The evolutionary race between pathogens and hosts

Microbiology, Immunity and Forensics · The immune response · note 5 of 5

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The evolutionary race between pathogens and hostsSpec 6.12

In short

The evolutionary race theory states that hosts and pathogens are in a continuing cycle of selection: mutations that help a pathogen evade defences are selected, then hosts with improved resistance are selected. Evasion mechanisms such as antigenic variation, hiding inside cells and suppressing immunity support the theory.

Pathogens have short generation times and high mutation rates, so they evolve quickly. A pathogen that survives host defences reproduces and passes on the allele. Hosts with a more effective immune response also survive and reproduce, so their offspring are better defended. The pressure from each side selects for change in the other: an evolutionary race. Evidence is shown by the many ways pathogens evade the immune system.

Evasion mechanisms shown by pathogens
MechanismExampleWhy it works
Antigenic variation: changing surface antigensInfluenza virus (mutations and reassortment give new surface proteins); HIV (reverse transcriptase makes many errors); Trypanosoma (switches its surface protein)Memory cells and antibodies for the old antigen no longer recognise the new type, so there is no secondary response and a new vaccine may be needed
Hiding inside host cellsHIV (inside helper T cells, as a latent provirus); Mycobacterium tuberculosis (inside macrophages); malaria parasite (liver and red blood cells)Antibodies cannot reach the pathogen inside the cell, and few or none of its antigens are displayed on the host cell surface
Killing or disabling immune cellsHIV destroys helper T cellsFewer B cells and killer T cells are activated, so the immune response collapses
Preventing digestion by phagocytesM. tuberculosis stops lysosome fusion; some bacteria have a capsulePathogen survives phagocytosis, or is not engulfed at all

These mechanisms are examples of adaptations produced by natural selection. Because the pathogen population keeps producing new variants, the host immune system, vaccines and drugs always have to respond to a moving target.

Exam tip:

To support the theory, name the mechanism, give the organism, and link it to the host: 'HIV mutates rapidly, so new antigen variants are not recognised by memory cells'.

Quick check

  1. How does lysozyme kill bacteria?

    Show answer

    It hydrolyses peptidoglycan in the cell wall, so the bacterium bursts by osmosis.

  2. How does interferon protect a neighbouring cell?

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    It switches on genes for enzymes that break down viral mRNA and block protein synthesis, so the virus cannot replicate.

  3. Which cell secretes antibodies?

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    The plasma cell (B effector cell).

  4. What is the difference between natural passive and artificial passive immunity?

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    Natural passive: antibodies pass from mother to baby. Artificial passive: ready-made antibodies are injected.

  5. Why does antigenic variation help a pathogen survive?

    Show answer

    Memory cells and antibodies for the old antigen do not recognise the new antigen, so there is no fast secondary response.

Written and checked against the Edexcel International A Level Biology (YBI11) specification · Updated October 2026

Frequently asked questions

What is the difference between innate and adaptive immunity?

Innate (non-specific) responses such as inflammation, lysozyme, interferon and phagocytosis act against any pathogen, quickly and in the same way. The adaptive (specific) response uses B and T cells whose receptors are complementary to one antigen, takes days at first, and produces memory cells for faster future responses.

How do antibodies work?

Antibodies are Y-shaped proteins made by plasma cells. The variable region on each arm has a shape complementary to one antigen. They bind to pathogens and toxins, clump pathogens together (agglutination), make them easier for phagocytes to engulf, and block attachment to host cells.

What do T helper cells and T killer cells do?

T helper cells are activated by antigen-presenting cells and release cytokines that stimulate B cells and T killer cells. T killer cells destroy body cells that display the antigen, such as virus-infected cells, by releasing perforin and enzymes. Both types also form T memory cells.

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