The Coevolution of Virulence: Tolerance in Perspective (original) (raw)
Figure 2
The importance of intercepts: pleiotropy.
Host genotypes will almost certainly show differences in ωo,n (genetic variation for life history characteristics is ubiquitous [37]), and in some cases these differences will be linked to variation in the traits that contribute to virulence (αn or _I_n) via pleiotropy (where one gene influences more than one trait). For example, hosts that possess alleles that confer more potent defences (ability to control I or α) may be less fit when parasites are not around because the allele that aids defence compromises the performance of other traits (compare ωoR and ωoS; R denotes resistance, S denotes susceptible). In other words, there may be a cost of possessing a defence mechanism [38], often referred to as a trade-off. It is even conceivable that ωo,n is lower than host fitness at low I, because individuals without enough parasites can experience difficulty with immune regulation: the hygiene hypothesis posits that allergy and autoimmunity result from immune systems lacking direction from parasites ([39]; see ωoH, which denotes hygiene). Thus, the rank order of ωo,n may be the opposite of the rank order of fitness when infected. Moreover, ωon may not be easily predicted from the relationship between parasite density and host fitness when infected—for example, when just a small number of parasites stimulates a damaging or energy-sapping immune response that is little amplified by further infection. Generally, the fitness of uninfected individuals need not be a linear extrapolation of the relationship between fitness and parasite density (I).