Host and vector adaptation in the tick-borne human pathogens Borrelia

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To be able to survive, parasitic vector-borne bacteria have developed a range of sophisticated means to adapt to their hosts and vectors. Their distribution is constrained by that of reservoir hosts and competent vectors. Ecological conditions, such as the availability of hosts, but also random processes such as genetic drift, can lead the bacteria to switch from one host type to another or to adapt to a new vector. Knowing which genes are involved in this adaptation can help to control those pathogens and identify novel disease prevention strategies. Here we plan to use population genomics methods to identify genetic factors involved in host and vector adaptation in two bacteria species responsible for Lyme disease: Borrelia garinii and B. bavariensis. Both species are present in Europe and Asia and both are human pathogens. They differ by the type of animal used as reservoir-host and B. bavariensis is composed of at least two separated populations using different tick vector species. In our study we will reconstruct the evolutionary history of these two species using strains from Eastern Asia, Western Europe and Russia. We will then study the evolution of genes that are candidates for playing a role in host and/or vector adaptation (encoding the so-called CRASP proteins for Complement Regulator-Acquiring Surface Proteins) and test whether these genes are under selective pressure. Next, we will identify novel genes under selection that might be responsible for host or vector adaptation in the two species under study. Finally, we will look for functional validation of the role played by those genes in infection and survival in the host or the vector. Our study will allow to unravel the genetic basis of host and vector adaptation in the two species under study and also to understand how host and vector switches can occur in Borrelia. This is of epidemiological importance as it will help to predict the spread of the different Borrelia species depending on the populations of hosts and vectors that might vary due to climate change. Our study will also ultimately contribute to the understanding of why certain Borrelia species are human pathogenic and how the genetic mechanisms involved in human immune system evasion evolved.