It is now generally accepted that most viral populations consist of various genetic variants rather than clones of a virus. The emergence of these viral variants is driven by virus-specific mutation rates, which vary greatly depending on a variety of factors, including replication patterns, polymerase fidelity, availability of repair mechanisms, and selection pressure. Together, these factors determine the rate of evolution of viruses (rate of evolution), which is manifested in the rate at which new virus variants emerge. Although some viruses evolve very quickly, such as the recent global pandemic, the SARS-CoV2 virus mutates impressively; But some viruses show a high degree of genetic stability and evolve very slowly. A classic example of the latter is African swine fever virus (ASFV).
African swine fever virus is a large, complex DNA virus first described in Kenya in 1921. It spreads for a long time between warthogs and soft ticks in an ancient jungle cycle. In 2007, the virus was carried to Eurasia and has since spread among wild boar and domestic pig populations. Although a distant virus of African swine fever virus has been identified in amoebas and shown some similarity with iris virus and pox virus, no viruses closely related to African swine fever virus have been identified. As a result, African swine fever virus has only recently been placed in the phylum Nuclear Cell Viruses, and since it is the only known member of its family Asfarviridae and genus Asfivirus, it is still considered a mystery in modern virology.
The genome of African swine fever virus is a single-molecule covalently closed double-stranded DNA up to 190 kbp in size with very high genetic stability. Modern strains show very high nucleotide sequence agreement with viral elements integrated into the molluscum tick genome at least 1.46 million years ago. Recent analyses of African swine fever virus strains introduced to Georgia in 2007 also support this observation. Despite more than a decade of circulation in the region, the virus strain has accumulated few mutations overall, and even fewer affecting virulence genes.
However, a recent study by the Friedrich Loeffler Institute (FLI) in Germany yielded unexpected results.
In 2020, African swine fever entered wild boar herds in eastern Germany. Whole-genome sequencing of the originally discovered virus, which showed similarities to the strain known to circulate in western Poland, was not particularly significant. But surprisingly, a number of African swine fever variants were subsequently identified in Germany, and these new variants were characterized by high-impact mutations affecting known non-blast virus open reading frames (ORFs), which had never been described before. While some changes affect regions of the viral genome that may be involved in potential immunomodulators or virulence factors, the effects of most mutations remain unknown. So they investigated these new genetic variants in more detail. A total of 5 lineages and 10 variants were identified.
Figure 1. Non-plague variants and lineages found in Germany
Although the genome of African swine fever virus has extremely high genetic stability, it is not unusual to find new genetic variants, and different types of variants have been recorded in the past. However, the special feature of the variant discovered by the German team is that within a year of the spread of African swine fever in Germany, at least 5 lineages of 10 variants have formed, and several geographical clusters have formed in Germany, which can be assigned to genetically different and hitherto undescribed subpopulations of the virus.
Figure 2. A spatial snapshot of the model output, with different variants in different colors, shows the dynamic development of the infection distribution (a-c) or maps the random variation of the final distribution (d-f). The pixels represent the boar social group, and the line is the administrative boundary.
In addition, the mutations of these new variants are high-impact mutations, and it is worth noting that all the new variants have a frameshift mutation at the 3' end of the DNA polymerase PolX gene O174L, suggesting its pathogenic role as a possible mutated gene. Although epidemiological models support the impact of increased mutation rates, how quickly the virus might evolve in this case remains unknown. They believe that this new factor has the potential to greatly affect the course of the ASFV pandemic, and the outcome is unknown.