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1.
Vet Microbiol ; 266: 109365, 2022 Mar.
Article in English | MEDLINE | ID: mdl-35151121

ABSTRACT

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.


Subject(s)
African Swine Fever Virus , African Swine Fever , Swine Diseases , African Swine Fever Virus/genetics , Animals , Ecosystem , Models, Theoretical , Swine , Virus Replication
2.
Vet Microbiol ; 237: 108421, 2019 Oct.
Article in English | MEDLINE | ID: mdl-31585648

ABSTRACT

This research is focused on the study of African swine fever virus (ASFV) survival in the leech Hirudo medicinalis. To detect the infection route of the virus in leeches, two introduction methods were used: blood-feeding from infected swine hosts and exposure to ASFV-contaminated water (leeches cultivated with ASFV). This study found that the survival of ASFV in leeches was much longer than that in leech-free medium. The persistent presence of the virus in leeches and leech excretion was detected in both groups. The virus excreted from both groups of leeches in the terminal stages of the experiment was able to induce productive infection in porcine alveolar macrophages. In an attempt to understand ASFV, transmission to pigs was conducted through the ingestion of leech-cultivated water and leeches that had fed on ASFV-infected animals or that were cultivated environmentally with the virus. The ingestion of some samples at 60-80 days after cultivation demonstrated successful ASFV transmission via per os infection. In conclusion, leeches can serve as a possible reservoirs for ASFV in the absence of its main hosts - pigs and some ticks of the genus Ornithodoros.


Subject(s)
African Swine Fever Virus/physiology , Hirudo medicinalis/virology , Animals , Coculture Techniques , Macrophages, Alveolar/virology
3.
J Comp Pathol ; 167: 50-59, 2019 Feb.
Article in English | MEDLINE | ID: mdl-30898298

ABSTRACT

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.


Subject(s)
African Swine Fever/pathology , Chemokine CXCL12/blood , Endothelium, Vascular/pathology , Nitric Oxide/blood , Vascular Endothelial Growth Factor A/blood , African Swine Fever/metabolism , Animals , Cell Cycle/physiology , Cell Proliferation/physiology , Endothelial Cells/metabolism , Endothelial Cells/pathology , Endothelium, Vascular/metabolism , Swine
4.
Vet Immunol Immunopathol ; 145(1-2): 551-5, 2012 Jan 15.
Article in English | MEDLINE | ID: mdl-22226551

ABSTRACT

African swine fever virus (ASFV) is the causative agent of African swine fever that is the significant disease of domestic pigs, with high rates of mortality. ASFV is double-stranded DNA virus whose genes encode some proteins that are implicated in the suppression of host immune response. In this study, we have modeled in vivo infection of ASFV for determination of interferon (IFN) status in infected pigs. We measured the level of IFN-α, -ß and -γ by enzyme-linked immunosorbent assay and showed that the level of IFN-α sharply decreased during infection. Unlike IFN-α, the level of IFN-ß and -γ increased from the 2nd and 4th days post-infection, respectively. Also, we analyzed the population dynamics of peripheral white blood cells of infected pigs due to their important role in host immune system. We showed that the atypical lymphocytes appeared after short time of infection and this result is in accordance with our previous study done in vitro. At the last day of infection about 50% of the total white blood cells were destroyed, and the remaining cells were represented mainly by small-sized lymphocytes, reactive lymphocytes and lymphoblasts.


Subject(s)
African Swine Fever Virus , African Swine Fever/immunology , Interferons/blood , Leukocyte Count/veterinary , African Swine Fever/blood , African Swine Fever Virus/immunology , Animals , Enzyme-Linked Immunosorbent Assay/veterinary , Interferon-alpha/blood , Interferon-beta/blood , Interferon-gamma/blood , Lymphocyte Count/veterinary , Lymphocytes/immunology , Swine/blood , Swine/immunology , Swine/virology
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