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.

Summary Pools of mosquitoes collected in the Murray Valley in February, 1974, during an encephalitis epidemic yielded 239 isolates of 11 distinct viruses. These included 39 isolates of MVE virus, an incriminated causative agent of encephalitis in man, and 111 isolates of kunjin virus, a probable causative agent. An additional isolate of MVE virus was recovered from the serum of a white‐faced heron, Ardea novaehollandiae. The other 9 viruses comprised the Alpha‐viruses Ross River and Sindbis, the Flavivirus, Edge Hill, the Bunyaviruses, koongol and Wongal, the underfined Kowanyama virus, and 3 previously undescribed viruses. One isolate of MVE virus was recovered from a total of 180 Culex australicus, and all other isolates of all viruses were from Culex annulirostris. The combined apparent infection rate of MVE and Kunjin viruses in Cx annulirostris was 1/913. The concurrent activity of so many seemingly transient arboviruses, their wide geographical distribution and temporal considerations all weaken the widely held hypothesis that during the pre‐epidemic period MVE virus is introduced into the Murray Valley by viraemic waterbirds from distant areas of tropical enzooticity.

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Proof of the existence of multiplication of myxoma virus in mosquitoes has been sought by a variety of experiments with Aedes aegypti and Anopheles annulipes. All were completely negative. All features of transmission are compatible with a purely mechanical and none is compatible with a ‘biological’ mechanism.In mechanical transmission important features of the infected animal host are the number and accessibility of viruliferous skin lesions, and the location and concentration of virus in these lesions.By inducing mosquitoes to probe through infectious skin lesions and subsequently permitting them to make many successive probes on marked skin sites on the backs of susceptible rabbits, it has been possible to obtain quantitative information on the median minimum virus load of probing mosquitoes, and the rates of loss due to probing and the passage of time.A preparation of myxoma virus suspended in normal rabbit serum had a half-lifetime of 11 days at 4° C., 5 days at 18–20° C., and 31 hr. at 27–28° C. Apart from losses due to probing (about 12% of the virus load per probe) viable virus on the proboscis of the mosquito probably disappears at about the same rates.

1. Australian wild rabbits which had recovered from myxomatosis acquired in the field contained in their serum antibodies which could be detected by complement-fixation or neutralization tests for a long period (more than 18 months) after their recovery. The titre of complement-fixing antibody fell fairly rapidly during the first few months, and remained at a steady level thereafter. No change could be detected in the titre of neutralizing antibodies throughout the observation period.2. Inoculation of such rabbits with myxoma virus was sometimes followed by the development of a local lesion at the inoculation site, and in these rabbits the titre of complement-fixing antibody rose, but there was no alteration in the neutralizing power of the serum. In other animals no lesion developed and there was no change in the antibody titre.3. Serum was collected from a total of 824 wild rabbits from seventeen localities in eastern Australia with varying histories of myxomatosis since December 1950. Examination of 135 of these sera by both neutralization and complement-fixation tests showed that the results obtained by the two methods were in close agreement.4. In many areas in which the disease was absent in the summer of 1950–1 and produced a violent epizootic in 1951–2, the majority (70–90 %) of the sera collected from rabbits 2–5 months after the height of the epizootic contained antibody to myxoma virus, i.e. the majority of the survivors had recovered from the disease.5. Counts of the rabbit population before and after a violent epizootic in the summer of 1951–2, and the proportion of immune animals amongst the survivors in these areas showed that the case-mortality rate was between 99·4 and 99·8%.6. Consideration of the results obtained in the serological surveys showed that the case-mortality rate was probably of this order (about 99·5%) in all areas in which there had been no disease or a negligible outbreak in 1950–1, whether they had a grade I or grade II kill in 1951–2.7. In certain other areas, in which a grade I outbreak in 1950–1 was followed by a grade II or poorer kill in 1951–2, the observed immune rate was considerably higher than would be expected if the case-mortality rate (assuming that the whole rabbit population was susceptible) was 99·5%. The possible causes of this are discussed. Survival of immune survivors from the first epizootic through the second may be a factor of some importance, but it is probably not the only factor involved.8. The areas just mentioned were exceptional. In most places there was either no build-up of population after the 1950–1 epizootic, or a second effective epizootic destroyed the majority of rabbits in the small population which had developed by reproduction of the survivors of the first outbreak.

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Summary Virulence tests were carried out on 300 strains of myxoma virus obtained from the rabbit‐infested parts of Australia during the year 1963‐1964. The general distribution of strains among virulence grades did not differ greatly from that found in the previous Australian survey in 1958‐1959. No highly virulent strains were recovered, and judging from the samples tested, the distribution of strains of various degrees of virulence was not influenced by recent inoculation campaigns. All strains were tested for the soluble antigens they produced in skin lesions in rabbits. One strain from Victoria and one from New South Wales failed to produce a soluble antigen which was a major component of the standard laboratory strain, and of all the other field strains tested.