Background and Aim: In modern scientific literature presents an understanding that African swine fever (ASF) ASF virus (ASFV) is remarkably stable in the environment, and carcasses of the pigs which were died after ASF, play a key role as ASFV reservoir. The aim of this study was to evaluate the possibility of the ASFV (different isolates) survival in bodies of dead animals, bones, remnants of bone marrow, residual organ matrix in natural conditions. Materials and Methods: Skeletons of ASFV infected pigs which were died and left/abandoned in forests or buried in Armenia at diverse time points and locations had been excavated and examined for the presence of ASFV genome by real-time polymerase chain reaction (PCR) assay and for infection abilities through in vitro (hemadsorption test and infection in porcine lung macrophages) as well as by intramuscular infection in healthy pigs. Results: Current exploration showed that in several samples (with different times of exposure) of excavated skeletons had been detected the presence of the virus gene (p72) using real-time PCR. However, in none of these porcine samples, infectious ASFV could be isolated. Data obtained by real-time PCR at frequent intervals indicated the presence of the virus gene (p72), especially within the case of the acute form of the disease. This can be explained by the highest levels of the virus during the latter case mentioned above. Conclusion: ASFV seems to be very sensitive to environmental temperature. The best place for ASFV long-term survival in the natural environment is bone marrow from intact big tubular bones (like femur or tibia) of buried carcasses. In artificial "graves," complete bones with not destructed bone marrow can preserve the virus gene (p72) for a very long time (more than 2 years). Infectious particles in underground conditions survive not so long: In complete bones with not affected bone marrow, possible presence of the virus for several months.

Our data allow assuming that new nosological form of ASF (genotype II) may present as a transitional form of the disease with the possibility of chronization

Aim: A genome-scale phylogenetic analysis was used to infer the evolutionary dynamics of Asfarviridae – African swine fever virus (ASFV) – and better define its genetic diversity. Materials and Methods: All complete ASFV genomes from NCBI's resource as of March 2020 were used. The phylogenetic analysis used maximum likelihood and neighbor-joining methods. The evolutionary models detection was done with the help of the package of programs MEGA-X. Algorithms were used to build phylogenetic trees for type B DNA polymerases of ASFV (n=34) and HcDNAV (n=2), as an external group. Results: An expedient categorization of the Asfarviridae family uses five clades. Genotype 1 (except for LIV 5/40 virus isolate) as well genotype 7 are assigned to the alpha clade; genotype 2 to the beta clade; genotypes 8, 9, and 10 to the gamma clade; genotype 5 to the delta clade; and genotypes 3, 4, and 20, as well as genotype 22 and the LIV 5/40 isolate to the epsilon clade. Branch lengths on the phylogenetic tree are proportional to genetic distance along the branch. Branches at the phylogenetic tree of Asfarviridae are much shorter than branches for Baculoviridae. Shorter branches in ASFVs population suggest that Asfarviridae evolved relatively recently and remain more closely related. Conclusion: We suggest applying more robust standards using whole genomes to ensure the correct classification of ASFV and maintain phylogeny as a useful tool.

Shortly after the establishment of African swine fever virus (ASFV) genotype II in 2007, cases of acute fatal infection were observed. However, after several years of circulation in the Eurasian region, the clinical signs of the disease changed. Currently, this disease can occur acutely, subclinically, chronically, or asymptomatically. Cases of the complete recovery of infected pigs, and the disappearance of ASFV from their tissues and secretions have been described. This form of the disease first appeared in Armenia at the end of 2011. This virus was described and identified as the Dilijan2011IMB strain. The goal of our research was to study the main features of clinical, pathological, immunological, virological, and genetic parameters involved in the development of new forms of African swine fever (ASF). Chronic ASF was characterized with low titers of the virus and a decrease in the intensity of hemadsorption. Additionally, a reduced intensity in clinical symptoms and pathoanatomical results was noted. The absolute, but not the relative number of immune cells changes; the neutropenia (in bone marrow and spleen), lymphopenia (in bone marrow), lymphocytosis (only in spleen), lymphoid cell depletion (in bone marrow), and pancytopenia (in bone marrow) observed in the chronic form of ASF were less pronounced compared to in the acute form. When comparing the late stage of chronic ASF to the acute form, the key cytological indicators in the spleen, lymph nodes, and blood were less severe in the chronic stage. Bone marrow failure in the chronic form, expressed in a pronounced decrease in all cell types, generally coincided with the data in the acute form of ASF. The same data were obtained after assessing serum TNF-alpha levels. Thus, we can conclude that the chronic form of ASF occurs due to a less pronounced immune response, as well as a decrease in virus titers in the blood and tissues of infected pigs.

African swine fever virus manipulates the cell cycle of infected G0 cells by inducing its progression via unblocking cells from the G0 to S phase and then arresting them in the G2 phase. DNA synthesis in infected alveolar macrophages starts at 10–12 h post infection. DNA synthesis in the nuclei of G0 cells is preceded by the activation of the viral genes K196R, A240L, E165R, F334L, F778R, and R298L involved in the synthesis of nucleotides and the regulation of the cell cycle. The activation of these genes in actively replicating cells begins later and is less pronounced. The subsequent cell cycle arrest at the G2 phase is also due to the cessation of the synthesis of cellular factors that control the progression of the cell cycle–cyclins. This data describes the manipulation of the cell cycle by the virus to gain access to the nucleotides synthesized by the cell. The genes affecting the cell cycle simply remain disabled until the beginning of cellular DNA synthesis (8–9 hpi). The genes responsible for the synthesis of nucleotides are turned on later in the presence of nucleotides and their transcriptional activity is lower than that during virus replication in an environment without nucleotides.