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.

Two commercial live virus infectious bovine rhinotracheitis (IBR) vaccines for intranasal administration and an inactivated polyvalent calf pneumonia vaccine were compared for safety and efficacy in calves against experimental IBR infections. All three products were clinically safe for use in young calves; a mild, transient, febrile response was induced by one of the live vaccines. Vaccinal virus was recovered for up to 16 days after vaccination from nasal secretions of all calves given live vaccine. Both live vaccines stimulated a serum neutralising antibody response, but the inactivated vaccine failed to elicit any serological response. Following intranasal challenge four months after the first dose of vaccine, all live virus vaccinates remained systemically healthy. A slight nasal discharge and a few rapidly healing ulcers of the nasal mucosa were the only abnormalities observed. Both the group given the inactivated vaccine and the unvaccinated controls developed clinical IBR with pyrexia, ocular and nasal discharges, severe ulceration of the nasal mucosa and tracheitis and tachypnoea to varying degrees of severity. Parenteral administration of dexamethasone six months after challenge induced reactivation of virus shedding followed by a rise in humoral antibody titre irrespective of the original vaccination history.

Rabbit antisera to the stump-tailed macaque polyomavirus (STMV) which had been shown by immunoelectron microscopy and indirect immunofluorescence to react with the polyomavirus found in FRhK-4 cells (FRKV), also gave precipitin lines in counter-immunoelectrophoresis (CIE) and double diffusion in gel (GD) when reacted with FRKV. The reactions in GD showed identity with that of a rabbit antiserum to FRKV. Naturally occurring antibody to FRKV (anti-FRKV) was found by CIE in 48 per cent of 353 cattle, 1/106 pigs and 1/20 goats but not in any of 13 other species including 45 rhesus monkeys and 97 humans. Each of 9 anti-FRKV positive samples from cattle, the goat serum, but not the pig serum gave a line of identity with the rabbit antiserum to FRKV in GD against FRKV. Detection of anti-FRKV in colostrum deprived newborn calves and in commercial foetal calf sera (FBS) indicates that intra-uterine infection of cattle with FRKV may occur. FRKV adapted readily to growth in secondary calf kidney cultures and grew more rapidly and to higher titres than in the FRhK-4 cultures. We conclude that FRKV is probably another strain of STMV and that the natural hosts of these viruses are cattle and not primates. Evidence of intra-uterine infection of cattle implies that infectious FRKV may be present in some FBS and may thus have gained entry into various susceptible cell lines, particularly primate kidney.

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