a positive ELISA.

VI. Answer in Detail (5-mark)

1. Explain the types of immunity with a diagram description.

Immunity is classified into two broad types:

Innate immunity (non-specific):

• Present from birth; provides immediate, non-specific defence.
• First line of defence: Physical barriers (skin, mucus, cilia) and chemical barriers (lysozyme in tears, HCl in stomach).
• Second line of defence: Phagocytes (neutrophils, macrophages) engulf pathogens; NK cells kill virus-infected cells; complement proteins lyse pathogens; inflammation and fever.
• No immunological memory — the response is the same on each exposure.

Acquired immunity (specific/adaptive):

• Develops after exposure to a specific antigen; has memory.
• Humoral immunity: B lymphocytes recognise antigens → differentiate into plasma cells → secrete specific antibodies (IgG, IgM, IgA, IgE, IgD). Memory B cells are formed.
• Cell-mediated immunity (CMI): T lymphocytes — T-helper cells (CD4+) coordinate the immune response via cytokines; cytotoxic T cells (CD8+) kill infected and tumour cells. Memory T cells formed.

Acquired immunity is further divided into:

• Active: Body produces own antibodies (natural infection or vaccination). Slow onset, long-lasting.
• Passive: Ready-made antibodies received (colostrum, antiserum). Fast onset, short-lived, no memory.

2. Describe the structure and replication of HIV. How does it cause immunodeficiency?

Structure:

• HIV is a spherical retrovirus (~120 nm diameter).
• Envelope: Derived from host cell membrane; embedded with glycoprotein spikes — gp120 (binds CD4 receptor) and gp41 (mediates fusion).
• Matrix protein (p17) lines the inner envelope.
• Capsid: Cone-shaped, made of p24 protein, encloses two identical single-stranded RNA genomes and three key enzymes — reverse transcriptase, integrase, and protease.

Replication cycle: 1. Attachment: gp120 binds CD4 receptor and co-receptor (CCR5 or CXCR4) on T-helper cells. 2. Entry: Viral envelope fuses with host cell membrane; capsid enters cytoplasm. 3. Reverse transcription: Reverse transcriptase converts viral RNA into double-stranded DNA. 4. Integration: Viral DNA enters the nucleus; integrase inserts it into the host genome as a provirus. 5. Transcription and translation: Host machinery transcribes viral mRNA → translates viral proteins. 6. Assembly and budding: New virions assemble at the cell membrane and bud off, destroying the host T cell.

Immunodeficiency:

• HIV specifically infects and kills CD4+ T-helper cells. As T cell count drops below 200/μL, the immune system collapses.
• Without T-helper cells, B cell activation and cytotoxic T cell responses are impaired.
• Opportunistic infections (Pneumocystis pneumonia, Candida, Toxoplasma, Mycobacterium) and cancers (Kaposi's sarcoma) develop — this stage is AIDS.

3. What is cancer? Discuss its causes, types, and treatment methods.

Definition: Cancer is a disease characterised by uncontrolled, abnormal cell division that forms a mass called a tumour.

Causes (Carcinogens):

• Physical carcinogens: UV radiation, ionising radiation (X-rays, gamma rays) cause DNA damage.
• Chemical carcinogens: Tobacco smoke (benzopyrene), aflatoxin (aspergillus mould on peanuts), asbestos.
• Biological carcinogens: Oncogenic viruses — HPV (cervical cancer), Hepatitis B/C (liver cancer), Epstein-Barr virus (Burkitt's lymphoma).
• Genetic factors: Mutations in proto-oncogenes (→ oncogenes) and tumour suppressor genes (p53, Rb inactivation).

Types of tumours:

• Benign: Localised, encapsulated, does not invade surrounding tissue or metastasise; usually not life-threatening.
• Malignant: Invasive, penetrates surrounding tissue, spreads via metastasis through blood and lymph; life-threatening.

Treatment methods:

• Surgery: Physical removal of the tumour; effective for localised benign and early-stage malignant tumours.
• Radiotherapy: High-energy X-rays or gamma rays destroy rapidly dividing cancer cells; damages DNA.
• Chemotherapy: Anti-cancer drugs (e.g., taxol, bleomycin, cisplatin) target rapidly dividing cells; side effects include hair loss and bone marrow suppression.
• Immunotherapy: Monoclonal antibodies (e.g., Herceptin for HER2+ breast cancer) or immune checkpoint inhibitors boost the body's immune response against cancer.
• Gene therapy: Restoring functional tumour suppressor genes (e.g., p53) or silencing oncogenes using RNA interference.

4. Explain the mechanism of vaccination. Why are booster doses given?

Mechanism: 1. A vaccine contains a weakened, killed, or inactivated pathogen, its toxoid, or a recombinant protein subunit (antigen). 2. When administered, the antigen is recognised by antigen-presenting cells (macrophages, dendritic cells). 3. These cells process the antigen and present it on MHC to T-helper cells. 4. T-helper cells activate B lymphocytes, which differentiate into:

5. On subsequent exposure to the real pathogen, memory cells trigger a rapid, strong secondary response (mainly IgG) — preventing disease.

• Plasma cells → produce specific antibodies (primary immune response; mainly IgM).
• Memory B cells → remain in circulation for years.

Why booster doses?

• Over time, antibody levels decline as plasma cells die.
• Booster doses re-expose the immune system to the antigen, re-activating memory cells.
• This produces a higher and longer-lasting antibody titre than the initial dose alone.
• Example: DTaP (Diphtheria, Tetanus, Pertussis) requires boosters at intervals to maintain protective immunity.

