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Strains of myxoma virus associated with a case-mortality rate in wild rabbits of 90—95% can be distinguished from those associated with a case-mortality rate of more than 99% by the use of a standardized virulence test carried out in groups of five laboratory rabbits, and tests carried out on laboratory rabbits are closely correlated with the results obtained with Australian wild rabbits. The test, which attempts to mimic natural mosquito transmission, consists of the intradermal inoculation in one site of about 5 rabbit-infectious doses of the virus, and the subsequent observation of the rate of progress of clinical symptoms and ultimate fate of the rabbit. The mean survival time provides a figure which allows satisfactory classification of all known myxoma virus strains into one of four grades of virulence, very attenuated strains being recognized by their low case-mortality rates.Using this test, 92 strains of myxoma virus have been compared. These comprised 6 laboratory strains, 62 strains recovered from Australian wild rabbits or from wild caught mosquitoes, between February, 1951 and March, 1955, 19 strains recovered from naturally infected rabbits in Europe between October, 1953 and August, 1955, 3 strains from South America, and 2 from California. Eight types have been described and illustrated, differentiation being based on their virulence and the clinical picture of the disease they cause in laboratory rabbits. The differences are summarized in Text-fig. 2. Four of the virus types produce recognizably different pocks on the chorioallantois of developing chick embryos.In Australia the repeatedly introduced standard laboratory strain of virus has been replaced by a moderately virulent strain, which appears to be better adapted for survival than either the highly virulent standard laboratory strain, or less virulent variants of which only a few had been recovered up to 1955. Strains of the type dominant in 1953–55 have appeared independently in many widely separated parts of Australia. Examination of these attenuated variants by pure clone techniques showed that the variability in symptomatology associated with them is not due to a mixture of virus strains, but to the expression of differences in innate resistance of the host animals which are obscured by the overwhelming virulence of the highly virulent strains.Only one introduction of a different strain of virus was made in Europe. All field strains recovered during the first two years after the introduction were of high virulence, but a few attenuated strains appeared in 1955, and they have since become widespread. One of them appears to be a relatively stable mixture of a highly virulent and a greatly attenuated strain.The collection of the large numbers of strains of virus described in this paper has been made possible only by the generous collaboration of many people. In Australia we would like to acknowledge the great help afforded us by Mr F. N. Ratcliffe, officer-in-charge of the Wildlife Survey Section, Commonwealth Scientific and Industrial Research Organization and his officers, especially Messrs J. H. Calaby, G. Douglas, A. L. Dyce, B. V. Fennessy, E. W. Lines, K. Myers, R. Mykytowycz, W. E. Poole and E. Waterhouse. Messrs B. D. Robinson and T. Pearce of the Lands Department of Victoria have also provided us with specimens, as have Mr G. Edgar, Director of the Veterinary Research Station, Glenfield, New South Wales, Dr D. Surrey Dane of the Institute of Medical and Veterinary Science, Adelaide, Mr D. Gooding, Department of Agriculture, Western Australia, and Messrs T. B. Alexander and A. F. Ryan, Department of Agriculture, Tasmania.We are indebted to Dr H. de B. Aragão of the Instituto Oswaldo Cruz, Rio de Janeiro, and Dr B. Szyfres, of the Laboratorio de Biologia Animal, Uruguay, for specimens from South America; Dr D. G. McKercher of the University of California School of Veterinary Medicine, Davis, California, for the Californian strains; Drs P. Lépine and H. Jacotot, of the Institut Pasteur, Paris, for strains from France; and Mr J. R. Hudson, of the Veterinary Laboratory, Weybridge, and Dr C. H. Andrewes of the National Institute for Medical Research, Mill Hill, for material from England.We are grateful to Dr S. Fazekas de St Groth and Dr G. S. Watson of this University for advice on the statistical treatment of the data.Mr V. Paral took the photographs.

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.

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When examined under similar conditions in the laboratory, the two strains of myxoma virus used to initiate the Australian and European epizootics, and three somewhat attenuated strains recovered in the field in Australia and France, were found to produce lesions containing approximately the same amount of virus, and were transmitted by mosquitoes with approximately equal efficiency. The laboratory variant neuromyxoma multiplied poorly in the skin and was very rarely transmitted by mosquitoes.The survival potential of different virus strains in the field is correlated with the length of time during which rabbits infected with different strains present to biting mosquitoes lesions containing high concentrations of virus. Sickness of the infected rabbit, and extensive viruliferous skin lesions, will increase its suitability as a source of virus for mosquitoes. These considerations explain the dominance of slightly attenuated strains of myxoma virus in the field in Australia.Species of mosquitoes, when tested under standard conditions in the laboratory, differ in their efficiency as vectors of myxomatosis. These differences may be related to differences in the method of feeding, and to structural differences in the mouthparts.Engorgement on an immune rabbit after probing through myxomatous skin lesions had no greater effect on the subsequent ability of mosquitoes to transmit myxomatosis than a similar blood feed on a normal rabbit.Nine serial mosquito-bite passages of the standard laboratory strain of virus, each involving one week in the rabbit and two weeks in the mosquito, had no effect on its pathogenic behaviour.

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Annually for 4 years groups of young Australian wild rabbits have been captured during non-epizootic periods from areas in which myxomatosis has occurred during the previous summer. The intensity of the preceding epizootic was measured by testing a sample of survivors for antibody. The captured young rabbits were raised in the laboratory until they were about 4 months old and then inoculated intradermally with small doses of the slightly attenuated myxoma virus strain Aust/Corowa/12–52/2 (KM 13), all samples of virus being derived from the same batch which has been stored at -70°C.The results show there is a significant negative correlation between the mortality rate and the degree of exposure to myxomatosis of the forbears of the tested animals. Passive and active immunization have been excluded and this result is ascribed to increased genetic resistance.We are greatly indebted to Mr. F. N. Ratcliffe, Officer in Charge of the Wildlife Survey Section of the Commonwealth Scientific and Industrial Organization, and to his officers, especially Messrs W. E. Poole, K. E. Myers, G. Douglas, B. V. Fennessy, H. Frith and K. Keith for their invaluable assistance in collecting rabbits and serum samples.We have had valuable discussions with Dr W. R. Sobey, Dr P. J. Claringbold and Dr G. S. Watson on genetical and statistical aspects of the problems under study.