ABSTRACT
Myxoma virus (MYXV) causes the lethal disease myxomatosis in European rabbits. The spread of MYXV in the Australian rabbit population in the summer of 1950/1951 was the first successful large-scale biological control of this species. Subsequent natural selection favored moderately attenuated viruses, which by allowing infected rabbits to survive for longer, had a greater chance of transmission. This meant more rabbits survived infection. The emergence of genetic resistance in the rabbit population further reduced the impact of myxomatosis and allowed some recovery of the rabbit population, particularly in the rangelands. Release of the European rabbit flea and later the Spanish rabbit flea as additional vectors for the virus helped to constrain rabbit population growth. In 1995, rabbit hemorrhagic disease virus (RHDV) spread into the Australian rabbit population as a second highly lethal biological control agent. In contrast to MYXV, there is little evidence of attenuation of RHDV, probably because rapid death of the animal with high titres of virus in the carcass is an effective transmission strategy. The evolution of RHDV is complex. A novel serotype of virus (RHDV2) emerged in Europe around 2010 and was detected in Australia in 2015. RHDV2 has become the dominant virus in Australia. Low virulence rabbit caliciviruses (RCVs) complicate the epizootiology of these viruses and recombine with them to form novel genotypes. There is evidence for emerging genetic resistance to RHDV in rabbit populations. This may be partially overcome by viruses able to use different cell-attachment factors. RHDV has also been released in New Zealand as a biological control.
