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At least 19 recordsLinked to original sources
PubMed1996

The lesional changes and pathogenesis in the kidney in African swine fever.

African swine fever is a viral haemorrhagic disease of pigs which has been used as a model for the study of viral haemorrhagic diseases in man. The acute course of the disease is characterized by acute proliferative glomerulonephritis, with viral replication in mesangial cells and occasional focal necrosis of the renal tubular system; hyperplasia of the collecting ducts is associated with evident virus replication. Haemorrhages have been attributed to endothelial dysfunction, aggravated by virus replication in endothelial cells in the final stages of the disease. The renal interstitium displays intense oedema and an infiltrate largely composed of macrophages. Virus replication has also been observed in fibroblasts and in the smooth-muscle cells of arterioles and venules. In subacute-chronic forms of the disease, various types of glomerulonephritis are observed, ranging from mesangial proliferative glomerulonephritis to focal and segmental hyalinosis associated with immune-mediated phenomena. No striking changes are reported in the renal tubular system. Interstitial haemorrhages are associated with diapedesis due to immunologically mediated events. The interstitium has also been found to contain a lymphohistiocytic infiltrate with abundant plasma cells. No evidence has been reported of viral replication in any cell population.

African Swine Fever↗
PubMed1995

A pathological study of the perisinusoidal unit of the liver in acute African swine fever.

African swine fever is an acute haemorrhagic disease of pigs which may serve as a model for the study of the pathogenesis of other viral haemorrhagic fevers. This paper describes an ultrastructural study of the sequence of lesions produced in the perisinusoidal functional unit of the liver of pigs inoculated with the Malawi '83 strain of African swine fever virus, which is classified as haemadsorbing and highly virulent. Virus replication was observed in Kupffer cells and monocytes from three days after inoculation, in hepatocytes and fat-storing cells at five and seven days after inoculation, and in sinusoidal endothelial cells at seven days after inoculation. Further observations included intravascular coagulation, which peaked at five days after inoculation, and fibroblast and myofibroblast transformation of fat-storing cells at seven days after inoculation. These results suggest that activated cells of the mononuclear phagocyte system may play a major role in this sequence of lesions and the possible role of the cytokines that may be released by these cells is discussed.

Acute Disease↗
PubMed2002

Swine fever: classical swine fever and African swine fever.

Because of the clinical and pathologic similarity to common endemic diseases, introduction of CSFV or ASFV strains of moderate to low virulence represents the greatest risk to North American swine herds. Producers, veterinarians, and diagnosticians should increase their awareness of these devastating diseases and request specific diagnostic testing whenever they are suspected. Production practices that improve biosecurity will reduce the risk of introduction of CSF and ASF and limit the spread if an incursion occurs. Additional resources. The following Web sites contain excellent color photographs that will assist producers and practitioners in identifying clinical signs and gross lesions associated with CSFV and ASFV: http://www.vet.uga.edu/vpp/gray_book/FAD and http://www.pighealth.com. The latter Web site and the OIE Web site (http://www.oie.int) offer updated information on current worldwide epizootics of ASF and CSF and other swine diseases. Details of biosecurity procedures can be found at http://www.agebb.missouri.edu; see publication G2340.

African Swine Fever↗
PubMed2005

Intra- and inter-genotypic size variation in the central variable region of the 9RL open reading frame of diverse African swine fever viruses.

African swine fever (ASF) viruses are characterised by numerous p72 genotypes, but by low levels of intra-genotypic variation, particularly in domestic pig associated genotypes. As it is precisely these viral lineages that are involved in outbreaks of the disease it is imperative that alternative, more informative gene regions be identified which are suitable for intra-genotypic resolution of relationships. To this end, the central variable region (CVR) of the 9RL open reading frame of diverse ASF viruses was amplified and product sizes scored and compared within and between genotypes. Results indicate that although product sizes are not genotype restricted, there is a high degree of intra-genotypic size variation particularly within the homogeneous p72 genotypes. Within one such genotype, the ESACWA virus genotype, 12 size-discrete CVR products were identified, four corresponding to viruses of west African origin and eight to viruses from countries where the disease is exotic, namely Europe, South America and the Caribbean. The high degree of size heterogeneity in the CVR of this genotype is significant and attests to the usefulness of the CVR gene marker in elucidating the epidemiology of African swine fever.

