Lagoviruses belong to the Caliciviridae family. They were first recognized as highly pathogenic viruses of the European rabbit (Oryctolagus cuniculus) and European brown hare (Lepus europaeus) that emerged in the 1970-1980s, namely, rabbit haemorrhagic disease virus (RHDV) and European brown hare syndrome virus (EBHSV), according to the host species from which they had been first detected. However, the diversity of lagoviruses has recently expanded to include new related viruses with varying pathogenicity, geographic distribution and host ranges. Together with the frequent recombination observed amongst circulating viruses, there is a clear need to establish precise guidelines for classifying and naming lagovirus strains. Therefore, here we propose a new nomenclature based on phylogenetic relationships. In this new nomenclature, a single species of lagovirus would be recognized and called Lagovirus europaeus. The species would be divided into two genogroups that correspond to RHDV- and EBHSV-related viruses, respectively. Genogroups could be subdivided into genotypes, which could themselves be subdivided into phylogenetically well-supported variants. Based on available sequences, pairwise distance cutoffs have been defined, but with the accumulation of new sequences these cutoffs may need to be revised. We propose that an international working group could coordinate the nomenclature of lagoviruses and any proposals for revision.

ELISA techniques developed for the veterinary diagnosis of Rabbit Haemorrhagic Disease (RHD) in domestic rabbits were used for studying the epidemiology of RHD in Australian wild rabbits. The combination of ELISA techniques that distinguished IgA, IgG and IgM antibody responses and a longitudinal data set, mainly based on capture-mark-recapture of rabbits, provided a reliable basis for interpreting serology and set the criteria used to classify rabbits' immunological status. Importantly, young with maternal antibodies, immune rabbits and rabbits apparently re-exposed to RHD were readily separated. Three outbreaks of RHD occurred in 1996-7. The timing of RHD outbreaks was mainly driven by recruitment of young rabbits that generally contracted RHD after they lost their maternally derived immunity. Young that lost maternal antibodies in summer were not immediately infected, apparently because transmission of RHDV slows at that time, but contracted RHD in the autumn when conditions were again suitable for disease spread.

This review considers the history of the discovery of the rabbit haemorrhagic disease virus (RHDV) and its spread throughout the world in domestic and wild rabbits, which led eventually to its deliberate release into Australia and New Zealand for the control of a major pest, the introduced wild rabbit. The physical and genetic structure of RHDV is now well understood, and its pathogenic effects are also well known. The epidemiology of rabbit haemorrhagic disease (RHD) has been clearly documented in the field in European countries, Australia and New Zealand. Since its initial spread through largely naïve populations of wild rabbits it has established a pattern of mainly annual epizootics in most areas. The timing of epizootics is dependent on climatic variables that determine when rabbits reproduce and the appearance of new, susceptible rabbits in the population. The activity of RHDV is also influenced by climatic extremes that presumably affect its persistence and the behaviour of insect vectors, and evidence is growing that pre-existing RHDV-like viruses in some parts of Australia may interact with RHDV, reducing its effectiveness. The timing of epizootics is further modified by the resistance to RHD shown by young rabbits below 5 weeks of age and the presence of protective maternal antibodies that also protect against fatal RHD. RHD has reduced rabbit abundance, particularly in dry regions, but rabbits in cooler, high-rainfall areas have been able to maintain their populations. In Australia and New Zealand, RHD has raised the prospects for managing rabbits in low rainfall areas and brought substantial economic and environmental benefits.

The calicivirus agent for rabbit hemorrhagic disease (RHD) escaped from an island quarantine station to the Australian mainland in October 1995. Within 2 wk it was detected at an established field study site where wild European rabbits (Oryctolagus cuniculus) were being monitored in the Flinders Ranges National Park (South Australia, Australia). During November 1995, RHD reduced the rabbit numbers on the site by 95%. Approximately 3% of the population survived challenge by RHD and developed antibodies. Most of the antibody-positive survivors were 3- to 7-wk-old when challenged. Many rabbits died underground, but counts of rabbit carcasses found on the surface indicated that approximately 1 million rabbits had died above ground in the National Park, and that > 30 million rabbits may have died in adjacent areas during the November epidemic.

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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.

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.