Rabbit myxoma virus, a member of the genus Leporipoxvirus, has been widely used in Australia to control populations of the European rabbit, which was introduced with disastrous results into Australia by European settlers. The history of the virus in Australia represents a fascinating story of viral evolution in the field and is one of the best studied examples of co-evolution of both a virus and its host. The story has important implications for our understanding of virus–host interactions.
Rabbit myxoma virus is native to the Americas, where it causes a localized skin fibroma in American rabbits. The virus is mechanically transmitted by mosquitoes. It does not replicate in the mosquito (it is not an arbovirus), but the mosquito can transmit the virus when mouthparts become contaminated by feeding on an infected rabbit with skin lesions. It was discovered early that, although the virus causes a trivial illness in American rabbits, it causes a systemic infection in European rabbits that is fatal more than 99% of the time, a disease called myxomatosis.
In Australia, a land of marsupials, the European rabbit was introduced for hunting or as potential food for foxes, which in turn had been introduced for the pleasures of fox hunting. The rabbits multiplied as rabbits proverbially do and became a plague. The enormous populations of these introduced rabbits depleted agricultural crops and also threatened to overwhelm a number of Australian marsupials by competing with them for the food supply. A significant percentage of Australian native mammals have gone extinct and rabbits have played an important role in the extinction of a number of them.
Rabbits have also caused problems from erosion by depleting large areas of ground cover. Campaigns in which people went out in large groups and killed as many rabbits as possible were undertaken in order to reduce the rabbit population, but it was a losing game. To make matters worse, the introduced foxes preferred the Australian fauna to the introduced rabbits anyway, and constituted a second plague on the native fauna, which have not evolved to deal with mammalian predators.
In an effort to eliminate or control the rabbit population, rabbit myxoma virus was introduced. At first this strategy was very successful and the rabbit population was reduced by an estimated 95%. It was believed that the virus would have to be broadcast every year in order to continue the campaign against the rabbits, but there was hope that the rabbit plague would end. However, soon after its release, new strains of virus arose that were less virulent. These strains prevailed because they persisted more successfully in the rabbit population—less virulent viruses remained within a host longer and were transmitted to new rabbits more successfully than virus that rapidly killed its host.
Furthermore, rabbits that survived infection with the less virulent strains were now immune to the virulent virus, making it more difficult to control the rabbits by reintroduction of a virulent strain (although rabbits have a short life span and herd immunity is not very important in resistance to disease). With time the virus became progressively less virulent but, interestingly, strains of very low virulence never became dominant components of the virus population. Very low virulence strains did arise, but did not persist, presumably because they were transmitted less efficiently than were strains of moderate virulence.
After a few years, the dominant strains were grades 3 and 4, which kill 50–95% of nonimmune, wild-type (i.e., not selected for resistance to myxomatosis) European rabbits. At the same time that less virulent virus strains were being selected, rabbits that were more resistant to myxomatosis were also being selected. The enormously high death rate caused by viral infection coupled with the short generation time of rabbits rapidly led to the selection of rabbits that exhibited increased resistance to the disease caused by the virus. Perhaps this is the reason that strains of low virulence first arose and then faded from the virus population. Notice that after seven epidemics of myxomatosis, virus strains of grade 3, the dominant strain in the virus population, now caused severe disease in less than 60% of selected rabbits, compared with 95% of unselected (wild type) rabbits.
With continuing passage of time, the virus and rabbit populations evolved such that rabbit myxoma virus was approximately as serious for the rabbit population as smallpox was for man, that is, about 40% mortality following viral infection. Nevertheless, the rabbit population, about 600 million before myxoma virus was introduced, has never completely recovered and is about half that today. Efforts are being made to select more virulent strains of virus that would kill a larger percentage of the rabbits. Rabbit calicivirus is also being used for control of rabbits.
The history of myxomatosis in Australia makes clear that a situation in which a virus rapidly kills the vast majority of its hosts is inherently unstable. There is selective pressure on the virus to attenuate its virulence and on the host to become resistant to the virus. Because both rabbits and rabbit myxoma virus multiply rapidly, the accommodation of the virus and host occurred rapidly.
Extracted from: James Strauss and Ellen Strauss (2008), Viruses and Human Diseases. ISBN: 978-0-12-373741-0