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Figure 2 | BMC Biology

Figure 2

From: The genetics of infectious disease susceptibility: has the evidence for epistasis been overestimated?

Figure 2

Genetic models of host-parasite interactions. Infection outcomes are shown for three different interaction models (haploid hosts and parasites with two loci and two alleles each), where R represents resistant individuals, I represents non-resistant individuals, and P represents partially resistant individuals. (a) Gene-for-gene-model. The mechanistic basis of the gene-for-gene model is that resistance by the host requires recognition of a gene product ‘elicitor’ produced by the parasite [15, 16]. Thus, a host is resistant if it contains one resistance allele that matches an avirulence allele (A or B) of the parasite. (b) Matching-allele model. In an architecture inspired by the self-nonself recognition systems of the animal immune system [14, 15], the matching-allele model assumes that a host can resist a parasite unless the parasite matches all of its interacting alleles. (c) Multiplicative matching-alleles model. This model is presented as a counterpoint to the matching-allele model, as it does not implicitly involve epistatic interactions between resistance alleles at different loci [4, 29]. Instead, the number of matched alleles determines host and parasite fitness in a multiplicative fashion, leading to intermediate, or partial, estimates of resistance.

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