Virulent African Swine Fever Virus Research Articles

African swine fever virus encodes a gene with extensive homology to type II DNA topoisomerases

Nucleotide sequencing of a virulent African swine fever virus (ASFV) isolate (Malawi LIL20/1) identified an open reading frame of 1191 amino acid residues encoding a protein of 134·9 kDa. This gene mapped to the SalI i and j restriction endonuclease fragments of the ASFV genome. The predicted polypeptide was found to share 21·1% identity over a 1077 amino acid region with the human type II DNA topoisomerase. The sequence is compared to other type II DNA topoisomerases and the possible roles in ASFV replication are discussed.

Genetic variation of african swine fever virus: Variable regions near the ends of the viral DNA

Restriction endonuclease maps of the variable DNA regions of African swine fever virus field isolates from the Iberian peninsula showed that the changes in length are located in the terminal-inverted repetitions and in unique sequences close to the DNA ends. Analysis of nine clones derived from the spleen of an infected pig revealed the existence of frequent length changes within the inverted terminal repetitions. In each clone, changes occurred symmetrically at both terminal-inverted repetitions, suggesting the existence of a terminal-inverted repetition transposition or correction mechanism. Large deletions in unique sequences were detected more frequently in the region located from 8 to 20 kb from the left DNA end. The analysis of this DNA segment from a virulent African swine fever virus isolated in Lisbon (LIS57) showed that this virus strain contains about 8 kb more DNA sequence than the prototype avirulent virus strain (BA71). Hybridization of the additional sequences from LIS57 virus with DNA from different virus field isolates revealed that this DNA region is highly variable in vivo and that it contains several repeated sequences. DNA sequences present around the deletion end points in the variable regions indicate that the deletion process may take place by both homologous and non homologous recombination.

Formula omitted] and [formula omitted] effects of moderately virulent African swine fever virus on mitogenesis of pig lymphocytes

Six pigs were infected oro-nasally with a moderately virulent African swine fever (ASF) virus from the Dominican Republic (DR II). The effect of virus infection on the pig's immune system was tested by measuring peripheral leucocyte numbers and the ability of mononuclear leucocytes (MNL) to respond by lymphocyte proliferation (LP) to the mitogens phytohemmagglutinin-P (PHA-P), concanavalin-A (Con-A), and pokeweed mitogen (PWM). All 6 pigs developed high viremias between 4 and 18 days post-inoculation (DPI) which became undetectable by 32 to 46 DPI. Virus was found in erythrocytes, plasma, and mononuclear leucocytes from peripheral blood. Overall, virus infection had only minor effects on the number of circulating leucocytes, lymphocytes, monocytes and granulocytes. At the early acute phase of infection slight neutrophilia and lymphocytopenia were observed with mildly elevated monocyte numbers and slightly depressed neutrophil numbers that continued from the time of evident reduction in viremia to beyond the period of viral clearance. The infected pigs readily produced high titers of ASF virus antibody shortly after the onset of viremia. No significant differences in LP responses of MNL from the 6 pigs to PHA-P, Con-A and PWM were observed after infection when compared to those obtained with MNL from normal pigs. The in vitro addition of infectious ASF virus to MNL from normal pigs did not affect LP responses to any of the three mitogens. These results do not support the hypothesis that immunosuppression is a consequence of ASFV infection of pigs.

The replication of virulent and attenuated strains of African swine fever virus in porcine macrophages.

The replication of virulent and attenuated strains of African swine fever virus (ASFV) was studied in pure cultures of swine macrophages. To ensure complete destruction of the macrophage monolayers about 50--100 times more virulent ASFV was needed than attenuated virus although both isolates could be used to establish persistently infected cultures. Interferon did not appear to influence virus yields from such cultures. Fluorescent and electron microscopy studies of infected macrophages suggested that the cycle of infection of the two isolates was different.

The Growth of Virulent African Swine Fever Virus in Pig Monocytes and Macrophages

The replication of virulent African swine fever virus (ASFV) in cultures of monocytes and macrophages derived from pig bone marrow (PBM) and pig leukocyte (PL) cells was investigated by light microscopy, immunofluorescence, haemadsorption and infective virus release. Monocytes showed a high rate of infection and complete destruction within 2 to 3 days, whereas macrophages had only a very low level of infection and survived to form persistently infected cultures. These observations may explain the decrease in sensitivity of PBM and PL cells for ASFV assay after extended periods of incubation and suggest that the macrophage may be one of the cell types concerned with virus persistence in the pig.

African swine fever virus replication in porcine lymphocytes.

Purified preparation of porcine lymphocytes were infected with three isolates of virulent African swine fever virus (ASFV). Electron microscopy showed the presence of small numbers of mature virus particles in degenerating cells. The titres of infective virus released were low and reached a maximum by 24 h after infection.