explain how vaccination programmes can help to control the spread of infectious diseases
Learning Objective
Explain how vaccination programmes can help to control the spread of infectious diseases.
1. Antibody Structure – Function Relationship
- Molecular architecture: Antibodies (immunoglobulins) are Y‑shaped glycoproteins composed of two identical heavy (H) chains and two identical light (L) chains linked by disulphide bonds.
- Variable (V) region – Fab fragment: The tips of the “Y” (V‑domains of both H and L chains) form the antigen‑binding site. Specificity for a particular epitope is determined here.
- Constant (C) region – Fc fragment: The stem of the “Y” (C‑domains of the heavy chains) interacts with complement proteins and Fc receptors on phagocytes, mediating effector functions.
- Primary functions:
- Neutralisation – Fab binds viral surface proteins or bacterial toxins, blocking attachment to host cells.
- Opsonisation – Fc tags pathogens for ingestion by macrophages and neutrophils.
- Complement activation – Fc initiates the classical complement pathway, leading to membrane‑attack‑complex formation and lysis.
2. Primary and Secondary Immune Responses
2.1 Primary immune response – step‑by‑step (≈5–7 days)
- Antigen entry & uptake – Pathogen‑associated antigens are captured by antigen‑presenting cells (APCs) such as dendritic cells.
- Processing & presentation – APCs degrade the antigen and display peptide fragments on MHC II molecules.
- Activation of naïve T‑helper cells – T‑cells recognise the peptide‑MHC II complex, become activated and secrete cytokines.
- Activation of naïve B‑cells – B‑cells that bind the same antigen via their B‑cell receptors receive help from T‑helper cells (CD40‑CD40L interaction + cytokines).
- Clonal expansion & differentiation – Activated B‑cells proliferate; most become plasma cells that secrete IgM (later class‑switch to IgG, IgA, etc.).
- Antibody production – Low‑affinity IgM appears in the blood after ~5 days; levels rise over the next 1–2 weeks.
- Memory‑cell formation – A subset of B‑cells become long‑lived memory cells, ready for rapid re‑activation.
2.2 Secondary (memory) response – rapid & enhanced
| Feature | Primary response | Secondary response |
|---|---|---|
| Speed of antibody appearance | 5–7 days (IgM first) | 1–3 days (predominantly IgG) |
| Antibody concentration | Modest rise (peak ≈10⁻⁶ M) | Higher peak (≈10⁻⁴ M), up to 10‑fold greater |
| Antibody class | IgM → IgG (class‑switch later) | IgG dominates from the start |
| Affinity for antigen | Low‑moderate affinity | High affinity due to affinity maturation |
| Memory cells | Generated but not yet active | Rapid activation of pre‑existing memory B‑cells |
3. Types of Immunity
| Immunity | Source | Mechanism | Typical duration |
|---|---|---|---|
| Active – Natural | Infection with the pathogen | Host produces its own antibodies & memory cells | Long‑lasting (often lifelong) |
| Active – Artificial | Vaccination | Vaccine antigens stimulate antibody and memory cell production | Long‑lasting; boosters may be required |
| Passive – Natural | Maternal antibodies (placenta, breast‑milk) | Pre‑formed antibodies provide immediate protection | Weeks–months |
| Passive – Artificial | Therapeutic antibody preparations (e.g., antivenom, monoclonal antibodies) | Direct administration of IgG/IgM gives immediate immunity | Short‑term; may need repeated doses |
4. How Vaccination Works
- Vaccines contain antigens that mimic a natural infection but do not cause disease. Main categories:
- Whole‑pathogen (live‑attenuated or inactivated)
- Subunit / recombinant proteins
- Polysaccharide capsular fragments
- Toxoids (inactivated toxins)
- Genetic material (DNA or mRNA) that directs host cells to produce the antigen
- The antigen is taken up by APCs, processed, and presented to T‑helper cells, which then activate B‑cells → antibody production + memory formation (see Section 2).
