OxfordAQA International AS and A-level Biology: Immunity and vaccination (9610) – Practice Questions

These are original questions written for Marlbridge, for revision and practice on this content. They are not reproduced past-paper questions, and they do not replicate the exam’s exact structure, question count or mark tariffs – examination boards hold copyright in their own papers. Use these alongside the official past papers from your board or school.

These questions cover section 3.2.5 (3.2.5.1 to 3.2.5.3, the defensive functions of mammalian blood) of the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1, for International AS exams from May/June 2017 and International A-level exams from May/June 2018. Learn the content first from the study guide and the revision notes. The course hub is OxfordAQA A-level Biology, the checklist lists every statement, and the free diagnostics give a quick check of your starting point.

Questions

1. (a) Define the term antigen. [2] (b) A kidney from a donor who is not an identical twin is transplanted into a patient. Explain why the patient’s immune system may attack the new kidney. [2]

2. Describe how a neutrophil destroys a bacterium after the bacterium has bound to its surface. [4]

3. An antibody is drawn as a Y shape. Region X is at the tip of each arm. Region Y is where the arms join the stem. Bonds Z link the four polypeptide chains. (a) Name X, Y and Z. [3] (b) Explain why an antibody against one bacterium does not bind to a different bacterium. [2]

4. A scanning electron micrograph shows a macrophage with a diameter of 54 mm on the image. The magnification is x3000. (a) Calculate the actual diameter of the macrophage in micrometres. [2] (b) A bacterium in the same image is 6 mm long. Calculate its actual length in micrometres. [2] (c) Explain the role of lysosomes in the macrophage. [2]

5. (a) State the type of immunity for which T cells are primarily responsible and the type for which B cells are primarily responsible. [2] (b) Explain why one of these types is described as humoral. [1] (c) Name the cells that secrete antibodies. [1]

6. A macrophage engulfs a bacterium. Describe how this leads to the production of antibodies against the bacterium. [6]

7. Explain how antibodies lead to the destruction of bacterial cells. [5]

8. A volunteer was injected with a vaccine on day 0 and given a booster on day 28. The table shows antibody concentration in the blood.

Day	0	7	14	21	28	31	34	41	56
Antibody (arbitrary units)	0	0	10	25	18	220	900	600	380

(a) Between which two days was antibody first detected? [1] (b) Calculate how many times greater the highest concentration after the second dose was than the highest after the first dose. [2] (c) Explain the differences between the response to the first dose and the response to the second dose. [4]

9. A man was vaccinated against influenza two years ago. This winter he caught influenza. (a) Explain why the earlier vaccine may not have protected him. [3] (b) Suggest why developing a vaccine against HIV is difficult. [2]

10. A child who has never been vaccinated against tetanus has a deep, dirty wound. A doctor injects tetanus antibodies and also starts a course of vaccination. (a) Explain why the antibody injection is given. [2] (b) Explain why the antibody injection alone would not protect the child for years. [2] (c) State the type of immunity the vaccine course provides and explain how it differs from that given by the injection. [2]

11. A disease has R = 8, where R is the mean number of new infections caused by a single case when nobody is immune. A simple model states that the minimum fraction of the population that must be immune to stop spread is 1 - 1/R. (a) Calculate the minimum percentage that must be immune. [2] (b) Only 95% of people given the vaccine become immune. Calculate the vaccination coverage needed. [2] (c) A town vaccinates 88% of its people. Calculate the percentage immune and state whether herd immunity is reached. [2]

12. A trial of a new vaccine gave the results below. Allocation to groups was random and neither participants nor staff knew who received the vaccine.

Group	Participants	Cases of disease over 3 months
Vaccine, all ages	9,000	27
Placebo, all ages	9,000	135
Vaccine, over 65 only	1,500	12
Placebo, over 65 only	1,500	30

Mild side effects occurred in 12% of the vaccine group and 4% of the placebo group. (a) Calculate the percentage of each all-ages group who developed the disease. [2] (b) Calculate the efficacy of the vaccine for all ages. [2] (c) Calculate the efficacy for the over-65 group. [2] (d) Evaluate the trial and its data. [4]

Answers

1. (a) A molecule, usually a protein, [1] that is recognised as foreign and triggers an immune response [1]. [2] (b) The donor cells carry surface molecules (antigens) that differ from the patient’s own [1]; the patient’s immune system recognises them as non-self and responds [1]. [2] Examiner insight: Defining an antigen only as “something that causes disease” misses transplants and other harmless foreign cells.

2. The neutrophil engulfs the bacterium, forming a phagosome [1]. Lysosomes fuse with the phagosome [1] and release hydrolytic enzymes [1], which digest the bacterium; the products are absorbed or removed [1]. [4] Examiner insight: Naming lysosomes is not enough on its own; a complete answer says that they fuse with the phagosome and what they release.

3. (a) X is the variable region [1]; Y is the hinge region [1]; Z are disulfide bridges [1]. [3] (b) The variable region has a specific tertiary structure, formed by its amino acid sequence, giving a particular binding-site shape [1]; the second bacterium has an antigen with a different shape that is not complementary [1]. [2] Examiner insight: Say “complementary” and link shape to amino acid sequence; “the antibody has the wrong shape” alone is a weaker explanation.

4. (a) 54 / 3000 = 0.018 mm [1] = 18 micrometres [1]. [2] (b) 6 / 3000 = 0.002 mm [1] = 2 micrometres [1]. [2] (c) Lysosomes contain digestive enzymes [1] and fuse with the phagosome so the engulfed bacterium is digested [1]. [2] Examiner insight: Convert units explicitly (1 mm = 1000 micrometres); state the unit with every answer so that the size of the value is clear.