Africa↗
PubMed1988

Epitopic diversity of African swine fever virus.

African swine fever (ASF) is caused by an icosahedral cytoplasmic, double stranded DNA virus. In the acute form of the disease, pigs die from disseminated intravascular coagulation (DIC) with extensive damage of the free and fixed macrophage systems and the reticular epithelial cells of the thymus; mortality is virtually 100%. In recent years, subacute and chronic forms of ASF have become more prevalent in the field, especially in outbreaks occurring outside the continent of Africa, and virus isolated from these outbreaks have often been of lesser virulence. In pigs experimentally infected with such isolates, a number of immunopathological manifestations have been encountered, e.g. hypergammaglobulinemia associated with necrotizing pneumonia, persistent infection in the presence of ASF-specific antibodies, and lack of demonstrable virus neutralizing antibodies. Nevertheless, the immune systems of pigs that have clinically recovered have not been impaired by the infection. We suggest that the heterogeneous composition of the virus population in a given isolate may be one of the causes of the anomalous immune responses. When a number of biological markers, i.e., hemadsorption characteristics, plaque size, infectivity, virulence, antigenic determinants, and genomic structure, were used to characterize the virus clones derived from various ASF virus (ASFV) isolates, considerable heterogeneity was apparent. In the present investigation, 20 monoclonal antibodies (MAb), which specifically identified the 14 kDa viral protein within the cytoplasmic membrane of the infected cells, were used to determine epitopic differences among a number of virus clones derived from various isolates. All of the non-African isolates examined contained two epitopically different groups of virus clones, and the reaction profiles obtained were distinctly different from those obtained with the clones of an African isolate (Tengani). It was concluded that an ASFV isolate is composed of a biologically diverse virus population with distinctly different members which are only identified after cloning.

African Swine Fever↗
PubMed1989

Infection of pigs with the Cameroon isolate (Cam/82) of African swine fever virus.

African swine fever (ASF) was produced in eight pigs by exposure to donors infected with the Cameroon/82 isolate of African swine fever virus. The primary clinical sign was pyrexia of more than 40 degrees C first observed 10 to 13 days post-exposure (dpe) in all pigs; other clinical signs were rarely observed. The most frequent post-mortem lesion was haemorrhage in the visceral lymph nodes. Other lesions included excess fluid in the abdominal cavity and petechial haemorrhages in the kidneys. Viraemia was first observed 1 to 2 days before the onset of pyrexia and maximal titres of more than 10(7.5) HAD50 per ml occurred 11 to 14 dpe. Virus excretion by the pharyngeal route was observed at 2 to 4 days before the onset of pyrexia and continued throughout the course of infection. Susceptible pigs, mixed directly with infected ones, contracted infection within 2 h; transmission time increased to 2 to 6 h when recipient pigs were separated by wire mesh from the infected pigs. The comparatively low mortality, ill-defined clinical signs and clinical recovery of many of the infected pigs show that the Cam/82 ASF virus is of relatively low virulence and thereby resembles recent European, South American and Caribbean isolates.

African Swine Fever↗
PubMed1993

The relative density of CD44-positive porcine monocytic cell populations varies between isolations and upon culture and influences susceptibility to infection by African swine fever virus.

