The evolutionary dynamics of local infection and global reproduction in host–parasite interactions

A fundamental question in both evolutionary biology and parasitology is why do different levels of virulence evolve in different parasites. Here we use explicitly spatial lattice models to show how the spatial relationships of infection and host reproduction determine the degree of virulence that will occur. When the reproduction of the host acts over larger spatial scales than the infection process higher virulence is predicted. In contrast to both the mean-field and the case where infection acts over larger spatial scales than reproduction, the transmission and virulence predicted are always finite as “self-shading” of infected individuals always occurs. This process may help to explain the evolution of the high virulence of larval diseases of insects where reproduction clearly acts over greater distances than infection.

[1]  R. May,et al.  The evolution of virulence in parasites and pathogens: reconciliation between two competing hypotheses. , 1994, Journal of theoretical biology.

[2]  Maurice W. Sabelis,et al.  The Dynamics of Multiple Infection and the Evolution of Virulence , 1995, The American Naturalist.

[3]  M. Keeling,et al.  The effects of local spatial structure on epidemiological invasions , 1999, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[4]  G. Dwyer.  On the Spatial Spread of Insect Pathogens: Theory and Experiment , 1992 .

[5]  S. Frank.  A kin selection model for the evolution of virulence , 1992, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[6]  F R Adler,et al.  Evolution of virulence: a unified framework for coinfection and superinfection. , 1998, Journal of theoretical biology.

[7]  David A. Rand,et al.  Invasion, stability and evolution to criticality in spatially extended, artificial host—pathogen ecologies , 1995, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[8]  W. Hamilton,et al.  The Evolution of Cooperation , 1984 .

[9]  R. Schinazi,et al.  On an interacting particle system modeling an epidemic , 1996, Journal of mathematical biology.

[10]  R M May,et al.  Epidemiology and genetics in the coevolution of parasites and hosts , 1983, Proceedings of the Royal Society of London. Series B. Biological Sciences.

[11]  Michael Begon,et al.  Host–pathogen systems in a spatially patchy environment , 1996, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[12]  J. Fuxa,et al.  Epizootiology of insect diseases , 1987 .

[13]  A. Sasaki.  Evolution of antigen drift/switching: continuously evading pathogens. , 1994, Journal of theoretical biology.

[14]  H J Bremermann,et al.  A game-theoretical model of parasite virulence. , 1983, Journal of theoretical biology.

[15]  Y. Iwasa,et al.  Optimal growth schedule of pathogens within a host: switching between lytic and latent cycles. , 1991, Theoretical population biology.

[16]  Akira Sasaki,et al.  Pathogen invasion and host extinction in lattice structured populations , 1994, Journal of mathematical biology.

[17]  M. Keeling.  Correlation equations for endemic diseases: externally imposed and internally generated heterogeneity , 1999, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[18]  A. Sasaki,et al.  ‘Small worlds’ and the evolution of virulence: infection occurs locally and at a distance , 1999, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[19]  Michael Begon,et al.  Long-term population dynamics of the Indian meal moth Plodia interpunctella and its granulosis virus , 1994 .

[20]  M. Boots,et al.  Cannibalism and the stage‐dependent transmission of a viral pathogen of the Indian meal moth, Plodia interpunctella , 1998 .

[21]  A. Sasaki,et al.  The evolution of parasite virulence and transmission rate in a spatially structured population. , 2000, Journal of theoretical biology.

[22]  Martin A. Nowak,et al.  Superinfection and the evolution of parasite virulence , 1994, Proceedings of the Royal Society of London. Series B: Biological Sciences.