Andrew Masterson
Andrew Masterson is a former editor of Cosmos.
In what can be described as a classic evolutionary arms race, in 1950 Australian authorities released a South American virus called myxoma to combat the burgeoning population of feral rabbits at the stage ravaging much of the country.
For decades, the strategy was extremely successful, causing rabbits to die from a combination of fever and skin lesions. So effective was the virus – affectionately nicknamed “myxo” by the locals – that the wild rabbit population dropped from 600 million to 100 million.
However, within surviving population was a small, but increasing, cohort of rabbits with a genetic resistance to myxoma. Exactly as evolutionary theory predicts, the bunnies immune to the virus were better adapted to survival and thus more effective in passing on their genes.
As a result, by 1990, Australia’s feral rabbit population was rebounding, with numbers up to an estimated 300 million. Scientists quickly started scouting for an alternative form of biological control – which they found in the form of another pathogen, calicivirus.
Research published in the journal Proceedings of the National Academy of Sciences, however, indicates that the rabbits’ triumph over myxo was by no means the end of the story. By the time scientists were trialling calcivirus, the myxoma virus was ready to stage a comeback.
A team led by Peter Kerr of the University of Sydney, Australia, decided to study myxoma samples collected in the 1990s. At the time, interest in the evolutionary development of the virus was pretty much non-existent: the rabbit population was surging and myxo’s reign as a biological control agent was over.
Revisiting them, Kerr and colleagues decided to test the virulence of the samples, and compare the results with those obtained by using archived samples collected in the 1950s.
The results were surprising. As rabbits had evolved immunity to the virus’ inflammatory effects, so the virus itself changed to trigger a new – and newly lethal – range of symptoms.
Introduced to lab rabbits that came from a lineage with no exposure to myxoma, the virus induced massive immune system suppression, which ushered in overwhelming bacterial infection and a development known as acute collapse syndrome, which is similar to sepsis.
“The rabbits infected with virus from the 1990s did not have a typical inflammatory response to the infection or develop fevers,” says co-author Isabella Cattadori, of Penn State University in Pennsylvania, US.
“This is further evidence that the virus is severely suppressing the immune response in these rabbits. The evolutionary arms race has produced a virus that instead of trying to evade the host’s immune response, directly attacks it.”
The scientists note that the 1950s strain of myxoma was also capable of suppressing the immune system, but to a much milder extent. The more efficient effect found in the later samples had to have evolved at some point after the 1980s.
While nowhere the scourge it once was, the myxoma virus still kills a lot of rabbits every year in Australia, although many of the fatalities are family pets. In Europe, domestic rabbits are routinely vaccinated against it.
Myxoma’s replacement as a biological control, calcivirus, has only been partly successful in containing the feral rabbit population.
In the early 2000s it was observed that many rabbit populations resident in lowland areas were immune to the pathogen. Researchers discovered that the bunnies had already been infected by a closely related but benign form of the virus, effectively inoculating them.