African swine fever (ASF) virus has been reported to infect cells of the monocyte family, probably macrophage-like cells, but there is variation in the apparent susceptibility of these cells. We have demonstrated that the phenotype and activity of porcine monocytic cells varies between different isolations and also upon culture. The variation during culture is dependent upon the phenotype of the cells at the time of isolation. As for the susceptibility of porcine monocytes/macrophages to infection by ASF virus, it was seen that this could be related to the variation in cell phenotype and activity. The susceptibility was determined by the relative density of particular subpopulations of cells present. Whilst inflammatory macrophages did not have an apparent role to play, phagocytic activity was influential. Furthermore, the expression of CD44 and the DH59 myeloid cell marker was important, whereas the relevance of MHC Class II expression was variable. Overall, it was concluded that susceptibility to infection required that a culture be dominated by CD44-positive cells which were non-inflammatory, of low phagocytic activity, and characterizable as being of the myeloid (DH59-positive) lineage.

African Swine Fever↗
PubMed1995

Pathological changes in the renal interstitial capillaries of pigs inoculated with two different strains of African swine fever virus.

African swine fever is a viral disease of pigs characterized predominantly by haemorrhagic lesions. This paper reports the lesions observed in the renal interstitial capillaries of pigs inoculated with African swine fever virus strains of differing virulence: the Malawi'83 strain (haemadsorbent and highly virulent) and the Dominican Republic'78 strain (haemadsorbent and moderately virulent). In pigs infected with the Malawi'83 strain, petechial haemorrhages and microhaemorrhages were observed 5 days after inoculation and lesions were evident in the renal capillaries. Signs of phagocyte activation were noticeable in endothelial cells, with enlarged fenestrations and even loss of endothelium, leaving the basement membrane of the vessels exposed. Platelet plugs and microthrombi were also observed in these vessels. At 7 days after inoculation these lesions had intensified, and were accompanied by virus replication in the endothelial cells. In pigs infected with the Dominican Republic'78 strain, haemorrhages were more abundant and more extensive, and although no endothelial cell lesions were observed, there was intense vasodilation with diapedesis of erythrocytes.

Africa↗
PubMed1980

A microtechnique for the titration for African swine fever virus.

African swine fever virus isolates were titrated in swine monocyte cultures established in microtitre trays. Although technically simpler and less laborious than conventional tube assays the microtitration assay was less sensitive, but for routine and comparative titrations offers distinct advantages.

African Swine Fever Virus↗
PubMed1981

Nucleoside triphosphate phosphohydrolase activities in African swine fever virus.

African swine fever virus contains nucleoside triphosphate phosphohydrolase activity which releases 32P phosphate from gamma-32P ATP at a rate of about 1 mumol/h mg of virus protein. The hydrolase activity is slightly stimulated by adding nucleic acids to the reaction mixture and under conditions of RNA synthesis. A study of the rate of ATP hydrolysis at different concentrations of ATP suggests the existence of two phosphohydrolase activities with apparent Km values of about 0.04 and 1 mM.

Adenosine Triphosphate↗
PubMed2006

Phenotype-based identification of host genes required for replication of African swine fever virus.

African swine fever virus (ASFV) produces a fatal acute hemorrhagic fever in domesticated pigs that potentially is a worldwide economic threat. Using an expressed sequence tag (EST) library-based antisense method of random gene inactivation and a phenotypic screen for limitation of ASFV replication in cultured human cells, we identified six host genes whose cellular functions are required by ASFV. These included three loci, BAT3 (HLA-B-associated transcript 3), C1qTNF (C1q and tumor necrosis factor-related protein 6), and TOM40 (translocase of outer mitochondrial membrane 40), for which antisense expression from a tetracycline-regulated promoter resulted in reversible inhibition of ASFV production by >99%. The effects of antisense transcription of the BAT3 EST and also of expression in the sense orientation of this EST, which encodes amino acid residues 450 to 518 of the mature BAT3 protein, were investigated more extensively. Sense expression of the BAT3 peptide, which appears to reversibly interfere with BAT3 function by a dominant negative mechanism, resulted in decreased synthesis of viral DNA and proteins early after ASFV infection, altered transcription of apoptosis-related genes as determined by cDNA microarray analysis, and increased cellular sensitivity to staurosporine-induced apoptosis. Antisense transcription of BAT3 reduced ASFV production without affecting abundance of the virus macromolecules we assayed. Our results, which demonstrate the utility of EST-based functional screens for the detection of host genes exploited by pathogenic viruses, reveal a novel collection of cellular genes previously not known to be required for ASFV infection.

