Haemostatic abnormalities in African swine fever/A comparison of two virus strains of different virulence (Dominican Republic '78 and Malta '78)

Abstract

African swine fever (ASF) virus strains cause haemorrhage by producing a variety of defects, which vary in severity from strain to strain. To distinguish the main haemostatic defects leading to haemorrhage, two groups of pigs were infected with moderately virulent (Dominican Republic '78) and less virulent (Malta '78) ASF virus strains. Mortality rate and severity of clinical observations were greater in pigs infected with DR '78 virus compared with pigs infected with Malta '78 virus. The animals became febrile from day 3 to 4 onwards at a time when the viraemia was high (10(7) to 10(8) HAD50/ml). No difference was found during the period observed in their pattern of viraemia or pyrexia. Thrombocytopenia developed in both groups but with different kinetics, suggesting two different mechanisms of sequestration of platelets. When coagulation tests were performed, significant abnormalities were found, including evidence for disseminated intravascular coagulation. These abnormalities were much less pronounced in the group infected with Malta '78. Antithrombin III activity did not change significantly in either group. Decreased plasminogen activity was found in the early phase of disease in DR '78 infected pigs. These results indicate that when haemorrhage does occur in DR '78 infected pigs, it is a consequence of more pronounced degrees of haemostatic impairment probably due to a marked endothelial injury and/or generation of procoagulant activity.

Macrophage Transcriptional Responses following In Vitro Infection with a Highly Virulent African Swine Fever Virus Isolate

“…In contrast, the virus causes an acute hemorrhagic fever with high mortality rates in pigs, although some low-virulence isolates have been reported (6,33,50,52,53).…”

Species-Specific Variation in RELA Underlies Differences in NF-κB Activity: a Potential Role in African Swine Fever Pathogenesis

“…This is thought, in part, to be the result of a proinflammatory cytokine storm driven by infected macrophages (9,15,16,(42)(43)(44)56). Initiation of a systemic inflammatory response results in severe hematological and vascular perturbations, ultimately leading to cardiovascular collapse in a manner not dissimilar to septic shock (3,17,18,20,21,40,52,53). In addition to hemorrhage, severe widespread apoptosis of infected macrophages and uninfected lymphocytes is a prominent feature of the disease; this is also likely related to markedly elevated proinflammatory cytokine levels (19,33,37,43).…”

Preclinical Diagnosis of African Swine Fever in Contact-Exposed Swine by a Real-Time PCR Assay

“…ASF occurs in several disease forms, ranging from highly lethal to subclinical infections depending on contributing viral and host factors (7,9,14,15,20). Hemostatic and hemodynamic changes (hemorrhage, edema, ascites, and shock) resulting from intravascular activation of coagulation are observed in pigs following infection with highly virulent strains of the ASF virus (ASFV) (31)(32)(33). ASFV infects cells of the mononuclear-phagocytic system, including fixed tissue macrophages and specific lineages of reticular cells; affected tissues show extensive necrosis following infection with highly virulent viral strains (20,24).…”