• Disease & pathogens: infectious disease = caused by a transmissible pathogen (bacteria, some fungi, all viruses).
• Tuberculosis (TB): caused by Mycobacterium tuberculosis; spread by droplets; can lie dormant in tubercles then reactivate.
• HIV: a retrovirus that infects and destroys helper T cells, eventually causing AIDS.
• Routes of entry: vectors, inhalation, ingestion, indirect contact, direct contact, inoculation.
• Barriers to entry: skin, gut/skin flora, stomach acid, lysozyme in secretions.
• Non-specific response: inflammation, interferons, phagocytosis — same reaction to ANY pathogen.
• Specific response: antigens trigger lymphocytes (T cells & B cells) that target ONE particular pathogen.
• Antibodies: Y-shaped proteins with variable regions that bind specific antigens; they neutralise, agglutinate, and block pathogens.
• Primary vs secondary response: first exposure is slow (symptoms appear); memory cells make re-exposure fast (often symptom-free).
• Active vs passive immunity: active = your body makes antibodies (long-term); passive = antibodies given to you (short-term).
• Vaccines: deliberately introduce antigens to trigger active immunity without causing disease.
• Evolutionary arms race: pathogens evolve evasion tricks (e.g. antigenic variation, hiding antigens) faster than hosts can keep up.

Tuberculosis (TB)

TB is caused by the bacterium Mycobacterium tuberculosis. Think of it like a burglar who doesn't just break in — it breaks in, hides inside your own security guards (phagocytes), and can stay dormant for years before causing trouble.

The clever (and dangerous) part: TB bacteria don't just get destroyed by phagocytes like most bacteria do — they can survive and reproduce inside phagocytes. A healthy immune system usually walls off these infected phagocytes into structures called tubercles, where the bacteria sit dormant (the primary infection). But if the immune system later becomes compromised — for example by an HIV infection — the bacteria can reactivate and overpower the body. This is the active phase, and it's why TB is a classic "opportunistic infection" in AIDS patients.

HIV

HIV (human immunodeficiency virus) is a retrovirus — it carries RNA instead of DNA and uses an enzyme called reverse transcriptase to convert its RNA into DNA once inside a host cell. Its target is devastatingly specific: it goes straight for helper T cells, the "generals" of your immune system that activate B cells and other immune responses.

⚠️ Exam wording trap: never write "the HIV virus" — HIV already stands for "Human Immunodeficiency Virus", so that phrase says "virus" twice!

How HIV replicates (step by step):

1. HIV attaches to a receptor on the helper T cell membrane.
2. The capsid enters the cell and releases its RNA.
3. Reverse transcriptase uses the viral RNA as a template to build a complementary DNA strand.
4. This single-stranded DNA is converted to double-stranded DNA and inserted into the host's own DNA.
5. The host cell's own enzymes are hijacked to build new viral components.
6. New viruses bud off from the host cell and go on to infect more helper T cells.

The three stages of HIV infection:

Six routes pathogens use to enter the body

Think of your body as a fortress — pathogens need SOME way in. Examiners love asking you to match a route to a real-world example, so learn these with their example diseases:

Barriers to pathogenic entry

Before the immune system even gets involved, your body has passive physical and chemical barriers — like a moat and walls before you even need soldiers:

• Skin: a physical barrier; if broken, the blood clotting mechanism seals the gap — though it takes time, so some pathogens may sneak in before a clot forms.
• Gut/skin flora: harmless resident microorganisms that compete with pathogens for resources, limiting pathogen numbers (this is why wiping out your gut flora with antibiotics can leave you vulnerable to infections like C. difficile).
• Stomach acid: hydrochloric acid creates an acidic environment unfavourable to most pathogens on food/drink (though some, like Salmonella, can survive it).
• Lysozyme: an enzyme in tears, saliva, and mucus that damages bacterial cell walls, causing them to burst (lyse).

Inflammation

When tissue is damaged, mast cells release histamine — a chemical signalling molecule. Histamine triggers a cascade:

Cells also release cytokines — another signalling molecule that further triggers the immune response in the infected area. This is why a wound becomes swollen, warm, and painful.

Interferons

Virus-infected cells produce interferons — anti-viral proteins with a three-pronged job:

• Inhibit viral protein production, stopping the virus replicating.
• Activate white blood cells of the specific immune response to destroy infected cells.
• Increase the non-specific response, e.g. by promoting inflammation.

Phagocytosis

Phagocytes are the "clean-up crew" — a type of white blood cell that removes dead cells and invading microorganisms. Here's the step-by-step mechanism, which is a classic long-answer exam question:

1. Chemicals released by pathogens (and by histamine from damaged cells) attract phagocytes to the site.
2. The phagocyte recognises the non-self antigens on the pathogen's surface.
3. The cell membrane extends around the pathogen, engulfing it — this is endocytosis — trapping it in a phagocytic vacuole.
4. Lysosomes fuse with the vacuole, releasing digestive enzymes (including lysozyme).
5. These enzymes digest the pathogen.
6. The phagocyte presents the pathogen's antigens on its own cell surface membrane, becoming an antigen-presenting cell.