5. Types of Vaccines
| Vaccine type | Example | Mechanism of action | Advantages | Disadvantages |
|---|---|---|---|---|
| Live‑attenuated | MMR (Measles‑Mumps‑Rubella) | Contains weakened, replicating pathogens that stimulate a strong, broad immune response. | Long‑lasting immunity; often a single dose. | Not safe for immunocompromised; requires cold chain. |
| Inactivated (killed) | Polio (IPV) | Pathogen is killed; antigens are recognised but cannot replicate. | Safe for immunocompromised; stable. | Weaker immunity; multiple doses needed. |
| Subunit / Recombinant | Hepatitis B | Only specific surface proteins are included. | Very safe; minimal side‑effects. | May require adjuvants and boosters. |
| Toxoid | Diphtheria, Tetanus | Inactivated toxins (toxoids) elicit neutralising antibodies. | Effective against toxin‑mediated disease. | Requires periodic boosters. |
| mRNA | COVID‑19 (Pfizer‑BioNTech, Moderna) | mRNA encodes a viral protein; host cells produce the antigen internally. | Rapid development; strong immune response. | Cold‑chain requirements; newer technology. |
6. Monoclonal Antibodies (mAbs)
Outline of the Hybridoma Method (3‑step summary)
- Immunise a mouse (or other suitable animal) with the target antigen.
- Fuse spleen‑derived B‑lymphocytes with an immortal myeloma cell line using polyethylene glycol, creating hybrid cells (hybridomas).
- Select & screen hybridomas (e.g., in HAT medium) for production of the desired antibody; clone the positive hybridoma to obtain a monoclonal population.
Applications
- Diagnostics: ELISA kits using mAbs detect SARS‑CoV‑2 antigens, hCG (pregnancy), cardiac troponin I, etc.
- Therapeutics: Trastuzumab (Herceptin) for HER2‑positive breast cancer; Adalimumab (Humira) for rheumatoid arthritis; monoclonal antibodies used as anti‑venoms and in passive immunisation against rabies.
7. How Vaccination Programmes Control Disease Spread
- Induction of herd immunity
When a sufficiently high proportion of the population is immune, the effective reproduction number (Re) falls below 1, preventing sustained transmission.
Re = R0 × (1 − p)
where R0 = basic reproduction number and p = proportion immune.
- Reduction of incidence and severity – Vaccinated individuals are less likely to become infected; breakthrough cases are usually milder and of shorter duration.
- Interrupting transmission chains – Fewer susceptible hosts break the chain of infection, especially in high‑density settings such as schools and workplaces.
- Protection of vulnerable groups – Infants, immunocompromised patients and pregnant women gain indirect protection through herd immunity.
- Economic and social benefits – Fewer cases lower healthcare costs, reduce absenteeism, and decrease mortality.
8. Real‑World Data Example – Measles
Measles has a high R0 (12–18), requiring >95 % coverage for herd immunity. The chart below illustrates the impact of achieving this threshold in Country X.
9. Factors Influencing the Success of Vaccination Programmes
- Vaccine coverage – Target thresholds vary (e.g., >95 % for measles, >80 % for polio).
- Vaccine efficacy – Proportion of vaccinated individuals who develop protective immunity.
- Population demographics – Age structure, birth rate, migration and urbanisation affect herd‑immunity calculations.
- Public confidence & misinformation – Attitudes toward vaccination strongly influence uptake rates.
- Logistical considerations – Cold‑chain maintenance, access to remote areas, trained personnel and reliable record‑keeping.
10. Case Study: Measles Elimination Efforts
Key statistics: In regions that have maintained >95 % two‑dose MMR coverage, measles incidence has fallen by >99 % within a decade.
Core strategies:
- Routine two‑dose schedule (first dose at 12 months, second dose at 4–5 years).
- Supplementary immunisation activities (SIAs) during outbreaks or in under‑vaccinated pockets.
- Robust surveillance, rapid case investigation and contact tracing.
11. Summary
Vaccination exploits the body’s ability to generate specific antibodies and long‑lived memory cells. By achieving high coverage, programmes create herd immunity, lowering the effective reproduction number (Re) below 1 and interrupting transmission. This protects both vaccinated and vulnerable unvaccinated individuals, reduces disease incidence and severity, and yields substantial economic and social benefits. A solid grasp of antibody structure, the primary/secondary immune response, and modern vaccine technologies equips students to understand how immunisation controls the spread of infectious diseases.