5. (a) T cells: cell-mediated immunity [1]; B cells: humoral immunity [1]. [2] (b) Humoral immunity works through antibodies in body fluids (blood and tissue fluid) [1]. [1] (c) Plasma cells [1]. [1] Examiner insight: Plasma cells are the cells that secrete antibody; answers that say “B cells” generally need to be more precise when the question asks which cells secrete.

6. The macrophage presents the bacterial antigen on its surface [1]. A T cell carrying a complementary receptor attaches to it [1] and is activated, helping to stimulate B cells [1]. A B cell with a complementary surface antibody binds the antigen [1] and divides by mitosis to form a clone [1]. Cells of the clone become plasma cells that secrete the antibody [1]. [6] Examiner insight: Sequence matters in a “describe how” question; listing the cells without saying what each one does earns little.

7. Antibodies bind to antigens on the bacterial surface, forming antigen-antibody complexes [1]. An antibody has two binding sites, so it can attach to two bacteria [1]; many antibodies link many bacteria into clumps (agglutination) [1]. Phagocytes bind to the antibody-coated or clumped bacteria and engulf them [1], and lysosomal enzymes digest them [1]. [5] Examiner insight: “Antibodies kill bacteria” does not describe a mechanism; name agglutination and phagocytosis and give the cause of each.

8. (a) Between day 7 and day 14 [1]. [1] (b) 900 / 25 [1] = 36 times [1]. [2] (c) After the second dose, antibody appeared much sooner (220 units within 3 days compared with 10 units at day 14) [1] and reached a much higher peak (900 compared with 25) [1]. Memory cells were formed by the first dose [1] and on re-exposure they divide rapidly into many plasma cells that secrete antibody [1]. [4] Examiner insight: Quote figures from the table to support each difference, and explain with memory cells rather than saying only that the body “remembers”.

9. (a) The antigens on the virus had changed (by mutation) [1]; antibodies and memory cells from the earlier vaccine were not complementary to the new antigens [1]; so no rapid secondary response occurred [1]. [3] (b) HIV mutates rapidly, so its antigens vary [1]; a vaccine would need to protect against many different forms of the antigen [1]. [2] Examiner insight: Link the cause (change in antigen) to the consequence (memory cells no longer match); stating that “the virus has become resistant” is a different idea.

10. (a) Antibodies give immediate protection [1]; the child’s own response would be too slow to deal with the toxin or bacteria already present [1]. [2] (b) The antibodies are not replaced and are broken down within weeks [1]; no memory cells are formed [1]. [2] (c) Active immunity [1]; the child makes its own antibodies and memory cells, giving long-term protection, whereas the injection gives short-term passive immunity [1]. [2] Examiner insight: A comparison needs both sides; saying only that the vaccine “lasts longer” earns less than naming memory cells.

11. (a) 1 - 1/8 = 0.875 [1], so 87.5% [1]. [2] (b) 87.5 / 0.95 [1] = 92.1% [1]. [2] (c) 88% x 0.95 = 83.6% immune [1]; this is below 87.5%, so herd immunity is not reached [1]. [2] Examiner insight: In part (c), a comparison with the threshold from part (a) is needed to answer “state whether”; the calculation alone is incomplete.

12. (a) Vaccine: 27 / 9000 x 100 = 0.3% [1]; placebo: 135 / 9000 x 100 = 1.5% [1]. [2] (b) (1.5 - 0.3) / 1.5 x 100 [1] = 80% [1]. [2] (c) Over-65 attack rates: 12 / 1500 = 0.8% and 30 / 1500 = 2.0% [1]; efficacy = (2.0 - 0.8) / 2.0 x 100 = 60% [1]. [2] (d) Random allocation, a placebo and double-blinding reduce bias, and the large groups make results more reliable [1]; the vaccine cut cases from 1.5% to 0.3%, so it appears effective [1]; it was less effective in the over-65 group (60% against 80%), and that subgroup is small [1]; follow-up of three months does not show long-term protection, and side effects were three times as common (12% against 4%) though described as mild [1]. Other valid points, such as the absence of a statistical test, can also gain credit. [4] Examiner insight: A good evaluation gives at least one strength and one limitation, each supported by a figure; repeating that the sample was “big” without saying why it matters is rarely enough.

Where marks are usually lost

• Defining an antigen without saying that it triggers an immune response.
• Writing that antibodies “destroy” or “kill” bacteria without naming agglutination or phagocytosis.
• Forgetting to say that each antibody has two binding sites when explaining agglutination.
• Missing out the lysosome or the enzymes when describing digestion after phagocytosis.
• Confusing plasma cells with memory cells.
• Saying vaccines contain antibodies, or that passive immunity produces memory cells.
• Mixing up units in magnification questions.
• Giving efficacy as the percentage of vaccinated people who became ill, instead of the reduction compared with placebo.
• Evaluating a trial without figures or a limitation.

Next steps

• Revise with the revision notes.
• Re-read the study guide.
• Go to the OxfordAQA A-level Biology hub and tick off the checklist.
• Try all free 10-minute diagnostics.
• Book a free trial class.

Official syllabus

OxfordAQA, International AS and A-level Biology (9610), Version 5.1: sections 3.2.5.1, 3.2.5.2 and 3.2.5.3. This page is an independent Marlbridge resource and is not endorsed by OxfordAQA.