The evolution of disease resistance and tolerance in spatially structured populations

Abstract

The ubiquitous challenge from infectious disease has prompted the evolution of diverse host defenses, which can be divided into two broad classes: resistance (which limits pathogen growth and infection) and tolerance (which does not limit infection, but instead reduces or offsets its negative fitness consequences). Resistance and tolerance may provide equivalent short-term benefits, but have fundamentally different epidemiological consequences and thus exhibit different evolutionary behaviors. We consider the evolution of resistance and tolerance in a spatially structured population using a stochastic simulation model. We show that tolerance can invade a population of susceptible individuals (i.e., neither resistant nor tolerant) with higher cost than resistance, even though they each provide equivalent direct benefits to the host, because tolerant hosts impose higher disease burden upon vulnerable competitors. However, in spatially structured settings, tolerance can invade a population of resistant hosts only with lower cost than resistance due to spatial genetic structure and the higher local incidence of disease around invading tolerant individuals. The evolution of tolerance is therefore constrained by spatial genetic structure in a manner not previously revealed by nonspatially explicit models, suggesting mechanisms that could maintain variation or limit the occurrence of tolerance relative to resistance.

The Innate Immune Signaling System as a Regulator of Disease Resistance and Induced Systemic Resistance Activity AgainstVerticillium dahliae

“…3). Therefore, the protective activity of K165 against V. dahliae is based on the activation of plant resistance rather than tolerance mechanisms, since tolerance does not limit infection but, instead, reduces or offsets its negative consequences on fitness (Horns and Hood 2012). The fls2 mutants exhibited high relative levels of V. dahliae DNA in agreement with the observed disease severity recordings at both time points, in contrast to efr-1, in which lower levels of the pathogen were observed relative to Col-0 ( Fig.…”

First principles of Hamiltonian medicine

“…Frank [32] used an inclusive-fitness model to show that higher relatedness selects for increased investment in resistance (avoidance of infection, in this case, through induction of immunity). Such resistance strategies may include altruistic, disease-related responses and behaviour by human hosts, which reduce pathogen transmission to kin [25,51,52]. Relatedness structure is also predicted to restrict the evolution of tolerance [51,52], in part, because tolerant individuals remain infectious.…”

“…Such resistance strategies may include altruistic, disease-related responses and behaviour by human hosts, which reduce pathogen transmission to kin [25,51,52]. Relatedness structure is also predicted to restrict the evolution of tolerance [51,52], in part, because tolerant individuals remain infectious. Such effects may be especially important owing to widespread trade-offs of investment in immune functions with investment in growth and reproduction, the usual two contexts for consideration of maximizing inclusive fitness.…”

Introduced and Native Congeners Use Different Resource Allocation Strategies to Maintain Performance during Infection

“…Ecologically, the high burdens that HOSP maintain may increase the frequency of parasite exposure for other avian hosts in the community (Restif and Koella 2004;Horns and Hood 2012), an outcome termed parasite spillback (Kelly et al 2009). As HOSP shed many coccidia but experience minimal health impacts themselves, spillback may enable HOSP to outcompete some native hosts (Kelly et al 2009).…”