The evolution of virulence in pathogens with frequency-dependent transmission

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Kara J O'Keefe1

  • 1Department of Ecology and Evolutionary Biology, Osborn Memorial Laboratories, Yale University, New Haven, CT 06520-8106, USA. kara.okeefe@yale.edu

Journal of Theoretical Biology
|December 24, 2004
PubMed

Insights

This study explores how virulence evolves in pathogens with frequency-dependent transmission, suggesting established principles may apply. It examines mortality and fecundity impacts, and spatial structure effects on sterility.

Area of Science:

  • Evolutionary biology
  • Epidemiology
  • Pathogen dynamics

Background:

  • Frequency-dependent transmission is key for sexually transmitted and vector-borne diseases.
  • Virulence has two components: increased host mortality and decreased host fecundity.
  • Sterilizing pathogens are common in frequency-dependent transmission systems.

Purpose of the Study:

  • To describe the evolution of virulence in pathogens with frequency-dependent transmission.
  • To compare virulence evolution principles between frequency-dependent and density-dependent transmission.
  • To investigate the role of spatial structure in the evolution of virulence.

Main Methods:

  • Theoretical modeling of host-pathogen dynamics.
  • Analysis of virulence components: mortality and sterility.
  • Examination of spatial population structure effects.

Main Results:

  • Principles of virulence evolution established for density-dependent pathogens may qualitatively apply to frequency-dependent pathogens.
  • Frequency-dependent transmission can lead to different host-pathogen numerical dynamics compared to density-dependent transmission.
  • Spatial structure influences the evolution of the sterility component of virulence.

Conclusions:

  • The evolution of virulence in frequency-dependent systems shares qualitative similarities with density-dependent systems.
  • Understanding virulence evolution requires considering both mortality and fecundity impacts.
  • Spatial dynamics are crucial for comprehending the evolution of pathogen-induced sterility.

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