5. Describe the life cycle of Plasmodium that causes malaria.

Plasmodium has a digenetic life cycle — it requires two hosts: humans (asexual phase) and female Anopheles mosquito (sexual phase).

In mosquito: 1. Female Anopheles mosquito bites an infected person and ingests gametocytes. 2. Gametocytes mature into male and female gametes in the mosquito gut. 3. Fertilisation forms a zygote → develops into an ookinete → becomes an oocyst on the gut wall. 4. Oocyst undergoes meiosis and releases sporozoites, which migrate to the mosquito's salivary glands.

In humans: 1. Infected mosquito bites a healthy person; sporozoites are injected into the bloodstream. 2. Sporozoites enter liver cells (hepatocytes) → undergo schizogony → produce merozoites (exo-erythrocytic cycle). 3. Merozoites are released from liver cells and infect red blood cells (erythrocytic cycle). 4. Inside RBCs, Plasmodium develops through trophozoite → schizont → merozoites → RBC ruptures, releasing merozoites (causing cyclic fever — chills and fever every 48–72 hours depending on species). 5. Some merozoites differentiate into male and female gametocytes, which circulate in blood, ready to be taken up by a mosquito.

Key species: P. vivax (most common, tertian fever), P. falciparum (most severe, malignant tertian), P. malariae (quartan fever), P. ovale (rare).

Major Infectious Diseases

HIV/AIDS — Flow

HIV enters CD4+ T cell → Reverse transcriptase converts RNA to DNA → DNA integrates into host genome → Viral proteins made → New virions bud off → T cell destroyed → Immunosuppression → AIDS

Antiretroviral drugs: NRTIs (block reverse transcriptase), PIs (block protease), HAART (combination therapy).

Cancer Treatment

• Surgery: Remove tumour.
• Radiotherapy: X-rays/gamma rays destroy rapidly dividing cells.
• Chemotherapy: Drugs (taxol, bleomycin) target dividing cells.
• Immunotherapy: Monoclonal antibodies (Herceptin for breast cancer).
• Gene therapy: Restore tumour suppressor genes.

Worked Examples

Example 1 — Active vs passive immunity (model answer)

Example 2 — Pathogen → disease matching

Example 3 — How vaccines work (model answer)

A vaccine introduces a weakened/inactivated antigen. The body mounts a primary immune response and forms memory cells. On later exposure to the real pathogen, these memory cells trigger a fast, strong secondary response — giving active, long-lasting immunity.

Common Mistakes

• Confusing active and passive immunity — vaccination = active; antiserum = passive.
• Saying HIV infects all white blood cells — it specifically infects CD4+ T-helper cells.
• Confusing benign and malignant tumours — benign stays localised; malignant metastasises.
• Forgetting that IgE is associated with allergy, not with general infection.

Common Mistakes to Avoid

• ❌ "Passive immunity produces memory cells." → ✅ Passive immunity provides ready-made antibodies; no memory cells are formed. Only active immunity produces memory.
• ❌ "HIV infects all white blood cells." → ✅ HIV specifically targets CD4+ T-helper lymphocytes, not neutrophils, B cells, or all leukocytes.
• ❌ "Benign tumours spread to other organs." → ✅ Benign tumours are localised and encapsulated; only malignant tumours metastasise.
• ❌ "IgM is the antibody involved in allergic reactions." → ✅ IgE mediates allergic reactions and anaphylaxis; IgM is the first antibody in a primary immune response.
• ❌ "Innate immunity remembers previous infections." → ✅ Innate immunity is non-specific and has no immunological memory; it responds the same way each time.
• ❌ "Vaccination gives passive immunity." → ✅ Vaccination provides active immunity — the body produces its own antibodies and memory cells.
• ❌ "Reverse transcriptase converts DNA to RNA." → ✅ Reverse transcriptase converts viral RNA to DNA, which then integrates into the host genome.
• ❌ "Colostrum provides active immunity." → ✅ Colostrum provides passive immunity (IgA transferred from mother); the baby does not produce these antibodies.

Exam Checklist

• [ ] Can I list the four types of immunity (innate, acquired, active, passive) with examples and whether each has memory?
• [ ] Can I name all five immunoglobulin classes (IgG, IgM, IgA, IgE, IgD) and their functions?
• [ ] Can I describe the structure and replication cycle of HIV (attachment → reverse transcription → integration → transcription → assembly → budding)?
• [ ] Can I explain why HIV causes immunodeficiency (CD4+ T cell depletion → opportunistic infections → AIDS)?
• [ ] Can I list the diagnostic tests for HIV (ELISA screening → Western blot confirmation) and tuberculosis (Mantoux test, BCG vaccine)?
• [ ] Can I differentiate benign and malignant tumours with at least four points of comparison?
• [ ] Can I name three categories of carcinogens (physical, chemical, biological) with two examples each?
• [ ] Can I explain the mechanism of vaccination and why booster doses are needed?
• [ ] Can I trace the Plasmodium life cycle through both mosquito and human hosts, naming each stage (sporozoite, merozoite, trophozoite, gametocyte)?
• [ ] Can I write the full expansion of HAART and list the drug classes it combines (NRTIs, NNRTIs, PIs)?
• [ ] Can I distinguish between the primary and secondary immune response (antibody type, speed, magnitude)?
• [ ] Can I explain opsonisation and complement activation as effector mechanisms of humoral immunity?