Foetuses of six seronegative gilts, two of which each respectively 35, 50 and 60 days pregnant, were inoculated intrauterinely with porcine parvovirus (PPV) and examined 7 and 11 days after inoculation. HI antibody was not detected in any of the foetuses although all but one gilt developed low levels of antibody. All but one of the foetuses inoculated with PPV died in utero prior to examination at 11 days after inoculation. Infection also spread to non-inoculated litter mates. Histological changes were mild in the gilts but there was widespread tissue necrosis in infected foetuses, and intranuclear inclusion bodies were observed in cells of the liver, lung, kidney and cerebellum. The increased survival of foetuses infected at later stages of gestation appeared to be related to increased numbers of mononuclear cells then present in many tissues.
Seven Anglo-Nubian goats, 5 months to 3 1/2 years old, developed clinical signs of increased respiratory rate, weight loss and exercise intolerance. Post-mortem examination of the goats revealed extensive consolidation of the lungs involving all lobes. Lesions, consisting of peribronchial and perivascular lymphoid cuffing, accumulations of homogeneous eosinophilic material in alveolar spaces, alveolar epithelialisation and thickening of alveolar septa as a result of lymphocytic infiltration, were detected histologically. A syncytial forming virus was consistently isolated from affected animals in explant cultures of lung, synovial membrane and choroid plexus. This agent had similar growth characteristics to the caprine arthritis-encephalitis (CAE) virus and the possible relationship between the respiratory disease and the diseases caused by the CAE virus is discussed.
A parvovirus was isolated during an outbreak of mummifications and abortions in a commercial piggery. Stillborn piglets from which virus was isolated or in which parvovirus antibody was detected had widespread inflammatory lesions. Lesions were also seen in apparently healthy piglets from affected litters.
Epstein-Barr virus (EBV) is a human herpes virus that infects over 90% of the world’s population and is linked to development of cancer. In immune-competent individuals, EBV infection is mitigated by a highly efficient virus-specific memory T-cell response. Risk of EBV-driven cancers increases with immune suppression (IS). EBV-seronegative recipients of solid organ transplants are at high risk of developing post-transplant lymphoproliferative disease (PTLD) due to iatrogenic IS. While reducing the level of IS may improve EBV-specific immunity and regression of PTLD, patients are at high risk for allograft rejection and need for immune-chemotherapy. Strategies to prevent PTLD in this vulnerable patient population represents an unmet need. We have previously shown that BZLF1-specific cytotoxic T-cell (CTL) expansion following reduced IS correlated with immune-mediated PTLD regression and improved patient survival. We have developed a vaccine to bolster EBV-specific immunity to the BZLF1 protein and show that co-culture of dendritic cells (DCs) loaded with a αDEC205-BZLF1 fusion protein with peripheral blood mononuclear cells (PMBCs) leads to expansion and increased cytotoxic activity of central-effector memory CTLs against EBV-transformed B-cells. Human–murine chimeric Hu-PBL-SCID mice were vaccinated with DCs loaded with αDEC205-BZLF1 or control to assess prevention of fatal human EBV lymphoproliferative disease. Despite a profoundly immunosuppressive environment, vaccination with αDEC205-BZLF1 stimulated clonal expansion of antigen-specific T-cells that produced abundant IFNγ and significantly prolonged survival. These results support preclinical and clinical development of vaccine approaches using BZLF1 as an immunogen to harness adaptive cellular responses and prevent PTLD in vulnerable patient populations.
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