A severe epidemic of rinderpest, affecting mainly wild ruminants, occurred between 1993 and 1997 in East Africa. Buffalo (Syncerus caffer), eland (Taurotragus oryx) and lesser kudu (Tragelaphus imberbis) were highly susceptible. The histopathological changes, notably individual epithelial cell necrosis with syncytia formation, were consistent with an infection with an epitheliotrophic virus. Serology, the polymerase chain reaction, and virus isolation confirmed the diagnosis and provided epidemiological information. The virus was related to a strain which was prevalent in Kenya in the 1960s, of a second lineage (II), and distinct from isolations of rinderpest virus in the region since 1986. The source of the virus was presumed to be infected cattle from the Eastern region of Kenya and Somalia. The pathogenicity of the virus varied during the epidemic. The mortality in buffalo populations was estimated to be up to 80 per cent, and population data suggested that the virus had an adverse effect on a wide range of species. The virus caused only a mild disease in cattle, with minimal mortality. The results confirmed the importance of wildlife as sentinels of the disease, but although wildlife were important in the spread of the virus, they did not appear to act as reservoirs of infection.

The Bo17 gene of bovine herpesvirus 4 (BoHV-4) is the only viral gene known to date that encodes a homologue of the cellular core 2 ␤-1,6-N-acetylglucosaminyltransferase-mucin type (C2GnT-M). To investigate the origin and evolution of the Bo17 gene, we analyzed its distribution among BoHV-4 strains and determined the sequences of Bo17 from nine representative strains and of the C2GnT-M gene from six species of ruminants expected to encompass the group within which the gene acquisition occurred. Of 34 strains of BoHV-4, isolated from four different continents, all were found to contain the Bo17 gene. Phylogenetic analyses indicated that Bo17 was acquired from a recent ancestor of the African buffalo, implying that cattle subsequently acquired BoHV-4 by cross-species transmission. The rate of synonymous nucleotide substitution in Bo17 was estimated at 5 ؋ 10 ؊8 to 6 ؋ 10 ؊8 substitutions/site/year, consistent with previous estimates made under the assumption that herpesviruses have cospeciated with their hosts. The Bo17 gene acquisition was dated to around 1.5 million years ago. Bo17 sequences from BoHV-4 strains from African buffalo and from cattle formed two separate clades, estimated to have split about 700,000 years ago. Analysis of the ratio of nonsynonymous to synonymous nucleotide substitutions revealed a burst of amino acid replacements subsequent to the transfer of the cellular gene to the viral genome, followed by a return to a strong constraint on nonsynonymous changes during the divergence of contemporary BoHV-4 strains. The Bo17 gene represents the most recent of the known herpesvirus gene acquisitions and provides the best opportunity for learning more about this important process of viral evolution.

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Cattle were vaccinated with a recombinant capripox-rinderpest vaccine designed to protect cattle from infection with either rinderpest virus (RPV) or lumpy skin disease virus (LSDV). Vaccination did not induce any adverse clinical responses or show evidence of transmission of the vaccine virus to in-contact control animals. Approximately 50% of the cattle were solidly protected from challenge with a lethal dose of virulent RPV 2 years after vaccination while at 3 years approx. 30% were fully protected. In the case of LSDV, all of 4 vaccinated cattle challenged with virulent LSDV at 2 years were completely protected from clinical disease while 2 of 5 vaccinated cattle were completely protected at 3 years. The recombinant vaccine showed no loss of potency when stored lyophylized at 4 degrees C for up to 1 year. These results indicate that capripoxvirus is a suitable vector for the development of safe, effective and stable recombinant vaccines for cattle.