AP Syllabus focus:
‘Pathogens rapidly evolve and can cause emergent diseases as they adapt to new hosts and environments.’
Pathogens can evolve on observable timescales because they reproduce quickly and generate abundant genetic variation. When novel variants spread in new hosts or conditions, outbreaks can occur and sometimes develop into emerging diseases.
Why pathogens evolve rapidly
Life-history features that speed evolution
Many pathogens (especially RNA viruses) evolve quickly because they often have:
Short generation times (hours to days), creating many opportunities for evolutionary change.
Large population sizes within hosts, increasing the number of new variants produced.
High mutation rates, particularly in RNA genomes with limited proofreading.
Strong selection from host immunity, transmission bottlenecks, and environmental change.
Sources of genetic variation
Rapid evolution requires heritable variation. In pathogens, variation can arise through:
Mutation during genome replication.
Recombination (exchange of genetic material) in viruses and microbes.
Reassortment in segmented viruses (mixing genome segments when two strains coinfect a host).
Reassortment is a form of genetic exchange unique to segmented viruses: when two strains coinfect the same cell, progeny virions can package a mixture of genome segments from each parent. The diagram contrasts reassortment with recombination, helping distinguish “whole segment swapping” from “within-segment template switching.” Source
Horizontal gene transfer in bacteria (acquiring genes from other cells), which can quickly add new functions.
Adaptation to new hosts and environments
Host shifts and “spillover”
A major route to emerging disease is cross-species transmission, when a pathogen infects a new host species and then adapts for onward spread.
This diagram summarizes spillover as a stepwise process linking reservoir-host infection dynamics to pathogen release, environmental persistence/transport, exposure of a recipient host, and within-host barriers that determine whether infection establishes. It emphasizes that failure at any barrier can prevent emergence, even when humans are frequently exposed. Source
Emerging disease: An infectious disease that has newly appeared in a population or is increasing rapidly in incidence, geographic range, or both.
Adaptation during or after spillover can be favored when variants:
Bind more effectively to receptors in the new host’s cells.
Replicate efficiently at the new host’s body temperature or tissue environment.
Evade or suppress immune responses long enough to transmit.
Transmit better via the dominant route available (respiratory, fecal–oral, vector-borne, contact).
Within-host vs between-host selection
Selection can act at multiple levels:
Within-host selection favors variants that replicate well inside an individual.
Between-host selection favors variants that transmit effectively to new hosts. These pressures can conflict; for example, very high replication may harm the host quickly and reduce transmission opportunities.
Environmental change and ecological opportunity
Pathogens encounter shifting conditions that alter which variants are favored, including:
New host availability (e.g., expanded contact between wildlife, livestock, and humans).
Changes in vector ranges (mosquitoes, ticks) driven by climate and land use.
Urbanization and crowding, which can increase transmission opportunities for well-adapted variants.
Travel and trade, which can move pathogens into immunologically naïve populations.
How emerging diseases arise and spread
Key steps in emergence
Emergence often involves a sequence of evolutionary and ecological events:
Introduction into a new host population (spillover or migration).
Establishment, when the pathogen can complete its life cycle and transmit.
Amplification, as transmission chains expand under favorable conditions.
Diversification, as ongoing mutation and selection generate lineages with different traits (e.g., transmissibility, immune escape).
Immune-driven evolution
Host immune responses create strong selection for variants that avoid recognition. Pathogens may evolve via:
Changes to surface proteins targeted by antibodies.
Altered epitopes that reduce immune binding while maintaining function.
Phenotypic plasticity in gene expression (in some microbes), changing what the immune system “sees.”
Bottlenecks and founder effects in transmission
Transmission frequently imposes a genetic bottleneck, where only a small subset of variants from the donor establish infection in the recipient.
A bottleneck reduces genetic diversity because only a small, non-representative sample of variants passes into the next population, allowing chance (genetic drift) to change allele frequencies. In pathogen transmission, this same sampling effect can make early infection genetically “narrow,” even if the donor carried many variants. Source
This can:
Reduce diversity temporarily in the new host.
Cause chance differences among transmission chains.
Still allow rapid evolution if mutation and replication quickly rebuild diversity.
Examples that illustrate rapid evolution and emergence
Influenza viruses: rapid change aided by mutation and genome segment mixing, facilitating outbreaks in populations with limited immunity.
Coronaviruses: adaptation to new hosts can follow spillover events, with selection favoring variants that transmit efficiently in humans.
HIV: high mutation rate and large within-host populations generate extensive variation, supporting rapid adaptation over time.
Ebola virus: emergence is associated with spillover and subsequent human-to-human transmission under certain ecological and social conditions.
FAQ
They compare historical clinical records with modern surveillance data.
Genomic sequencing can reveal whether lineages diverged recently or have circulated undetected for longer.
Sustained spread is more likely when:
The pathogen can transmit efficiently between individuals in the new host
The infectious period overlaps with opportunities for contact
The initial introduction occurs into dense or highly connected populations
Multiple spillovers often produce several distinct lineages closely related to animal strains.
A single spillover typically yields a more monophyletic cluster with diversification occurring after introduction.
If vectors expand geographically, the environment changes in a way that increases transmission opportunity.
The pathogen may already be compatible with the vector and host, so ecology rather than new mutations drives emergence.
Researchers use cell cultures and organoids from different species to test entry/replication differences.
They also use reverse genetics to introduce candidate mutations and measure phenotypic effects under controlled conditions.
Practice Questions
Explain why RNA viruses can evolve rapidly compared with many cellular organisms. (2 marks)
Short generation time and/or large population size increases opportunities for selection (1).
High mutation rate due to error-prone replication/lack of proofreading increases genetic variation (1).
Describe how a pathogen can cause an emerging disease after entering a new host species. Include both evolutionary and ecological factors. (5 marks)
Spillover/cross-species transmission introduces pathogen to a new host population (1).
Heritable variation arises (e.g., mutation/recombination/reassortment) (1).
Natural selection favours variants better able to infect/replicate in the new host (e.g., receptor binding, temperature, immune evasion) (1).
Selection favours variants with improved transmission between hosts (1).
Ecological conditions enable spread (e.g., high contact rates, travel, vector presence, naïve hosts) (1).
