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SUMMARYComparative antigenic and nucleic acid analyses were carried out on two new atypical rotavirus isolates coming respectively from chickens (D/132) and pigs (E/DC-9). Indirect immunofluorescence showed that each virus carried different group antigens which were also distinct from those of previously described rotavirus groups. By genome profile analysis each virus had a pattern of genomic RNAs clearly distinct from those of the other rotavirus groups. Comparative terminal fingerprinting of corresponding genome segments from the two viruses showed large differences between them, indicating that all of their genomic RNAs had significant differences in sequence both from each other and from the three previously defined rotavirus groups. On the basis of these results, extension of the number of rotavirus groups from three to five is proposed, with isolates D/132 and E/DC-9 being the type members of groups D and E respectively.

Primary chick kidney cells were infected with avian infectious bronchitis virus (IBV) and examined by electron microscopy. Virus particles entered the cells by viropexis and distinction could be made between engulfment by cell processes (phagocytosis) and entry by micropinocytosis in coated transport vesicles. Virus maturation occurred by budding into either the cisternae of the endoplasmic reticulum or cytoplasmic vacuoles, and evidence was obtained to suggest that the viral surface projections could be attached during the budding process. Late in infection large numbers of virus particles were present, mainly in cytoplasmic vacuoles, and the majority were released by cell lysis. Release by fusion of vacuoles with the plasma membrane was also observed, and individual virions could be transported from the endoplasmic reticulum to the surface within coated vesicles.

The virus recovered from cases of European brown hare syndrome in the U.K. contains one major capsid protein of approximately 60 k molecular weight and morphologically resembles known caliciviruses. It has been compared with a European isolate of rabbit haemorrhagic disease calicivirus and, although it shows some antigenic similarity, it is not identical. In transmission and protection studies the virus from U.K. hares failed to produce disease in rabbits and did not effectively protect against subsequent challenge with the rabbit calicivirus.

Haemagglutination and ELISA tests, and negative contrast electron microscopy, have been used to identify rabbit haemorrhagic disease virus in naturally occurring cases of the disease and in experimentally infected rabbits in the United Kingdom. Haemagglutination tests alone are not satisfactory for the diagnosis because non-haemagglutinating isolates of the virus, otherwise indistinguishable from others, have been found in some outbreaks. Haemagglutination inhibition tests have shown that a proportion of both commercial laboratory and wild rabbits in the UK are seropositive to the virus although they have not been associated with clinical disease. This observation, made previously in other parts of Europe, may indicate the longstanding circulation of a related but non-pathogenic strain of virus. Naturally occurring antibody appears to afford a high degree of protection against experimental challenge with virulent virus.

A new, widespread and important disease of rabbits, rabbit haemorrhagic disease (RHD), is concisely reviewed and discussed. RHD is an acute, infectious condition of adult rabbits and morbidity and mortality, after a relatively short incubation period, can be very high. The disease appears typically as a necrotizing hepatitis with associated haemorrhaging, and death occurs as a result of generalized organ dysfunction. RHD is caused by a calicivirus, antigenically related to a similar virus found in brown hares but distinct from other known caliciviruses, and is spread to susceptible rabbits by a number of routes and vectors. The disease is easily identified and can be effectively controlled in commercial and domestic rabbit populations by slaughter and vaccination regimes. The occurrence of pre-existing cross-reacting antibody in a proportion of rabbits unchallenged by the disease implies the presence of non-pathogenic strains of the virus. This antibody protects against disease on subsequent exposure to RHD. Uniquely, pre-existing antibody does not occur in rabbits in Australia where, after accidental release, the virus is currently spreading rapidly.

An extensive collection of blood samples from adult wild rabbits, from areas where Rabbit Haemorrbagic Disease (RHD) had not been recorded, was obtained from sites across the U.K. and parts of Eire over the winter of 1994195. Sera from 946 animals were examined for antibodies to RHD. Antibody was found in all populations, varying between 20 and 100% depending on locality, and overall 64% of rabbits were seropositive in midwinter, supporting the view that non-pathogenic RHD or RHD-like caliciviruses, which are not producing clinical disease, circulate within rabbit populations. The serological response to these agents appears to confer significant immunity on rabbits subsequently exposed to the virulent RHD virus, so the disease will not be as devastating as myxomatosis was in the early 1950s (99% mortality) but at least one-third of the c. 40 million rabbits in the U.K. are susceptible.

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