Immune Response and Vaccination – Primary vs Secondary Response

BiologyHealth & DiseaseAges 16–17

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A pathogen enters the body: phagocytes destroy some of it, B lymphocytes are activated, secrete antibodies and leave memory cells behind. A graph of pathogen load and antibody concentration over time shows that the secondary response is faster and stronger than the primary one. Compare natural infection with vaccination, booster doses and the threshold at which symptoms appear.

Lesson: Immunity in humans; vaccines and disease prevention

What it shows

This model follows one pathogen inside the body. Phagocytes give a fast but limited non-specific defence. B lymphocytes that recognise the antigen divide and become plasma cells, which secrete specific antibodies after a lag of several days; some become memory cells. At the next exposure, memory cells respond within about two days and produce far more antibody, so the pathogen is removed before it reaches the symptom threshold. A vaccine supplies antigen that cannot multiply, so it builds memory without the illness. Units are relative and the curves show trends, not a particular disease.

How to use

Choose a Scenario and press Run. Watch the red pathogen curve and the blue antibody curve on the logarithmic graph, and read the table row for each exposure. Change Growth rate, Antibody half-life and Exposure day, or add events yourself with + Vaccine and + Infection at the current day. Drag across the graph to scrub back and forth in time.

Parameters you can change

  • Scenario Natural infection twice, One vaccine dose, then exposure to the pathogen, Two doses (booster on day 28), then exposure, Not vaccinated, exposed to the pathogen, Custom (use the buttons to add events)
  • Pathogen growth rate 1–3 /day
  • Antibody half-life 5–40 days
  • Day of exposure to the pathogen 35–150 day

Questions to explore

  1. Why does a second infection cause no symptoms even though antibody levels in the blood have already fallen a lot?
  2. How does vaccination differ from natural infection in antibody level and in the risk to the person protected?
  3. When is a booster dose useful, and how does it change the antibody curve?