In 1859 the English settler Thomas Austin shipped 13 rabbits from his family’s farm in Somerset to Australia, releasing them on his estate for hunting. Populations exploded in size and spread across the continent with devastating consequences for Australian agriculture and ecology. The solution came in the form of the myxoma virus. This virus causes benign infections in its natural host, cottontail rabbits, but on transfer to European rabbits causes the lethal disease myxomatosis. It was released in the 1950s in Australia, Britain and France, causing the collapse of populations. This resulted in a unique replicated natural experiment, that has become a textbook example of evolution following disease emergence. By sequencing the exomes of rabbits from museum specimens before the pandemic and modern populations, we found that natural selection had acted on standing genetic variation in immunity genes across the genomes, with the parallel evolution if resistance having a common genetic basis. We have recently shown that one of the most strongly selected loci encodes classical MHC-I molecules that present viral peptides to T cells. Across the three populations, the same allele has risen in frequency. The high levels of standing genetic variation maintained in MHC genes has therefore likely allowed populations to rapidly adapt to a novel pathogen. The MHC alleles differ in properties such as surface expression and the extent to which they are down-regulated by the virus, and we are currently investigating whether these traits are the targets of natural selection.​