Abstract
The evolution of pathogen virulence has received considerable attention during the last decades (Van Baalen and Sabelis 1995; Frank 1996; Day and Proulx 2004). In this note we will discuss two major theories of virulence evolution in the context of clonal plant— pathogen interactions and argue that they can lead to contradictory predictions when applied to very long-lived hosts such as clonally propagating plants. We propose that clonal plants and their pathogens may be especially suitable systems for empirically testing hypotheses of virulence evolution. A generally accepted theory of virulence evolution is based on the trade-off between pathogen transmission and within-host pathogen reproduction (Frank 1996; Lipsitch and Moxon 1997; Day 2003; Andre and Hochberg 2005), the latter being positively correlated with pathogen virulence (see Table 1 for definitions). Pathogens can benefit for a long time from hosts with low intrinsic mortality rates, provided that they exploit them prudently (low virulence), while severe host exploitation (high virulence) shortens the time during which a pathogen can benefit from the host. This effect can be seen as a mortality cost of virulence (Day and Proulx 2004). As a consequence, high host longevity should select for lower levels of virulence. Conversely, increased virulence should be favoured in shortlived hosts (Gandon et al. 2001 and references therein; Day and Proulx 2004), due to the necessity to spread quickly to new hosts and due to the lower mortality costs of virulence (Ewald 1994; Day and Proulx 2004). Depending on the specific host-pathogen interaction a whole range of evolutionary stable strategies can be expected. The optimal strategy
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