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Q: What does H2 Biology Notes (9477, 2026): Extension 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.
TL;DR Use this guide to connect immune response mechanisms, pathogen strategies, antibiotics/resistance, and epidemiology
metrics so you can handle Paper 2 data and Paper 3 evaluation essays with confidence.
Status: SEAB H2 Biology (9477, first exam 2026) syllabus last checked 2026-01-12. Extension Topic A scope (immunity, pathogens, antibiotics, epidemiology) and Paper 3/4 assessment hooks remain unchanged. [1]
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 (somatic recombination, hyper-mutation, class switching) [1]
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 antibody production; secondary response is faster and typically higher-affinity because of memory cells and affinity maturation. Use antibody titre graphs to illustrate-likely Paper 2 data question. [2]
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/macrophages process antigens and present via MHC II to helper T cells. [2]
Helper T cells (CD4+): Secrete cytokines that activate B cells and support cytotoxic responses. [2]
Cytotoxic T cells (CD8+): Recognise infected cells via MHC I and induce apoptosis. [2]
B cells: Differentiate into plasma cells producing antibodies and memory B cells. [2]
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, and a hinge region. Fc vs Fab roles: Fab binds antigen; Fc mediates effector functions such as complement activation. [1][2]
Diversity mechanisms:
Somatic recombination (V(D)J): Gene-segment rearrangement creates many unique variable regions for B-cell receptors and antibodies. [1][2]
Hyper-mutation and affinity maturation: Mutations in immunoglobulin variable regions, followed by selection for higher-affinity binders. [1][2]
Class switching (isotype switching): Rearrangement changes the heavy-chain constant region (e.g. IgM → IgG/IgA/IgE) while preserving variable-region specificity, altering effector function. [1][2]
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.
Concept 4: Vaccination strategies and debates
Mechanism: Vaccines present antigens to stimulate adaptive immunity without causing disease; memory cells underpin longer-term protection. [2]
Herd immunity: When enough people are immune, transmission becomes harder and susceptible individuals are indirectly protected; the needed coverage depends on transmissibility (R0). [1][2]
Success story: Smallpox eradication is a canonical case study that vaccination can break transmission cycles at population scale. [1][3]
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 and strain selection.
Concept 5: Pathogenesis of key agents
Influenza virus: Segmented RNA genome; antigenic drift and antigenic shift allow immune evasion and can contribute to epidemics/pandemics. Influenza infects epithelial cells of the respiratory tract. [1][2]
HIV: A retrovirus that infects and damages helper T cells. Reverse transcriptase produces a DNA copy that can integrate into the host genome (provirus), enabling persistent infection; progressive immune dysfunction can lead to AIDS. [1][2]
Mycobacterium tuberculosis: Airborne transmission; infection can lead to granuloma (tubercle) formation and latent vs active disease dynamics. [1][2]
Compare disease courses, tissue tropism, and immune evasion strategies.
Concept 6: Antibiotics and resistance
Modes of action (penicillin example): Beta-lactams inhibit peptidoglycan cross-linking by targeting transpeptidase enzymes (penicillin-binding proteins), weakening the cell wall of actively dividing bacteria. [1][2]
Other classes (briefly): macrolides inhibit protein synthesis (50S subunit), quinolones block DNA gyrase. [2] Stress that antibiotics do not target viruses-common exam misconception.
Design a Kirby-Bauer disk diffusion susceptibility test: sterile technique, a confluent lawn, antibiotic disks on Mueller–Hinton agar, measurement of zone diameters, and interpretation using a standard chart. [2]
Concept 7: Epidemiology metrics
R0: Average secondary infections from a single case in a wholly susceptible population. Use R0>1 to predict outbreak growth and R0<1 for decline. [1]
Outbreak vs epidemic vs pandemic: Terms used to describe increasing geographic spread of infectious diseases (e.g. influenza). [1]
Control strategies: Quarantine, contact tracing, vaccination, antivirals/antibiotics, sanitation.
Calculation drill
Given an R0 value, explain qualitatively why higher transmissibility requires a higher coverage of immune individuals to interrupt transmission, and discuss practical constraints (cold chain, public acceptance). [1]
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, such as “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.
Where can I find the full H2 Biology Notes series? Start at the H2 Biology Notes hub and then branch into the extension topics after Core Ideas 1–4.
Where can I download a PDF of these Extension A notes? Use the “Download PDF” button on this page, or open the direct PDF link:
H2 Biology Extension A notes PDF.
How do I use Extension A for Paper 2 vs Paper 3? For Paper 2, practise explaining mechanisms from a dataset (e.g. antibody titres or outbreak curves). For Paper 3, train evaluative paragraphs that balance biological reasoning with public health constraints.
