Figure 1.
Two ways in which host relatedness may effect a pathogen's ability to host shift.
The bars at the tips of the trees show a measure of pathogen infection success, with the bar in red representing the pathogen's natural host species. (A) The pathogen is less successful in host clades more distantly related to its natural host. (B) “Patches” of highly susceptible—or highly resistant—clades of hosts, may be scattered across the host phylogeny independently from their distance from the natural host. All of the species in the clade labelled “a” are equally distantly related from the pathogen's natural host. However, the species in the clade marked “b” are highly susceptible, despite being distantly related to the natural host.
Table 1.
Factors that evolutionary theory predicts will affect the likelihood that the correct set of mutations will arise to adapt a pathogen to a new host.
Figure 2.
Examples of parallel adaptations following host shifts.
(A) Parallel genetic changes in five replicate lines of Hibiscus chlorotic ring spot virus. The white boxes represent the viral genome, and the coloured blocks represent mutations. The virus naturally infects Hibiscus plants, but following five passages in an alternate host, (Chenopodium quinoa) the same eight mutations repeatedly occur [57]. (B) Parallel genetic changes in codon 30 of the gag gene (Met to Arg) following three independent transfers of SIVcpz into humans [59]. When a chimp was subsequently infected with HIV-1, the residue reverted back to Met. The coloured blocks represent either a Met (yellow) or Arg (blue) at codon position 30 in the HIV gag gene. (C) Parallel changes in protein function following independent transfers of SIVs from chimpanzees (HIV-1) and sooty mangabeys (HIV-2) into humans. SIV Nef protein does not antagonise tetherin in humans, and so other HIV proteins have evolved the ability to antagonise tetherin [64]. The exception to this is HIV-1 group O viruses, which do not appear to have evolved anti-tetherin activity. In HIV-1 group N viruses the evolution of anti-tetherin activity in Vpu may have come at a cost, as Vpu no longer degrades CD4 receptors to aid the release of viral particles [61]. The coloured gene names in the schematic represent the gene that provides the anti-tetherin function in that host and viral lineage.
Figure 3.
Examples of how patterns of host shifts can affect the distribution of pathogens across the host phylogeny.
Each column shows the presence of a different pathogen, with a coloured circle representing the presence of that pathogen. In panel A, pathogens preferentially shift between closely related hosts, while in B closely related host species have similar levels of susceptibility to infection, regardless of the source of the pathogen (with two increases in host resistance occurring at the asterisks on the host phylogeny). Both processes result in closely related host species harbouring similar pathogens, and in some host clades harbouring more pathogen species. However, in A, but not B, host species with more close relatives tend to have more pathogens. For example, the phylogenetically isolated species at the bottom of the tree is not infected by any of the three pathogens in A, but is in B.