Experimental models of ecological niches for African swine fever virus.

In this study, we investigated the possible biological factors affecting the survival of the African swine fever virus (ASFV) in the environment and their potential to influence the ecology of the ASFV. Specifically, we tested the survival and replication of ASFV in four phylogenetically distinct organisms: Paramecium caudatum, Dendrobaena alpine, Aedes aegypti andXeropicta derbentina using qReal-Time PCR and hemadsorbtion analysis. Levels of ASFV in earthworms (Dendrobaena alpina) and soil declined at similar rates, suggesting that earthworms likely have no influence on the ecology of the ASFV. Ciliates (Paramecium caudatum) significantly increase the rate of ASFV disappearance from the aquatic environment, probably using the virus as a food source. Mosquitoes (Aedes aegypti) do not provide significant support for the persistence of ASF virus in the environment, with no evidence for transmission to their offspring or pigs that ingested mosquitoes. ASFV persisted for much longer in air-breathing land snails (Xeropicta derbentina) than in the soil. Moreover, transcription of viral genes was maintained within the snail, although the question of full-fledged viral replication is still open. In addition, the active movements of snails suggests that they could play a role in the spread of the virus. The virus is likely to be localized in the intestines of snails as it is regularly excreted from their feces. These results highlight the importance of investigating invertebrates for understanding ASFV surviving, spreading and transmission in natural populations with zoonotic transmission potential.

Serum Concentrations of Vascular Endothelial Growth Factor, Stromal Cell-Derived Factor, Nitric Oxide and Endothelial DNA Proliferation in Development of Microvascular Pathology in Acute African Swine Fever.

There is significant evidence that pathology of the microcirculation occurs in African swine fever (ASF); however, the mechanisms by which it develops are largely unknown. In the present experimental infection study, we show that an increase in vascular permeability in the initial stages of acute ASF is dependent on viraemia and elevation of the concentration of serum nitric oxide (NO). Macrophages activated by ASF virus (ASFV) are stimulated to produce NO and simultaneously to sensitize the endothelial cells through the action of vascular endothelial growth factor Β (VEGFΒ), which is followed by an increase in VEGF-mediated endothelial permeability. In the later stages of disease, the endothelial cells undergo DNA proliferation, which may additionally provoke capillary leakage, point haemorrhages and migration of blood cells into tissues. The possible mechanism of a shift in the cell cycle from the G1 to S and G2 stages could be a direct effect of ASFV. The terminal stages of disease are characterized by triggering of compensatory mechanisms such as stimulation of the synthesis of stromal cell-derived factor-1.