IB DP Biology: Defence against disease: immunity, HIV and vaccines (DP Biology)

This study guide covers section C3.2 (Defence against disease) of the IB Biology guide, first assessment 2025, for DP Biology. Statements C3.2.1 to C3.2.18 are for both SL and HL, and the guide lists no additional higher level material for the section, so nothing here is HL only.

Use it with the revision notes and the practice set. See also the IB DP Biology hub, the printable checklist, the syllabus guide and the free 10-minute diagnostics.

What this unit covers

Statement	What you must be able to do	Level
C3.2.1	Name the types of pathogen and give examples	SL and HL
C3.2.2	Explain skin and mucous membranes as physical and chemical barriers	SL and HL
C3.2.3	Outline blood clotting	SL and HL
C3.2.4	Distinguish innate from adaptive immunity	SL and HL
C3.2.5	Describe how phagocytes control infection	SL and HL
C3.2.6	Describe lymphocytes and where they are found	SL and HL
C3.2.7	Explain what antigens are	SL and HL
C3.2.8	Explain activation of B-cells by helper T-cells	SL and HL
C3.2.9	Explain clonal expansion to plasma cells	SL and HL
C3.2.10	Explain immunity and memory cells	SL and HL
C3.2.11	Describe HIV transmission	SL and HL
C3.2.12	Explain how HIV leads to AIDS	SL and HL
C3.2.13	Explain how antibiotics work and why they fail against viruses	SL and HL
C3.2.14	Explain evolution of multiresistant bacteria	SL and HL
C3.2.15	Give examples of zoonoses	SL and HL
C3.2.16	Explain how vaccines work	SL and HL
C3.2.17	Explain herd immunity	SL and HL
C3.2.18	Evaluate COVID-19 data, using percentage change and difference	SL and HL

C3.2.1 Pathogens

A pathogen is an organism that causes disease. The term is usually kept for viruses, bacteria, fungi and protists. Examples: cholera (the bacterium Vibrio cholerae), COVID-19 (a virus), athlete’s foot (a fungus), malaria (the protist Plasmodium). Archaea are not known to cause human disease. Other organisms, such as parasitic worms, also cause disease, which is why the guide speaks of a broad range.

Nature of science: careful observation led to progress. Ignaz Semmelweis noticed that childbed fever was far commoner in Vienna wards staffed by people who had come from dissections, and handwashing reduced it. John Snow mapped cholera cases in London and linked them to a water pump. Neither knew the exact pathogen, yet both found ways to control the disease.

C3.2.2 and C3.2.3 First lines of defence

Skin is a physical and a chemical barrier. The outer layer is tough, made of dead cells filled with keratin, and few microorganisms can pass through it. Skin glands secrete oily and acidic substances that discourage growth of many microorganisms. Mucous membranes line the airways, gut and reproductive tract. Mucus is sticky and traps microorganisms. In the airways, cilia sweep the mucus upwards to be swallowed. Mucus and tears also contain enzymes that damage bacterial cell walls.

If the skin is cut, blood clotting seals it:

1. Platelets (cell fragments) release clotting factors at the wound.
2. The factors start a cascade, a chain of reactions in which each step activates the next.
3. The cascade produces thrombin.
4. Thrombin converts soluble fibrinogen into insoluble fibrin.
5. Fibrin forms a mesh that traps erythrocytes, making a clot that dries to a scab.

The clot stops blood loss and blocks entry of pathogens. No more detail is required.

C3.2.4 Innate and adaptive immunity

Feature	Innate	Adaptive
Target	Broad categories of pathogen	A specific pathogen
Change over a lifetime	None	Improves with each exposure
Memory	No	Yes, memory cells
Cells you need	Phagocytes	Lymphocytes (B-cells and T-cells)

You do not need any other innate component than phagocytes.

C3.2.5 Phagocytes

Phagocytes are white blood cells. They move by amoeboid movement: the cell changes shape and extends parts of its cytoplasm, so it can squeeze out of the blood through capillary walls to reach infected tissue. At the site of infection:

• the phagocyte recognises molecules on the pathogen as foreign
• it engulfs the pathogen by endocytosis, enclosing it in a vesicle
• lysosomes fuse with the vesicle and release digestive enzymes that break the pathogen down.

Phagocytes respond to broad categories of pathogen, so this is innate immunity. Link: lysosomes are covered in organelles and cell specialization.

C3.2.6 to C3.2.10 The adaptive response

Lymphocytes are the cells of the adaptive system. They circulate in blood and are also held in lymph and concentrated in lymph nodes. You have a very large number of different B-cells, each able to make one specific antibody.

Antigens are recognition molecules. Most are proteins or glycoproteins on the outer surface of a pathogen. Antigens also occur on erythrocytes: if blood of a different group is transfused, its antigens can trigger antibody production in the recipient.

The sequence (clonal selection):

1. A B-cell with a matching antibody on its surface binds the antigen.
2. A helper T-cell, itself activated by the same type of antigen, contacts the B-cell and signals to it.
3. Only a B-cell with both signals is activated.
4. Few B-cells match any one antigen, so the activated cell divides by mitosis many times, making a clone.
5. Most of the clone become plasma cells, which secrete large quantities of the same antibody.
6. Some become memory cells, which survive for a long time.

Immunity means being able to clear an infectious disease from the body. It depends on memory cells. On re-exposure they produce plasma cells faster, giving a quicker and larger antibody response.

Worked example 1: size of a clone

A single activated B-cell divides every 6 hours. How many cells after 4 days, if all divide? How long until there are at least 10 000?