African Swine Fever Virus↗
PubMed1995

Isolation and characterization of TK-deficient mutants of African swine fever virus.

African swine fever virus induces the synthesis of thymidine kinase (TK) in BHK TK-negative cells as an immediate early protein. The TK gene is not essential for growth of ASFV in cell culture and a stable viral strain deficient in TK has been isolated (E70NTKp). The genetic lesion of this ASFV TK- strain was identified by TK gene nucleotide sequencing, showing a nucleotide deletion leading to a -1 frameshift and a nonsense codon residue downstream of the deletion. The availability of this viable ASFV variant deficient in TK activity allows the insertion of foreign genes in the ASFV genome for genetic and biochemical studies.

African Swine Fever Virus↗
PubMed1996

Involvement of the endoplasmic reticulum in the assembly and envelopment of African swine fever virus.

African swine fever (ASF) virus is a large enveloped DNA virus assembled in the cytoplasm of cells. In this study, the membrane compartments involved in the envelopment of ASF virus were investigated. A monoclonal antibody recognizing p73, the major structural protein of ASF virus, was generated to analyze the binding of p73 to membranes during the assembly of the virus. Approximately 50% of the intracellular pool of p73 associated with membranes as a peripheral membrane protein. Binding was rapid and complete within 15 min of synthesis. Subcellular membrane fractionation showed that newly synthesized p73 molecules cosedimented with endoplasmic reticulum (ER) membranes and remained associated with the ER during a 2-h chase. A similar distribution on gradients was recorded for p17, a structural membrane protein of ASF virus. The results suggested that the ER was involved in the assembly of ASF virus. A protease protection assay demonstrated a time-dependent envelopment of the membrane bound, but not cytosolic, pool of p73. Envelopment of p73 took place 1 h after binding to membranes and was completed 1 h before the first detection of p73 in virions secreted from cells. Envelopment was unaffected by brefeldin A and monensin, drugs that block membrane transport between the ER and Golgi. Taken together the results provide evidence for the binding of ASF virus structural proteins to a specific membrane compartment and implicate a role for the ER in the assembly and envelopment of ASF virus.

African Swine Fever Virus↗
PubMed2026

A smartphone-integrated plasmonic biosensor for amplification-free detection of African swine fever virus.

African Swine Fever Virus (ASFV) poses a catastrophic threat to global swine production, with recent outbreaks across Europe, Asia, and the Caribbean, significantly elevating the biosecurity risk to the United States' billion-dollar pork industry. Current diagnostic gold standards are laboratory-dependent and introduce critical delays in outbreak response. To address this gap, a plasmonic biosensor based on functionalized gold nanoparticles (GNPs) was developed for the rapid, amplification-free detection of ASFV. GNPs were surface-functionalized with 11-mercaptoundecanoic acid (MUDA) and combined in situ with ASFV-specific oligonucleotide probes targeting a conserved region of the p72 (B646L) gene. The detection mechanism relies on acid-induced aggregation: hybridization of target ASFV DNA to the probe generates a rigid duplex that shields the nanoparticles from acid-induced destabilization, maintaining a ruby-red color, whereas in the absence of target DNA the GNPs aggregate, producing a visible red-to-blue color shift. The optimized plasmonic biosensor demonstrated 100% analytical specificity, with no cross-reactivity against a panel of 19 non-target bacterial genomic DNA samples representative of the swine environment. Detection limits determined by the IUPAC 3σ criterion were 285 copies per reaction for Probe 1 and 402 copies per reaction for Probe 2, within the same order of magnitude as the qPCR reference assay run on the same dilution series (approximately 312 copies per reaction) under the experimental conditions used here. A smartphone-based Bio-Analytics App employing an RGB color-conversion algorithm served as a quantitative reader, yielding signal-to-noise ratios (S/N) that strongly correlated with benchtop spectrophotometric readings (A520/A620 ratio, R2 = 0.96) and achieved diagnostic concordance with qPCR binary calls. This platform offers a robust and low-cost (∼$2 per test), amplification-free approach to ASFV screening with potential for point-of-need deployment, subject to future validation in clinical specimens.

