Comparison of the genome sequences of non-pathogenic and pathogenic African swine fever virus isolates

Abstract

The genomic coding sequences, apart from the inverted terminal repeats and cross-links, have been determined for two African swine fever virus (ASFV) isolates from the same virus genotype, a non-pathogenic isolate from Portugal, OURT88/3, and a highly pathogenic isolate from West Africa, Benin 97/1. These genome sequences were annotated and compared with that of a tissue culture-adapted isolate, BA71V. The genomes range in length between 170 and 182 kbp and encode between 151 and 157 open reading frames (ORFs). Compared to the Benin 97/1 isolate, the OURT88/3 and BA71V isolates have deletions of 8–10 kbp that encode six copies of the multigene family (MGF) 360 and either one MGF 505/530 copy in the BA71V or two copies in the OURT88/3 isolate. The BA71V isolate has a deletion, close to the right end of the genome, of 3 kbp compared with the other isolates. The five ORFs in this region include an additional copy of an ORF similar to that encoding the p22 virus structural protein. The OURT88/3 isolate has interruptions in ORFs that encode a CD2-like and a C-type lectin protein. Variation between the genomes is observed in the number of copies of five different MGFs. The 109 non-duplicated ORFs conserved in the three genomes encode proteins involved in virus replication, virus assembly and modulation of the host's defences. These results provide information concerning the genetic variability of African swine fever virus isolates that differ in pathogenicity.

Molecular characterisation of African swine fever viruses from Nigeria (2003–2006) recovers multiple virus variants and reaffirms CVR epidemiological utility

“…2a), thereby confirming their genotype I designation. Similarly, all Nigerian viruses were identical to each other across the 780 bp region spanning the 5'ends of the B125R and B646L (p72) genes, and to other West African genotype I viruses, such as Ben97/1 (Chapman et al 2008) for which homologous data were available (results not shown). In contrast, five size-and sequence-discrete CVR variants were obtained for the Nigerian 2003-6 viruses analysed, corresponding to virus variants containing between 20 and 36 tetrameric repeats (Fig.…”

Related strains of African swine fever virus with different virulence: genome comparison and analysis

“…As referred to above for OURT88/3 (Chapman et al, 2008), NHV is also non-haemadsorbing, with similar deletions as in OURT88/3 for both the lectinlike EP153R and CD2-like EP402R. Haemadsorption is not directly related to virulence, since there are virulent field strains lacking this feature (Gonzague et al, 2001;Pan & Hess, 1984), and deletion of EP402R (8DR) or EP153R (8CR) from Malawi Lil-20/1 did not reduce virulence for domestic pigs, although deletion of 8DR caused a delay in viral spread (Borca et al, 1998;Neilan et al, 1999).…”

“…Further genomic factors have to be contemplated. Ba71V has an extra deletion of 3.2 kb in the RVR of its genome, resulting in loss of several ORFs conserved in all natural strains of ASFV sequenced to date (Chapman et al, 2008), and also in the present L60 and NHV -I7L, -I8L, -I9R, -I10L and -I11L. These may have an important role for replication in macrophages and/or virulence, but they are still mostly uncharacterized, except for I10L encoding an extra copy of structural viral protein p22, similar to KP177R present in the LVR (Dixon et al, 1994).…”

“…The novel ASFV genomes were annotated with the aid of Genome Annotation Transfer Utility software (Tcherepanov et al, 2006), using the OURT88/3 strain as a reference and following the ORF nomenclature scheme proposed by Chapman et al (2008). Analysis and comparison of genome sequences was performed using Jalview (Waterhouse et al, 2009), Base-By-Base (Hillary et al, 2011) and viral Genome Organizer (Upton et al, 2000).…”

“…In more recent years, sequences from strains of different origin and genotypes have become available along with comparative analyses (Chapman et al, 2008(Chapman et al, , 2011de Villiers et al, 2010). Most of the variation among ASFV genomes results from the presence of different numbers of multi-gene family (MGF) genes in the left and right variable regions (LVR and RVR, respectively).…”