Beyond the Red Queen: are elevated parasite evolutionary rates driven by host shifts?

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Evolution is change over time. Most people know of evolution in terms of responses to man-made influences - bacteria evolve resistance to antibiotics; industrial pollution led to the evolution of dark forms of the peppered moth. However, in natural systems, evolution is most rapid in genes that contribute to parasite infectivity and to the ability of the organisms they infect to stop parasites from propagating. Forty years ago, Leigh Van Valen produced a theory as to why genes involved in parasite infectivity and host resistance should evolve more quickly than others. This theory noticed that evolution would be rapid where there was 'mutual antagonism'. Hosts evolve to resist infection by parasites, so parasites must adapt to circumvent this resistance (or die). Reciprocally, as the parasites adapt to better infect their hosts, so the hosts must adapt (or die). This creates a continual cycle termed antagonistic coevolution, where parasite virulence and host defence genes continually adapt, and counter adapt, in an arms race. This continuous 'catch up' between hosts and parasites parallels a scene from Lewis Carrol's famous book, Through the Looking Glass, in which Alice (a.k.a. Alice in Wonderland) runs rapidly with the evil Red Queen, yet gets nowhere. Red Queen interactions are widely accepted as 'the' reason why genes involved in host defence and parasite virulence evolve quickly. However, it is possible that it is only a partial explanaiton. This proposal seeks to test an alternative explanation for fast evolution of parasite genes rarely examined to date: parasite virulence genes evolve rapidly because parasites occasionally switch host species. Host switching occurs quite commonly in parasites. We have all heard about it- HIV moved from primates into humans about 70 years ago, and Swine Flu and Avian flu have raised our awareness of new influenza shifting from pigs and birds into humans. It is likely that host switching by a parasite represents a very strong selective force. Following a host switch, the entire environment of the parasite is different, and a parasite in its new host is likely to perform poorly. Thus, there is great scope for adaptation of the parasite to its new host, and it must rapidly evolve to better exploit the host. It is clear that parasites do 'switch' hosts quite commonly, and very likely this is accompanied by a bout of strong natural selection that may explain why parasite 'virulence' genes evolve rapidly. In this project, we will test the theory that host shifts drive fast parasite evolution. In the laboratory, we will produce host shift events for a bacterium, moving the bacterium from its native host into a new 'foreign' one. We will leave this bacterium in its new host species for a year, and then recover it. We will investigate whether the host shift has resulted in the bacterium evolving more quickly in terms of gene sequence, and whether it has evolved in terms of its ability to prosper in its new host. We will also examine the diversity of the bacterium across host species which it has colonised through host switching in nature. By comparing the differences seen between bacterial strains in the wild to those following laboratory host shifts, we can ask if natural diversity is likely driven by the host shift events it has encountered in the past