Antigens: self vs non-self

Antigens are like ID badges on the surface of every cell — proteins or glycoproteins that let the immune system tell friend from foe.

This is also why organ transplants can be rejected — the recipient's immune system sees the donor organ's antigens as "non-self" and attacks it.

Antibody structure

Antibodies (immunoglobulins) are secreted by plasma cells and have a distinctive Y-shape, built from four polypeptide chains:

• Two long "heavy" chains and two short "light" chains, joined by disulfide bonds.
• Each chain has a constant region (same within an antibody class) and a variable region (unique amino acid sequence per antibody).
• The variable region forms the antigen binding site — this is what gives each antibody its specificity.
• A flexible hinge region (where the heavy chains join) lets the two "arms" move to different angles when binding antigens.

How antibodies disable pathogens (3 ways)

1. Block receptors: bind to the receptors pathogens use to enter host cells, preventing infection.
2. Neutralise toxins: act as anti-toxins by binding to toxins (e.g. diphtheria, tetanus toxins).
3. Agglutination: cause pathogens to clump together — this reduces spread through the body AND lets a phagocyte engulf many pathogens at once.

T cells

T cells are produced in the bone marrow but mature in the thymus (hence "T"). Mature T cells each carry a unique T cell receptor, structurally similar to an antibody, specific to one antigen type.

A T cell is activated when it binds to its matching antigen on an antigen-presenting cell (which could be a macrophage, an infected body cell, or the pathogen itself). Once activated, it divides by mitosis to make genetically identical clones — all carrying the same receptor.

B cells

B cells mature in the bone marrow (hence "B"). Each B cell has many copies of a unique antibody receptor on its surface — essentially a membrane-bound antibody.

If the matching antigen enters the body, that specific B cell binds to it, forming an antigen-antibody complex. Combined with signalling molecules from T helper cells, this activates the B cell, which then divides repeatedly by mitosis into:

Primary vs secondary immune response

On first exposure to an antigen, very few T and B cells have the matching receptor, so it takes several days for the right cells to be found, activated, and to divide/differentiate — meanwhile you experience symptoms. This is the primary response.

Both T and B cells produce memory cells during this process, which persist in the blood long after the infection clears. If the SAME antigen appears again, these memory cells trigger a secondary response that is dramatically faster and stronger — often clearing the pathogen before symptoms even appear. This is what "being immune" to a disease actually means.

Active vs passive immunity

Vaccines

A vaccine deliberately introduces antigens into the body to trigger artificial active immunity — without causing the actual disease. Vaccines may contain:

• Dead or weakened (attenuated) pathogens
• Less harmful strains of a pathogen
• Isolated antigens alone
• Genetic material coding for the antigens

Because vaccination causes memory cells to form, a future encounter with the real pathogen triggers a fast, strong secondary response — which is why vaccinated people typically don't show symptoms of the disease they've been vaccinated against.

The evolutionary arms race

Hosts and pathogens are locked in a constant back-and-forth: hosts evolve better immune defences, pathogens evolve better ways to dodge them, and round it goes. This is sometimes called an evolutionary arms race.

Key Terms

Quick-fire facts examiners love to test

• T cells mature in the thymus; B cells mature in the bone marrow.
• Antibodies have 4 polypeptide chains: 2 heavy + 2 light, joined by disulfide bonds.
• The variable region gives antibody specificity; the constant region is the same within a class.
• Lysozyme is found in tears, saliva, and mucus — it damages bacterial cell walls.
• Histamine causes vasodilation + increased capillary permeability = inflammation.
• Primary response = slow, symptoms appear. Secondary response = fast, often symptom-free.
• HIV destroys helper T cells specifically — this cripples both B cell activation and T killer cell activation.
• Active immunity = memory cells = long-term. Passive immunity = no memory cells = short-term.

• I can describe how TB is transmitted and explain the primary vs active phase
• I can describe the full replication cycle of HIV, step by step
• I can explain the difference between HIV and AIDS
• I can list all six routes of pathogen entry with an example disease for each
• I can name the body's physical/chemical barriers to infection and explain how each works
• I can describe inflammation as a step-by-step process involving histamine
• I can explain the three roles of interferons
• I can describe phagocytosis from attraction to antigen presentation
• I understand the difference between self and non-self antigens
• I can label and explain the structure of an antibody
• I can explain three ways antibodies disable pathogens
• I can explain the roles of T helper, T killer, and T memory cells
• I can explain the roles of plasma cells and B memory cells
• I can explain clonal selection in my own words
• I can explain why the secondary response is faster than the primary response
• I can compare active and passive immunity across all features (source, speed, memory cells, duration)
• I can explain how vaccines work and why they need updating (antigenic variation)
• I can explain at least two evasion mechanisms each for HIV and TB