The non-pathogenic Australian rabbit calicivirus RCV-A1 provides temporal and partial cross protection to lethal Rabbit Haemorrhagic Disease Virus infection which is not dependent on antibody titres

The endemic non-pathogenic Australian rabbit calicivirus RCV-A1 is known to provide some cross protection to lethal infection with the closely related Rabbit Haemorrhagic Disease Virus (RHDV). Despite its obvious negative impacts on viral biocontrol of introduced European rabbits in Australia, little is known about the extent and mechanisms of this cross protection. In this study 46 rabbits from a colony naturally infected with RCV-A1 were exposed to RHDV. Survival rates and survival times did not correlate with titres of serum antibodies specific to RCV-A1 or cross reacting to RHDV, but were instead influenced by the time between infection with the two viruses, demonstrating for the first time that the cross protection to lethal RHDV infection is transient. These findings are an important step towards a better understanding of the complex interactions of co-occurring pathogenic and non-pathogenic lagoviruses

Rabbit haemorrhagic disease: are Australian rabbits (Oryctolagus cuniculus) evolving resistance to infection with Czech CAPM 351 RHDV?

Rabbit haemorrhagic disease is a major tool for the management of introduced, wild rabbits in Australia. However, new evidence suggests that rabbits may be developing resistance to the disease. Rabbits sourced from wild populations in central and southeastern Australia, and domestic rabbits for comparison, were experimentally challenged with a low 60 ID50 oral dose of commercially available Czech CAPM 351 virus - the original strain released in Australia. Levels of resistance to infection were generally higher than for unselected domestic rabbits and also differed (0-73% infection rates) between wild populations. Resistance was lower in populations from cooler, wetter regions and also low in arid regions with the highest resistance seen within zones of moderate rainfall. These findings suggest the external influences of non-pathogenic calicivirus in cooler, wetter areas and poor recruitment in arid populations may influence the development rate of resistance in Australia

Increased virulence of rabbit haemorrhagic disease virus associated with genetic resistance in wild Australian rabbits (Oryctolagus cuniculus)

The release of myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV) in Australia with the aim of controlling overabundant rabbits has provided a unique opportunity to study the initial spread and establishment of emerging pathogens, as well as their co-evolution with their mammalian hosts. In contrast to MYXV, which attenuated shortly after its introduction, rapid attenuation of RHDV has not been observed. By studying the change in virulence of recent field isolates at a single field site we show, for the first time, that RHDV virulence has increased through time, likely because of selection to overcome developing genetic resistance in Australian wild rabbits. High virulence also appears to be favoured as rabbit carcasses, rather than diseased animals, are the likely source of mechanical insect transmission. These findings not only help elucidate the co-evolutionary interaction between rabbits and RHDV, but reveal some of the key factors shaping virulence evolution

Rabbit haemorrhagic disease: virus persistence and adaptation in Australia

In Australia, the rabbit haemorrhagic disease virus (RHDV) has been used since 1996 to reduce numbers of introduced European rabbits (Oryctolagus cuniculus) which have a devastating impact on the native Australian environment. RHDV causes regular, short disease outbreaks, but little is known about how the virus persists and survives between epidemics. We examined the initial spread of RHDV to show that even upon its initial spread, the virus circulated continuously on a regional scale rather than persisting at a local population level and that Australian rabbit populations are highly interconnected by virus-carrying flying vectors. Sequencing data obtained from a single rabbit population showed that the viruses that caused an epidemic each year seldom bore close genetic resemblance to those present in previous years. Together, these data suggest that RHDV survives in the Australian environment through its ability to spread amongst rabbit subpopulations. This is consistent with modelling results that indicated that in a large interconnected rabbit meta-population, RHDV should maintain high virulence, cause short, strong disease outbreaks but show low persistence in any given subpopulation. This new epidemiological framework is important for understanding virus–host co-evolution and future disease management options of pest species to secure Australia's remaining natural biodiversity

Emerging epidemiological patterns in rabbit haemorrhagic disease, its interaction with myxomatosis, and their effects on rabbit populations in South Australia

The impact of rabbit haemorrhagic disease (RHD) on wild rabbit populations was assessed by comparing population parameters measured before the introduction of RHD into Australia in 1995 with population parameters after RHD. We used data from an arid inland area and a moist coastal area in South Australia to examine the timing and extent of RHD outbreaks, their interaction with myxomatosis and their effect on breeding, recruitment and seasonal abundance of rabbits. From this we propose a generalised conceptual model of how RHD affects rabbit populations in southern Australia. RHD decreased long-term average numbers of rabbits by 85% in the arid area. In the coastal area, RHD decreased numbers of rabbits by 73% in the first year but numbers gradually recovered and were only 12% below pre-RHD numbers in the third year. Disease activity generally begins a month or two after the commencement of breeding in autumn or winter, peaks in early spring and ceases to be apparent in summer. Where the disease is most active, the pattern of population change is almost the inverse of the former pattern. During the breeding season, RHD severely suppresses rabbit numbers. Compensatory recruitment of late-born young, protected by maternal antibodies until the disease becomes inactive at the end of spring (also the end of breeding), allows the observed rabbit abundance to increase during summer, albeit to lower levels than before RHD. Maternal antibodies are lost during summer and the population becomes susceptible to RHD. The seasonal peak in myxomatosis activity is pushed back from late spring to early summer or autumn. Survivors of myxomatosis breed after opening rains in autumn but many succumb to RHD before raising their litters. The reduced abundance of rabbits and changed pattern of seasonal abundance have potential consequences for vegetation recovery.Gregory Mutze, Peter Bird, John Kovaliski, David Peacock, Scott Jennings and Brian Cook

Trip Covariates

Details of each trapping trip, including 'date'; whether the trip was classified as an outbreak of rabbit haemorrhagic disease virus ('RHDV') or myxoma virus ('MV'); intervals between trips ('Ints') = time between one trip and the next, expressed as a ratio of the mean interval between trips (58 days)—the last interval is the time between the last trapping trip and the last dead recovery; trapping effort ('SEffort'), the number of rabbits known to be alive ('KTBA'), estimated population size based on a POPAN model ('POPAN') and associated lower and upper confidence limits ('POPANlcl' and 'POPANucl'); and the number of days since the first trip. Data collected by Biosecurity, South Australia, Department of Primary Industries and Regions

Plotting output of multi-state, dead-recovery model

This script is for plotting the output from the multi-state model script. Run the models and save the output first. Notes- Immunity state / previous exposure categories: N - Immunity to neither virus M - Immunity to myxoma virus only R - Immunity to rabbit haemorrhagic disease virus (RHDV) only B - Immunity to both viruses Age groups: Kittens ≤ 600 g (may have residual maternal immunity to RHD) Adults > 600 g (unlikely to have residual maternal immunity