4 days is 96 hours, so 96 ÷ 6 = 16 divisions. Number of cells = 2¹⁶ = 65 536. 2¹³ = 8192 (too few) and 2¹⁴ = 16 384, so 14 divisions are needed: 14 × 6 = 84 hours (3.5 days). This is why the primary response takes days: one cell is far too few.

Worked example 2: interpreting antibody data

A fictional patient is given a harmless antigen twice. Antibody concentration peaks at 40 arbitrary units after the first dose and at 640 units after the second, the second peak arriving sooner.

Percentage change = (640 − 40) ÷ 40 × 100 = 1500% (16 times higher). Explanation: the first dose produced memory cells, so on the second dose many more B-cells were ready to divide and form plasma cells.

C3.2.11 and C3.2.12 HIV and AIDS

HIV (human immunodeficiency virus) passes in body fluids that contain infected cells or virus: blood, semen, vaginal fluids and breast milk. Mechanisms: unprotected sex, shared needles, from mother to child (in pregnancy, birth or breastfeeding) and transfusion of unscreened blood. HIV is not passed by casual contact such as touching or sharing a room.

HIV infects and kills only certain lymphocytes, the helper T-cells. With fewer helper T-cells, fewer B-cells are activated, so less antibody is made. The person cannot fight opportunistic infections, which seldom harm a healthy person. AIDS (acquired immunodeficiency syndrome) is the stage at which these infections occur.

Worked example 3: helper T-cell counts

Counts (per mm³ of blood) for a fictional person: 900 at diagnosis, 560 after 3 years, 310 after 6 years and 180 after 8 years. Percentage change over 8 years = (180 − 900) ÷ 900 × 100 = −80%. Over the first 3 years = (560 − 900) ÷ 900 × 100 = −37.8%. The fall explains why infections appear late: the system still copes while numbers are high.

C3.2.13 and C3.2.14 Antibiotics and resistance

Antibiotics block processes in bacteria that do not occur in eukaryotic cells, so they harm the pathogen but not the host. Examples: penicillin stops bacteria building their cell walls (animal cells have none), and some antibiotics block bacterial ribosomes, which differ from eukaryotic ribosomes.

Antibiotics fail against viruses because viruses have no metabolism or cell wall of their own and no ribosomes. They live inside host cells and use the host’s machinery, so there is no bacterial process to block.

Resistance evolves by natural selection. A mutation makes a few bacteria resistant. The antibiotic is a selection pressure that kills the others. Survivors reproduce and pass on the allele, and resistance genes can also be passed between bacteria. Strains resistant to several antibiotics are multiresistant. To slow this: use antibiotics only when needed, finish the prescribed course, and avoid routine use in farm animals.

Nature of science: screening chemical libraries is a new technique producing new antibiotics.

Worked example 4: resistant population

A culture has 10 resistant cells. The antibiotic kills all non-resistant cells. Resistant cells divide every 30 minutes. After 6 hours: 6 ÷ 0.5 = 12 divisions, so 10 × 2¹² = 40 960 cells. The new population is almost entirely resistant.

C3.2.15 Zoonoses

Zoonoses are infectious diseases that transfer from other species to humans, by varied routes.

Disease	Pathogen	Route
Tuberculosis (some cases)	Bacterium Mycobacterium bovis	Unpasteurised milk or close contact with infected cattle
Rabies	Virus	Bite from an infected mammal, saliva entering the wound
Japanese encephalitis	Virus	Mosquito bite; pigs and wading birds carry the virus
COVID-19	Virus (SARS-CoV-2)	Respiratory droplets and aerosols between people, after transfer from animals

COVID-19 shows how a transfer can have profound consequences, because the virus then spread between people worldwide.

C3.2.16 and C3.2.17 Vaccines and herd immunity

A vaccine contains antigens, or DNA or RNA coding for antigens. Cells make the antigen, the immune system responds and memory cells form, but the person does not get the disease.

Herd immunity: when enough of a population is immune, transmission is greatly impeded, so people who cannot be vaccinated, such as young babies, are protected too. Members of a population depend on each other. The percentage needed varies with the disease.

Nature of science: research is published for evaluation, but media may report before evaluation finishes. Vaccine side effects are minimal but not nil.

C3.2.18 Evaluating COVID-19 data

Percentage change = (new − original) ÷ original × 100. Percentage difference = difference ÷ mean of the two values × 100.

Worked example 5

Fictional weekly cases in Eastmere rose from 2400 to 9600. Percentage change = 7200 ÷ 2400 × 100 = +300%.

Hospital admissions per 100 000 people over four weeks: 84 unvaccinated, 12 vaccinated. Difference = 72; mean = 48; percentage difference = 72 ÷ 48 × 100 = 150%. Percentage change from unvaccinated to vaccinated = (12 − 84) ÷ 84 × 100 = −85.7%.

Herd immunity: 17 000 of 20 000 people immune is 85%.

When you evaluate data, ask: Is the figure a rate per 100 000 or a raw count? How large was the sample? Were the groups otherwise similar? Was testing the same throughout? Does correlation show cause?

Common errors

• Saying antibiotics kill viruses, or that bacteria “become used to” them. Mutation is random, and selection does the rest.
• Writing that vaccines “contain antibodies”.
• Forgetting that B-cells need a helper T-cell as well as antigen.
• Saying HIV is AIDS. HIV is the virus; AIDS is the later condition.
• Using the wrong denominator for percentage change.

Official syllabus

IB Biology guide, first assessment 2025, published by the International Baccalaureate Organization, section C3.2.