Parasitology

Research Article

Applying predator-prey theory to modelling immune-mediated, within-host interspecific parasite interactions

ANDY FENTONa1 c1 and SARAH E. PERKINSa2

a1 School of Biological Sciences, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK

a2 Center for Infectious Disease Dynamics, 208 Mueller Lab, Penn State University, State College, PA, 16803, USA

SUMMARY

Predator-prey models are often applied to the interactions between host immunity and parasite growth. A key component of these models is the immune system's functional response, the relationship between immune activity and parasite load. Typically, models assume a simple, linear functional response. However, based on the mechanistic interactions between parasites and immunity we argue that alternative forms are more likely, resulting in very different predictions, ranging from parasite exclusion to chronic infection. By extending this framework to consider multiple infections we show that combinations of parasites eliciting different functional responses greatly affect community stability. Indeed, some parasites may stabilize other species that would be unstable if infecting alone. Therefore hosts' immune systems may have adapted to tolerate certain parasites, rather than clear them and risk erratic parasite dynamics. We urge for more detailed empirical information relating immune activity to parasite load to enable better predictions of the dynamic consequences of immune-mediated interspecific interactions within parasite communities.

(Received July 28 2009)

(Revised October 28 2009)

(Accepted October 31 2009)

(Online publication February 15 2010)

Correspondence:

c1 Corresponding author: School of Biological Sciences, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK. Tel: +0151 795 4473. Fax: +0151 795 4408. E-mail: a.fenton@liverpool.ac.uk

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