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Rift Valley Fever virus (RVFV) causes recurrent outbreaks of acute life-threatening human and livestock illness in Africa and the Arabian Peninsula. No licensed vaccines are currently available for humans and those widely used in livestock have major safety concerns. A One Health vaccine development approach, in which the same vaccine is co-developed for multiple susceptible species, is an attractive strategy for RVFV. Here, we utilized a replication-deficient chimpanzee adenovirus vaccine platform with an established human and livestock safety profile, ChAdOx1, to develop a vaccine for use against RVFV in both livestock and humans. We show that single-dose immunization with ChAdOx1-GnGc vaccine, encoding RVFV envelope glycoproteins, elicits high-titre RVFV-neutralizing antibody and provides solid protection against RVFV challenge in the most susceptible natural target species of the virus-sheep, goats and cattle. In addition we demonstrate induction of RVFV-neutralizing antibody by ChAdOx1-GnGc vaccination in dromedary camels, further illustrating the potency of replication-deficient chimpanzee adenovirus vaccine platforms. Thus, ChAdOx1-GnGc warrants evaluation in human clinical trials and could potentially address the unmet human and livestock vaccine needs.

Twelve complete African swine fever virus (ASFV) genome sequences are currently publicly available and these include only one sequence from East Africa. We describe genome sequencing and annotation of a recent pig-derived p72 genotype IX, and a tick-derived genotype X isolate from Kenya using the Illumina platform and comparison with the Kenya 1950 isolate. The three genomes constitute a cluster that was phylogenetically distinct from other ASFV genomes, but 98–99 % conserved within the group. Vector-based compositional analysis of the complete genomes produced a similar topology. Of the 125 previously identified ‘core’ ASFV genes, two ORFs of unassigned function were absent from the genotype IX sequence which was 184 kb in size as compared to 191 kb for the genotype X. There were multiple differences among East African genomes in the 360 and 110 multicopy gene families. The gene corresponding to 360-19R has transposed to the 5′ variable region in both genotype X isolates. Additionally, there is a 110 ORF in the tick-derived genotype X isolate formed by fusion of 13L and 14L that is unique among ASFV genomes. In future, functional analysis based on the variations in the multicopy families may reveal whether they contribute to the observed differences in virulence between genotpye IX and X viruses. © 2015, Springer Science+Business Media New York.

We describe a horizontal survey of African swine fever virus (ASFV) prevalence and risk factors associated with virus infection in domestic pigs in two contrasting production systems in Kenya. A free range/tethering, low input production system in Ndhiwa District of South-western Kenya is compared with a medium input stall fed production system in Kiambu District of Central Kenya. Analysis of variance (ANOVA) of data derived from cluster analysis showed that number of animals, number of breeding sows and number of weaner pigs were a significant factor in classifying farms in Nhiwa and Kiambu. Analysis of blood and serum samples using a PCR assay demonstrated an average animal level positivity to ASFV of 28% in two independent samplings in South-western Kenya and 0% PCR positivity in Central Kenya. No animals were sero-positive in either study site using the OIE indirect-ELISA and none of the animals sampled exhibited clinical symptoms of ASF. The farms that contained ASFV positive pigs in Ndhiwa District were located in divisions bordering the Ruma National Park from which bushpig (Potamochoerus larvatus) incursions into farms had been reported. ASFV prevalence (P<0.05) was significantly higher at distances between 6 and 16. km from the National Park than at distances closer or further away. One of the 8 bushpigs sampled from the park, from which tissues were obtained was PCR positive for ASFV. The data therefore indicated a potential role for the bushpig in virus transmission in South-western Kenya, but there was no evidence of a direct sylvatic virus transmission cycle in Central Kenya. ASF control strategies implemented in these areas will need to take these epidemiological findings into consideration. © 2012 Elsevier B.V.

The presence of antibodies against African swine fever (ASF), a complex fatal notifiable OIE disease of swine, is always indicative of previous infection, since there is no vaccine that is currently used in the field. The early appearance and subsequent long-term persistence of antibodies combined with cost-effectiveness make antibody detection techniques essential in control programmes. Recent reports appear to indicate that the serological tests recommended by the OIE for ASF monitoring are much less effective in East and Southern Africa where viral genetic and antigenic diversity is the greatest. We report herein an extensive analysis including more than 1000 field and experimental infection sera, in which the OIE recommended tests are compared with antigen-specific ELISAs and immuno-peroxidase staining of cells (IPT). The antibody detection results generated using new antigen-specific tests, developed in this study, which are based on production of antigen fractions generated by infection and virus purification from COS-1 cells, showed strong concordance with the OIE tests. We therefore conclude that the lack of success is not attributable to antigenic polymorphism and may be related to the specific characteristics of the local breeds African pigs. © 2012 Elsevier B.V.

The role of the ancestral sylvatic cycle of the African swine fever virus (ASFV) is not well understood in the endemic areas of eastern Africa. We therefore analysed the ASF infection status on samples collected from 51 free-ranging warthogs (Phacocherus africanus) and 1576 Ornithodorus porcinus ticks from 26 independent warthog burrows at a single ranch in Kenya. Abattoir samples from 83 domestic pigs without clinical symptoms, originating from specific locations with no recent reported ASF outbreaks were included in this study. All samples were derived from areas of central Kenya, where ASF outbreaks have been reported in the past. Infection with ASFV was confirmed in 22% of O. porcinus pools, 3.22% of adult warthog serum samples and 49% of domestic pig serum samples by using p72-based PCR. All of the warthog sera were positive for anti-ASFV antibodies, investigated by using ELISA, but none of the domestic pig sera were positive. Twenty O. porcinus-, 12 domestic pig- and three warthogderived viruses were genotyped at four polymorphic loci. The ASFV isolates from ticks and domestic pigs clustered within p72 genotype X. By contrast, ASF viruses genotyped directly from warthog sera, at same locality as the tick isolates, were within p72 genotype IX and genetically similar to viruses causing recent ASF outbreaks in Kenya and Uganda. This represents the first report of the co-existence of different ASFV genotypes in warthog burrow-associated ticks and adult wild warthogs. The data from this and earlier studies suggest transfer of viruses of at least two different p72 genotypes, from wild to domestic pigs in East Africa. © 2011 SGM.

Complete sequencing of p54-gene from 67 European, American, and West and East African Swine Fever virus (ASFV) isolates revealed that West African and European ASFV isolates classified within the predominant Genotype I according to partial sequencing of p72 were discriminated into four major sub-types on the basis of their p54 sequences. This highlighted the value of p54 gene sequencing as an additional, intermediate-resolution, molecular epidemiological tool for typing of ASFV viruses. We further evaluated p54-based genotyping, in combination with partial sequences of two other genes, for determining the genetic relationships and origin of viruses responsible for disease outbreaks in Kenya. Animals from Western and central Kenya were confirmed as being infected with ASFV using a p72 gene-based PCR assay, following outbreaks of severe hemorrhagic disease in domestic pigs in 2006 and 2007. Eleven hemadsorbing viruses were isolated in macrophage culture and genotyped using a combination of full-length p54-gene sequencing, partial p72-gene sequencing, and analysis of tetrameric amino acid repeat regions within the variable region of the B602L gene (CVR). The data revealed that these isolates were identical in their p72 and p54 sequence to viruses responsible for ASF outbreaks in Uganda in 2003. There was a minor difference in the number of tetrameric repeats within the B602L sequence of the Kenyan isolates that caused the second Kenyan outbreak in 2007. A practical implication of the genetic similarity of the Kenyan and Ugandan viral isolates is that ASF control requires a regional approach. © 2008 Springer Science+Business Media, LLC.