A unifying perspective on pathogen specificity

Linking microevolutionary processes to macroevolutionary patterns

I have always been interested coevolutionary interactions, particularly host-parasite interactions. I have often wondered if the local patterns of interaction between host and parasite (e.g. local adaptation) can scale up and lead to patterns of host specificity. Having a thorough understanding of these selective forces may help us better understand the conditions for disease emergence and perhaps disease virulence evolution.


Population genetics is concerned with the processes that generate evolutionary change within species and populations. A major question in evolutionary biology is whether these same processes ultimately generate patterns of diversity at higher organizational levels. While interactions between species such as hosts and their parasites (or plants and pollinators, herbivores and plants) have long been implicated as a means of generating patterns of diversification (Ehrlich and Raven, 1964,Thompson, 1994, 2005), the process by which microevolutionary forces generate macroevolutionary patterns is not well understood for coevolutionary systems.

Highly specific interactions between pairs of species can result in population level patterns. Both theoretical and empirical studies show that genetic specificity combined with specific gene flow patterns lead to parasites tracking of local host populations (Dybdahl and Storfer, 2003,Gandon et al., 1996,Gandon and Michalakis, 2002,Kaltz and Shykoff, 1998). In a mutualism between plant and pollinator, the seeming match between the length of a flower corolla and bill may be the result of strong selective pressure. Although we have many good examples of the processes that work at the population level, we have little evidence as to how those processes generate patterns of diversity among interacting species (Thompson, 2005). At the macroevolutionary scale, the processes leading to the observed patterns of host specificity have remained unclear.

The authors of a recent perspective piece in Evolution have addressed this exact issue by asking:

“Can microevolutionary adaptive processes acting at the within-species level explain macroevolutionary patterns across host and pathogen taxa?” (Antonovics et al., 2013)

What processes can explain why most pathogens cannot infect all encountered hosts ?

Schematic of host range (modified from Poulin (2007))

Schematic of host range (modified from Poulin (2007))

Understanding host specificity: The amount that a parasite specializes on different hosts is determined by how often it encounters potential hosts as well as its capacity to utilize and adapt to them (Combes, 1991). Poulin (2007) describes the range of hosts that a parasite or pathogen uses as the result of two different kinds of filters. Let us imagine all of the potential hosts for a particular pathogen as the large circle in the figure. The first filter represents the small set of hosts that a pathogen encounters (the inner blue circle). The second filter is those hosts that are compatible with the pathogen (the pie wedge). That is, those hosts that the pathogen can infect. The combination of these filters (the inner green edge) is the reduced host range and represents the host specificity of a pathogen.

What makes some hosts compatible and some resistant? Why are some pathogens able to infect only a few hosts? As Antonovics et al. (2013) say

“even though farmers are repeatedly exposed to spores of wheat rust pathogens, they do not get infected by them”

Host resistance: What are the mechanisms that determine host resistance? The authors contrast two types of host resistance to pathogens: evolved resistance and nonhost resistance. Evolved resistance occurs when hosts evolve specific or general resistance to regularly encountered pathogens. This evolved resistance can be the result of specific defenses and countermeasures (reciprocal adaptations) generated via coevolution with a virulent pathogen or a more general host resistance mechanism. However, the authors point out that these evolved responses will be geared only towards sympatric pathogens where the hosts have prolonged contact. In contrast, nonhost resistance occurs when pathogens cannot infect a particular novel host because the pathogen is specialized on its own source host. That is, nonhost resistance is not the result of evolution of resistance in the host, but evolved pathogen specialization to an alternative host.

These two different mechanisms of host resistance may explain the broader patterns of host specificity. In order to compare the relative importance of these two contrasting mechanisms, the authors synthesized the results of empirical data on infection experiments with host and pathogens across broad host genetic distances. Typically these results are from one of two kinds of study. Type I) Infection experiments where a pathogen (dark box) is taken from a single host source and then used to infect (dotted lines) hosts from a broad range of genetic distances to the source host (light boxes). Here, genetic distance from the target of infection to the source host for the pathogen increases from left to right.

Type I experiment: Single pathogen infecting multiple host targets

Type I experiment: Single pathogen infecting multiple host targets

Evolved resistance to this single pathogen is expected to decline as the distance from source host increases because these less related hosts are less likely to contain the evolved resistance. In the diagram to the right, the source host evolved resistance with the pathogens. Hosts from sympatric populations may contain similar resistance, but allopatric hosts are less likely to share this evolved resistance.

Type II) Infection experiments where pathogens are taken from multiple host sources (light boxes) from a broad range of genetic distances and then used to try and infect (dotted lines) the target host (dark gray box). Here, genetic distance of the pathogen sources increases from left to right.

Type II experiment: Multiple pathogens infecting single target host

Type II experiment: Multiple pathogens infecting single target host

Non-evolved host resistance increases as pathogens come from more distant hosts because those pathogens are specific to those hosts. The pathogen specificity to their source hosts prevents them from infecting novel hosts. In the above diagram to the right, pathogens that originate from hosts of different families (recall the wheat rust example above) may be unable to infect a unrelated target host. However, pathogens that have evolved with nearby allopatric populations may not be too specialized and may be infect novels hosts. That is, the hosts lack resistance to these nearby pathogens.

The evidence: The authors complied data from both of these kinds of experiments and provide there results in their Figure 3 (Antonovics et al., 2013). Interestingly, the compiled metadata were most consistent with nonhost resistance where host resistance increases with increased phylogenetic distance of the pathogen host source.

Prediction of non-evolved host resistance

Prediction of non-evolved host resistance

Antonovics et al. (2013) contrasted these two mechanisms of host resistance. The first, evolved resistance, is due to evolutionary changes occurring in the host in response to pathogens. The second, nonhost resistance, is the result of evolutionary changes occurring in the pathogen. The contrasting evolutionary origins of host defense provided a new testable framework for studying host specificity.

Are you looking to explore this topic more? The authors provide an invaluable table of testable hypotheses regarding their proposed mechanisms of host resistance. It is well worth checking out the full details of the paper.

Are you convinced by the evidence? Are the mechanisms of host resistance sufficient to generate the patterns of host specialization? Answering this question may provide evidence of one of the puzzles of coevolution by drawing a connection between processes at the population level and patterns at higher levels of organization. The testable hypotheses outlined in the paper provide mechanisms which can be applied broadly. Ultimately, understanding the landscape of host resistance may give us a better understanding of emerging human disease and cross-species transmission (Lloyd-Smith et al., 2009).


  • Antonovics J, Boots M, Ebert D, Koskella B, Poss M, et al. (2013) The Origin of Specificity by Means of Natural Selection: Evolved and Nonhost Resistance in Host–Pathogen Interactions. Evolution 67: 1-9. DOI: 10.1111/j.1558-5646.2012.01793.x
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One comment on “A unifying perspective on pathogen specificity

  1. […] Well, scaling evolutionary patterns of infections are interesting matters. Nothing in biology makes sense devoted some length to a recent paper I agree I need to read. And I’ll do, so I refer you to the post there. […]

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