No abstract

Three discrete regions of the African swine fever virus (ASFV) were analysed in the genomes of a wide range of isolates collected from wild and domestic pigs in Sardinia, over a 31-year period (1978-2009). The analysis was conducted by genotyping based on sequence data from three single copy ASF genes. The E183L gene encoding the structural protein p54 and part of the gene encoding the p72 protein were used to delineate genotypes, before intra-genotypic resolution of viral relationships by analysis of tetramer amino acid repeats within the hypervariable central variable region (CVR) of the B602L gene. The data revealed that these isolates did not show significant variation in their p72 and p54 sequence when compared between different isolates showing a remarkable genetic stability of these genome regions. In particular, the phylogeny revealed that all the Sardinian isolates belong to the same largest and most homogeneous p72 genotype I together with viruses from Europe, South America, the Caribbean and West Africa, and p54 genotype Ia which comprises viruses from Europe and America. The analysis of B602L gene revealed a minor difference in the number of tetramer repeats, placing the Sardinian isolates into two clusters, accordingly to their temporal distribution, namely sub-group III and sub-group X, this latter showing a deletion of 12 tetramer repeats located in the centre of the array. The genetic variation of this fragment suggests that one sub-group could be derived from the other supporting the hypothesis of a single introduction of ASFV in Sardinia.

African Swine Fever (ASF) is a haemorrhagic disease, which can cause high mortality in domestic pigs and wild boars; it does not affect humans but has a devastating socioeconomic impact. It can be transmitted directly through animal contact or indirectly via contaminated food and equipment. Humans can mechanically transport the ASF virus (ASFV) by human-mediated activities (the 'human factor') (EFSA AHAW Panel, 2014). The ongoing epidemiological wave in Europe originated in 2007 in Georgia and spread to other European countries in 2014; ASFV genotype II was responsible for these outbreaks, which affected both wild boar and domestic pigs (Blome et al., 2020). Since then, the disease has spread westward in Europe, with the epidemic reaching Germany (Sauter-Louis et al., 2020). At the same time, a long-distance jump transmitted the virus from infected countries to previously ASF-free countries, such as Belgium (Linden et al., 2019).It is suspected that the transmission via the human factor occurred in mainland Italy, which is also the latest European country to report the spread of ASF, where the first ASFV genotype II-positive wild boar was found in the Piedmont region (northwest region of the country) in January 2022 (ADIS, 2022). Subsequently, several other positive cases were reported in the wild boar population across the Liguria and Piedmont regions, a mountainous area between the This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Previous genetic characterization of African swine fever virus isolates from the Italian island of Sardinia, where the virus has been present since 1978, has largely been limited to a few selected genomic regions. Here, we report the complete genome sequence of the isolate 47/Ss/08 collected during an outbreak in 2008.

To date, in countries where infectious bovine rhinotracheitis (IBR) is widespread, its control is associated with deleted marker vaccines. These products lack one or more genes responsible for the synthesis of glycoproteins or enzymes. In Europe, the most widely used marker vaccine is one in which glycoprotein E (gE−) is deleted, and it is marketed in a killed or modified-live form. Using this type of immunization, it is possible to differentiate vaccinated animals (gE−) from those infected or injected with non-deleted (gE+) products using diagnostic tests specific for gE. The disadvantage of using modified-live gE-products is that they may remain latent in immunized animals and be reactivated or excreted following an immunosuppressive stimulus. For this reason, in the last few years, a new marker vaccine became commercially available containing a double deletion related to genes coding for gE and the synthesis of the thymidine-kinase (tk) enzyme, the latter being associated with the reduction of the neurotropism, latency, and reactivation of the vaccine virus. Intramuscularly and intranasally administered marker products induce a humoral immune response; however, the mother-to-calf antibody kinetics after vaccination with marker vaccines is poorly understood. This review discusses several published articles on this topic.