Q: What does EXTENSION TOPICS, Topic A - Infectious Diseases cover?
A: Integrate immunology, pathogen biology, epidemiology, and public health strategy so the 2026 H2 Biology infectious diseases extension questions become an opportunity to score.
Why this extension matters
Real-world relevance: Pandemic literacy and antimicrobial resistance are assessed through data handling, case studies, and ethical evaluation.
Integration: Requires command of cell biology (immune cells), genetics (somatic recombination), and population biology (epidemiology).
Assessment trend: Paper 3 essays and Paper 4 data questions frequently use infectious disease narratives to test synthesis.
Syllabus map
Innate vs adaptive immunity, active vs passive immunity
Roles of B cells, T cells, antigen-presenting cells, memory cells
Antibody structure (IgG) and diversity generation (V(D)J recombination, somatic hypermutation, class switching)
Vaccination principles, herd immunity, risks
Viral pathogenesis (influenza, HIV) and bacterial infection (Mycobacterium tuberculosis)
Modes of action of antibiotics (penicillin focus) and resistance issues
Adaptive immunity: Distinguish active vs passive, natural vs artificial immunity. Outline lymphatic organ roles (bone marrow, thymus, lymph nodes).
Primary vs secondary response: Primary response features slower, lower-affinity antibodies; secondary response is rapid, high-affinity due to memory cells. Use antibody titre graphs to illustrate-likely Paper 2 data question.
Practice check
Sketch a flowchart showing antigen entry through innate barriers, antigen presentation, clonal selection, and effector responses. Annotate timelines for primary and secondary exposure.
Concept 2: Lymphocyte orchestration
Antigen-presenting cells (APCs): Dendritic cells process antigens, present via MHC II to helper T cells.
Helper T cells (CD4+): Secrete cytokines, activate B cells and cytotoxic T cells.
Cytotoxic T cells (CD8+): Recognise infected cells via MHC I and induce apoptosis.
B cells: Differentiate into plasma cells producing antibodies and memory B cells.
Explain co-stimulation (CD28-B7 interaction) and why absence prevents activation-links to immunological tolerance.
Concept 3: Antibody structure and diversity
IgG architecture: Y-shaped molecule with two heavy and two light chains, variable (V) and constant (C) regions, disulfide bonds, hinge region. Complement-binding Fc region vs antigen-binding Fab regions.
Diversity mechanisms:
Somatic recombination (V(D)J): Random joining of variable (V), diversity (D), and joining (J) gene segments.
Junctional diversity: Addition/removal of nucleotides by TdT.
Somatic hypermutation: Activated B cells introduce point mutations in V regions; affinity maturation via selection in germinal centres.
Class switching: Cytokine-guided recombination changes heavy chain constant region (e.g. IgM to IgG), preserving antigen specificity but altering effector function.
Data connection
Analyse sequence data from antibodies pre- and post-immunisation; identify evidence of somatic hypermutation (increased point mutations in V regions) and relate to affinity increases.
Herd immunity: Threshold coverage approximated by 1−R01. For measles (R0≈18), coverage >94% needed.
Success story: Smallpox eradication-stable DNA virus, easily recognisable rash, no animal reservoir.
Risks and concerns: Adverse reactions, contraindications (immunocompromised patients and live vaccines), cold chain logistics, vaccine hesitancy misinformation. Prepare balanced arguments for exam evaluation tasks.
Exam prompt idea
“Discuss how vaccination strategies must adapt for rapidly mutating RNA viruses such as influenza.” Include antigenic drift, strain selection, potential mRNA booster flexibility.
Concept 5: Pathogenesis of key agents
Influenza virus: Segmented RNA genome enabling antigenic shift via reassortment. Infects respiratory epithelium, causing cell death and systemic symptoms. Immune evasion through antigenic drift, NS1 protein blocking interferon response.
HIV: Retrovirus targeting helper T cells via CD4 and CCR5/CXCR4 co-receptors. Reverse transcriptase introduces mutations; integrates as provirus; progressive CD4 decline leads to AIDS. Discuss latency, treatment (ART combination therapy), and global health impact.
Mycobacterium tuberculosis: Airborne transmission; granuloma formation; latent vs active disease. Virulence factors (mycolic acid cell wall) resist phagosome-lysosome fusion.
Compare disease courses, tissue tropism, and immune evasion strategies.
Concept 6: Antibiotics and resistance
Modes of action (penicillin example): Beta-lactam ring inhibits transpeptidase, preventing peptidoglycan cross-linking and leading to osmotic lysis of actively dividing bacteria.
Other classes (briefly): macrolides inhibit protein synthesis (50S subunit), quinolones block DNA gyrase. Stress that antibiotics do not target viruses-common exam misconception.
Design a Kirby-Bauer antibiotic susceptibility experiment: sterile technique, lawn inoculation, antibiotic discs, measuring zones of inhibition, and applying antibiogram charts.
Concept 7: Epidemiology metrics
R0: Average secondary infections from a single case in a wholly susceptible population. Use R0>1 to predict outbreak growth, R0<1 for decline.
Outbreak vs epidemic vs pandemic: Localised spike, regional/national spread, global spread respectively. Provide recent examples (Dengue clusters, SARS, COVID-19).
Control strategies: Quarantine, contact tracing, vaccination, antivirals/antibiotics, sanitation.
Calculation drill
If R0=3.2, the herd immunity threshold is 1−3.21≈0.6875. Calculate required vaccination coverage for a population of 5 million and discuss practical challenges (cold chain, public acceptance).
Exam technique outlook
Paper 2: Expect data interpretation on antibody titres, vaccination impact graphs, or TB infection curves.
Paper 3: Prepare essays synthesising immune response, pathogen strategies, and public health-e.g. “Explain how HIV compromises immune defence and how biomedical interventions mitigate the disease.”
Paper 4: Practise enzyme assays simulating antibiotic action or ELISA simulations; record MMO/PDO/ACE evidence thoroughly.