Journal Article↗
PubMed1986

Neutralization of African swine fever virus by sera from African swine fever-resistant pigs.

Sera from African swine fever-resistant pigs with infection-inhibitory activity decreased virus replication in infected porcine buffy coat cultures. This same effect was observed even after virus was adsorbed. The infection-inhibition was not reversed by removing the immune serum from the assay cultures. Reduction of African swine fever virus replication by immune sera was demonstrated by fluorescent focus assay on MS cell line cultures. Virus-neutralization tests showed a persistent fraction of non-neutralized virus, which was not demonstrable by infection-inhibition tests. One hypothesis for explaining this difference is proposed.

African Swine Fever↗
PubMed1986

In vitro and in vivo association of African swine fever virus with swine erythrocytes.

The association of African swine fever virus (ASFV) with swine erythrocytes in vivo, in high titers, was verified by inoculating 30 pigs with 17 ASFV isolates and assaying their plasma and washed erythrocyte fractions for residual virus. Viral antigens were specifically localized on the surface of in vitro and in vivo swine erythrocytes, using the fluorescent antibody technique and 3 monoclonal antibodies specific for ASFV. The same monoclonal antibodies immunoprecipitated virus-specific polypeptides of molecular weights 13 kd and 73 kd from ASFV-infected Vero cells. Erythrocytes from viremic swine infected with Lisbon-60, Dominican Republic, Badajoz-M98, or Cameroon isolates of ASFV were studied by transmission electron microscopy. Virus was found in membrane depressions at the surface of erythrocytes. These surface depressions resembled stages of smooth surfaced pits. Erythrocytes from viremic pigs were fragile osmotically.

African Swine Fever↗
PubMed1998

The African swine fever virus thymidine kinase gene is required for efficient replication in swine macrophages and for virulence in swine.

African swine fever virus (ASFV) replicates in the cytoplasm of infected cells and contains genes encoding a number of enzymes needed for DNA synthesis, including a thymidine kinase (TK) gene. Recombinant TK gene deletion viruses were produced by using two highly pathogenic isolates of ASFV through homologous recombination with an ASFV p72 promoter-beta-glucuronidase indicator cassette (p72GUS) flanked by ASFV sequences targeting the TK region. Attempts to isolate double-crossover TK gene deletion mutants on swine macrophages failed, suggesting a growth deficiency of TK- ASFV on macrophages. Two pathogenic ASFV isolates, ASFV Malawi and ASFV Haiti, partially adapted to Vero cells, were used successfully to construct TK deletion viruses on Vero cells. The selected viruses grew well on Vero cells, but both mutants exhibited a growth defect on swine macrophages at low multiplicities of infection (MOI), yielding 0.1 to 1.0% of wild-type levels. At high MOI, the macrophage growth defect was not apparent. The Malawi TK deletion mutant showed reduced virulence for swine, producing transient fevers, lower viremia titers, and reduced mortality. In contrast, 100% mortality was observed for swine inoculated with the TK+ revertant virus. Swine surviving TK- ASFV infection remained free of clinical signs of African swine fever following subsequent challenge with the parental pathogenic ASFV. The data indicate that the TK gene of ASFV is important for growth in swine macrophages in vitro and is a virus virulence factor in swine.

African Swine Fever↗