Recognition and polymorphism in host-parasite genetics

Abstract

Genetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host-parasite polymorphisms: plant-pathogen interactions, nuclear-cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.

Wolbachiahost shifts: routes, mechanisms, constraints and evolutionary consequences

“…In that sense, they may be essential in generating the raw heritable variations underlying the evolution of the many phenotypes that Wolbachia displays, including its ability to survive in a new host (Licht, 2018). Reciprocally, host shifts may also boost Wolbachia genetic diversity by exposing diverse lineages to diverse new environments, that is, diverse selective constraints (Frank, 1997; Read & Taylor, 2001). Host shifts may also contribute to Wolbachia genomic variations in a more proximate manner, by generating co‐infections by several Wolbachia strains, that are indeed of common occurrence (Perrot‐Minnot et al ., 1996; Kondo et al ., 2002) and open the possibility for recombination between both close and distant Wolbachia lineages (Jiggins et al ., 2001; Werren & Bartos, 2001; Jiggins, 2002; Baldo et al ., 2006; Atyame et al ., 2011; Ellegaard et al ., 2013).…”

Hot Spots, Cold Spots, and the Geographic Mosaic Theory of Coevolution

“…Although mathematically convenient, linear fitnesses arise naturally when individual fitness is determined via random pairwise, between-species interactions (e.g., Hofbauer and Sigmund 1988;Gavrilets 1997), including matching-alleles and gene-for-gene interactions (e.g., Frank 1994). In particular (6) and (7) correspond to average genotypic fitnesses assuming a matching-alleles model in which alleles X 1 and Y 1 are "matched" as are alleles X 2 and Y 2 .…”

Within-Host Population Dynamics and the Evolution of Microparasites in a Heterogeneous Host Population

“…(These and other forms of host heterogeneity have been observed in a number of host-parasite systems; e.g., Fenner and Ratcliffe 1965;Anderson and May 1982;May and Anderson 1983;Ebert and Hamilton 1996;Zhong and Dobson 1996;Woolhouse et al 1997). However, these models have largely been aimed at explaining the observed stable polymorphism in host susceptibility and parasite virulence found for many parasitehost systems (Antonovics and Thrall 1994;Frank 1994;Gupta and Hill 1995;Morand et al 1996). The question of how host heterogeneity affects the evolution of parasite virulence has, until recently, been less thoroughly explored.…”

“…Virulent parasites can evolve if there are trade-offs between ␣ and ␤ or v, with evolved virulence levels determined by the shape of the tradeoff (Anderson and May 1982;May and Anderson 1983). Numerous extensions of the basic susceptible-infectious-recovered (SIR;Bailey 1975) approach have explored the way in which virulence evolution is affected by factors such as mutation (Bonhoeffer and Nowak 1994;Bergstrom et al 1999), co-or superinfection (Levin and Pimentel 1981;Frank 1992;Nowak and May 1994;May and Nowak 1995;Mosquera and Adler 1998), the mode of transmission (Lipsitch et al 1995a,b;Bergstrom et al 1999), host susceptibility Antonovics and Thrall 1994;Frank 1994;van Baalen 1998;Gandon and Michalakis 2000), and host heterogeneity (Regoes et al 2000).…”