Primary and Secondary Immune Response

Q1.1 — Primary vs secondary peak comparison

Lag time: after dose 1 (primary), the response takes approximately 14 days to reach a modest peak of ~2 IU/mL. After dose 2 (secondary), the response peaks within approximately 5–7 days (graph shows a much faster rise) and reaches ~10 IU/mL — approximately 5× higher. [1 mark for lag comparison; 1 mark for magnitude comparison with approximate values from the graph.]

Q1.2 — Why titre declines but does not fall to zero (3 marks)

Plasma cells are short-lived and stop producing antibody as the infection/vaccine antigen is cleared [1]. Antibody molecules themselves are broken down (catabolised) over weeks to months, so titre falls [1]. However, long-lived memory B cells (and some long-lived plasma cells in bone marrow) persist and continue to secrete low levels of antibody, preventing titre from reaching absolute zero [1].

Q1.3 — Why the booster produces the largest, fastest response (3 marks)

The booster triggers a secondary immune response, driven by memory B cells accumulated during both the primary and secondary responses of doses 1 and 2 [1]. This large pool of pre-committed memory cells can differentiate into plasma cells within hours, bypassing the slow naive clonal selection needed in the primary response [1]. The result is a faster response (rise within days rather than two weeks) and a higher peak titre (the lesson states 10–100× primary peak) because more plasma cells are produced from the expanded memory pool [1].

Q2 — Cause-and-effect chain

Effect 1: A primary immune response is triggered — dendritic cells engulf cowpox antigens and present them in lymph nodes, where naive B and T cells encounter them for the first time.

Effect 2: Clonal selection identifies and activates the matching B cell; clonal expansion produces a large population of plasma cells (secreting anti-cowpox antibodies) and memory B and T cells.

Effect 3: Memory B and T cells persist in lymphoid tissue for months to years, storing the immune system's "record" of the cowpox antigen epitopes (which are shared with smallpox).

Effect 4: The pre-existing memory cells recognise the shared antigens as familiar and mount an immediate secondary immune response — plasma cells flood the blood with high-affinity IgG antibodies within 1–3 days.

Overall outcome: Smallpox virus is neutralised and cleared before it can replicate to disease-causing levels — Phipps shows no smallpox symptoms and is effectively immune.

Q3.1 — MMR vs flu vaccine dose schedules (3 marks)

A live-attenuated vaccine (e.g. MMR) contains a weakened but living pathogen that replicates briefly inside the body, presenting many different antigens over time — this closely mimics natural infection [1]. The resulting primary (and secondary after dose 2) immune response is strong and generates large numbers of long-lived memory B and T cells, with antibody levels often persisting above the protective threshold for decades [1]. An inactivated (killed) vaccine cannot replicate, so it presents antigens only briefly; the immune response is weaker, generates fewer and shorter-lived memory cells, and antibody titres decline below the protective threshold sooner — hence boosters are required annually (flu also mutates, making last year's memory cells less effective against new strains) [1].

Q3.2 — Why measles needs a higher herd immunity threshold than polio (3 marks)

Measles has a much higher basic reproduction number (R₀ ≈ 12–18) compared to polio (~5–7), meaning one measles case infects far more susceptible people on average [1]. For herd immunity to work, the proportion of immune individuals must be high enough that the pathogen cannot find a new susceptible host at every transmission step — the formula is approximately 1 − (1/R₀), so higher R₀ requires higher immunity proportion [1]. For measles (R₀ ≈ 15), approximately 1 − (1/15) ≈ 93–95% of the population must be immune; for polio (R₀ ≈ 6), approximately 1 − (1/6) ≈ 80–85% is sufficient. Even a small drop in measles vaccination coverage below 95% leaves enough susceptible individuals that the virus can sustain transmission chains [1].

Q3.3 — Predict effect of falling uptake (2 marks)

If MMR uptake falls from 95% to 85%, population immunity would drop below the ~95% herd immunity threshold for measles [1]. Transmission chains would re-establish, and the rate of measles cases would increase significantly — unvaccinated individuals, immunocompromised people, and infants too young to be vaccinated would bear the greatest risk, as seen in the 2019 Australian resurgence [1].

Q4 — Comparison table completed