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A rabbit once kept by Charles Darwin is helping scientists to understand how the mammals became resistant to myxomatosis, a deadly disease widely used as a biological control during the 1950s.
Myxomatosis caused widespread death among European rabbit (Oryctolagus cuniculus) populations in Australia, France and the UK. But some of the animals soon developed immunity to the virus.
Researchers from the University of Cambridge and the CIBIO (Research Centre in Biodiversity and Genetic Resources) in Porto, Portugal, wanted to see if they could find any genetic under pinning to the resistance. They looked at the DNA of rabbits from both before and after the release of the disease, including one owned by Darwin and still held at the Museum.
Dr Joel Alves, now a postdoctoral researcher at the University of Oxford and lead author of the study, says, 'We compared rabbits collected before the virus outbreak in the 1950s with modern populations that evolved resistance, and found that the same genes had changed in all three countries.
'Many of these genes play a key role in the rabbit immune system.'
The results have been published in a paper in Science.
Myxomatosis is caused by the myxoma virus. Although it is thought to have originated in Europe, it was first identified to be infecting laboratory rabbits in Uruguay in 1896.
The disease is spread either by direct contact with infected animals or after being bitten by a flea or mosquito that has recently fed on an infected rabbit. It was found to be widespread but sublethal in American rabbit species.
It was not until the mid-twentieth century that scientists considered using the virus as a biological control for the more susceptible European rabbits that had run rampant throughout Australia.
Rabbits were first introduced to Australia in October 1859 when the English settler Thomas Austin released 24 breeding animals onto his estate near Melbourne. He had introduced them so that gentlemen would have something to shoot for sport and was initially praised for his forward thinking.
But the animals spread rapidly and bred in such numbers that within a decade millions of rabbits were being trapped every year, with seemingly little impact on their numbers. By as early as 1887 the government was looking for ways to control numbers and limit damage done to grasslands and pastures.
In 1950, it was decided that the myxoma virus would be released to control the rabbit plague after experiments showed a 99.8% fatality rate for infected individuals. In under three months the disease spread thousands of kilometres, killing hundreds of millions of rabbits in its wake.
The disease was illegally introduced into France when in 1952 Dr Paul-Félix Armand-Delille used it on his private estate to eradicate the rabbits. Within two years myxomatosis had wiped out 90% of France's rabbit population.
From the mainland, the disease made it to the UK by 1953, where once again it was used as a biocontrol agent, and is thought to have killed off 99% of the UK's rabbits.
The problems came with the few rabbits that survived the onslaught, as their resistance soon spread to the rest of the population. Numbers began to climb once more.
The fact that three fairly isolated populations of rabbits all developed the ability to withstand the disease within such a short period of time offers an interesting window into how such immunity evolves.
The team of researchers analysed the remains of close to 200 rabbits from Australia, France, the UK and the USA held in the collections of universities and museums dating from between 1865 and 2013. These even included one owned by Charles Darwin, housed at the Natural History Museum.
'It wasn't easy to get samples from so many long-dead rabbits,' says Joel. 'Not all natural history museums keep rabbits, because they are not very exotic compared to other species.'
By taking DNA samples from these specimens and sequencing nearly 20,000 genes, the team were able to track exactly which changes had occurred within the separate rabbit populations before and after the release of the virus.
They found an impressive parallel evolution between the three populations. Rather than there being a single genetic shift that gave the rabbits resistance, each population made lots of little ones.
'Often evolution works through big changes in single genes,' explains Joel, 'but our findings show that resistance to myxomatosis likely evolved through lots of small effects spread across the genome.'
Crucially, these all occurred in the same genes relating to immunity.
This suggests that the underlying ancestral variation in the genetics of the European rabbit was still there in the populations introduced both to the UK in the thirteenth century and Australia in the nineteenth century. This allowed all three populations to rapidly evolve the same resistance.