Allocation to sexual versus nonsexual disease transmission.

Published

Journal Article

Many diseases have both sexual and nonsexual transmission routes, and closely related diseases often differ in their degree of sexual transmission. We investigate the evolution of transmission mode as a function of host social and mating structure using a model in which disease transmission is explicitly dependent on the numbers of sexual and nonsexual contacts (which are themselves a function of population density) and per-contact infection probabilities. Most generally, and in the absence of trade-offs between the degree of sexual transmission and effects on host fecundity and mortality, nonsexual transmission is favored above the social-sexual crossover point (the host density at which the number of nonsexual contacts exceeds the number of sexual contacts), while sexual transmission is favored below this point. When changes in allocation to the two transmission modes are accompanied by changes in mortality or fecundity, both mixed and pure transmission strategies can be favored. If invading genotypes differ substantially from resident genotypes, genetic polymorphism in transmission mode is possible. The evolutionary outcomes are predictable from a knowledge of the equilibrium population sizes in relation to the social-sexual crossover point. Our results also show that predictions about dynamic outcomes, based on rates of invasion for single pathogens into healthy populations, do not adequately describe the resulting disease prevalence nor predict the subsequent evolutionary dynamics; once invasion of a pathogen has occurred, the conditions for spread of a second pathogen are themselves altered. If the host is considered as a single resource, our results show that two pathogens may coexist on a single resource if they use that resource differentially and have differential feedbacks on resource abundance; such resource feedback effects may be present in other biological systems.

Full Text

Duke Authors

Cited Authors

  • Thrall, PH; Antonovics, J; Wilson, WG

Published Date

  • January 1998

Published In

Volume / Issue

  • 151 / 1

Start / End Page

  • 29 - 45

PubMed ID

  • 18811422

Pubmed Central ID

  • 18811422

Electronic International Standard Serial Number (EISSN)

  • 1537-5323

International Standard Serial Number (ISSN)

  • 0003-0147

Digital Object Identifier (DOI)

  • 10.1086/286100

Language

  • eng