ABSTRACT The EAV-HP group of chicken endogenous retrovirus elements was previously shown to be defective, with large deletions of the pol gene. In this report, we demonstrate that genomes of other Gallus species also maintain EAV-HP elements with similar deletions. The chicken EAV-HP1 locus was detected in both red ( Gallus gallus gallus ) and Sonnerat's ( Gallus sonneratii ) jungle fowl with identical integration sites, indicating that these elements had integrated before separation of the Gallus species. Furthermore, we demonstrate for the first time that the G. sonneratii genome carries EAV-HP elements with intact pol regions.
Increased levels of plasma corticosterone following administration of the hormone at 1, but not 2, weeks after exposure to avian leukosis virus (ALV) at hatching, significantly increased cloacal shedding of ALV in chickens that lacked maternal antibody (MAB) to ALV. Exposure of 2-week-old chickens, which had been exposed to virus at hatching, to heat- or cold-stress for 21 days had no effect on ALV infection and shedding. MAB significantly reduced or eliminated shedding in treated as well as in control chickens. Induced moulting or raised circulating corticosterone in adult hens did not influence the incidence of ALV infection or shedding.
Summary Studies have been made with the immunosuppressive drug cyclosporin A (CsA) to examine its value in the establishment of lymphoid tumour cell lines from Marek's disease (MD) lymphomas and from lymphoid cell cultures exposed to MD virus in vitro. CsA was shown to depress the proliferative response of normal spleen cells to phytohaemagglutinin, Coricanavalin A and pokeweed mitogen, and to a lesser extent to lipopolysaccharide. Short‐term proliferative responses of lymphoma cells were either not affected, depressed or stimulated by CsA. The efficiency of establishment of lymphoid cell lines from long‐term cultures of lymphoma cells was not increased by CsA, and the drug had a depressive effect on the proliferation of cell lines in the lympho‐cytoid stage. The majority of lymphoblastoid cell lines studied were stimulated by CsA. Interleukin 2 partially overcame the suppressive effect of CsA on the cell lines, and enhanced the stimulatory effects. Cultures of lymphoid cells exposed to MD virus in vitro were usually depressed by CsA; a few stimulatory combinations were observed, but these were not considered to be of biological significance. These results indicate that CsA suppresses normal T‐cell responses in the chicken, but that some MD‐associated lymphoid cells are stimulated by the drug, in some instances at least by a direct effect.
We describe the construction of a recombinant baculovirus containing the cloned DNA encoding the gp85 envelope glycoprotein of HPRS-103 (subgroup J) avian leukosis virus fused to the carboxy-terminus of the affinity tag glutathione-S-transferase. The fusion protein was efficiently secreted into the supernatant medium of the infected insect cell culture and could be purified in a single step using immobilized glutathione. An enzyme-linked immunosorbent assay using the recombinant protein was found to be specific and sensitive for detection of HPRS-103 virus-specific antibodies in the sera of infected birds.
HPRS-103, the prototype of avian leukosis virus (ALV) subgroup J, is a recently identified retrovirus associated with myeloid leukosis in meat-type chickens. Although this virus shows high sequence identity to other ALV subgroups within the gag and pol genes, its env gene is highly diverged (with only about 40% sequence identity) from other ALV subgroups. On the other hand, the sequence of the env gene of HPRS-103 was 75% identical to that of E51, a member of the EAV family of endogenous avian retroviruses. It is reported here that the chicken genome also contains another EAV-related element, EAV-HP, showing much greater sequence identity (over 97%) to the HPRS-103 env gene. Southern blotting analysis showed that EAV-HP-related sequences were distinct from EAV-O and were present in all lines of chicken examined and in grey jungle fowl, but were absent from several other avian species. The potential role of these endogenous sequences in the evolution of ALV subgroup J viruses is discussed.
HPRS-103, the prototype of avian leukosis virus (ALV) subgroup J, was isolated in 1989 from meat-type chickens from commercial flocks where it induces myelocytic myeloid leukosis (ML). The HPRS-103 env gene differs considerably from other ALV subgroups but shows high identity (75–97%) to env-like sequences of the different members of the EAV family of endogenous avian retroviruses. Recently, we have isolated several viruses related to HPRS-103 from cases of ML. Although these isolates showed properties of ALV subgroup J, the majority of them resisted neutralization by HPRS-103-specific serum, suggesting antigenic variation. The nucleotide sequence of the env gene of the variant viruses showed several substitutions resulting in amino acid changes especially clustered in the variable regions hr1, hr2 and vr3. Analysis of the data suggests that selection pressure, probably from the immune response, is driving the antigenic variation among the isolates. Phylogenetic analysis of the sequences showed the evolutionary relationships of the isolates with HPRS-103 and the EAV family of endogenous avian retroviruses. The epidemiological significance of the antigenic variation and the emergence of variant viruses are discussed.
The inoculation of turkeys with large doses of a virulent strain of Marek's disease virus (GA strain), but not of two other virulent strains (HPRS-16 and JM), was found to induce a disease resembling Marek's disease of the chicken. The most prominent lesions were lymphocytic leukaemia and lymphoid and reticular hyperplasia in the spleen and the liver. These developed after a prolonged latent period and the early histological changes (lymphoid cell destruction and reticuloendothelial cell hyperplasia) reported in chickens were not observed. Twelve cell lines were established from suspensions of spleen cells or of buffy coat cells from infected turkeys. These cells expressed both Marek's disease tumour-associated surface antigen and T-cell antigens. The cells carried the Marek's disease virus genome and when inoculated into chickens induced typical Marek's disease lymphomas. Nine of the cell lines were infected with an avian leukosis virus, but three lines were free of such infection. All cell lines had normal turkey karyotypes.
Avian leukosis virus of subgroup J (ALV-J), isolated in the late 1980s, predominantly causes myelocytic myeloid leukosis in meat-type chickens. In the past few years, we have observed the occurrence of lesions indicative of erythroblastosis in ALV-J-infected flocks and, in this paper, we report the isolation of ALV-J strains from such flocks. Three of these isolates were acutely transforming viruses, as shown by their ability to transform bone marrow cell cultures. The bone marrow cultures transformed by these virus isolates were very similar to the myeloid cells transformed by the ALV-J strain 966. However, the infection of meat-type chickens with these isolates either as embryos or as 1-day-old chicks resulted in the induction of erythroblastosis as well as myelocytomatosis. Other histopathological changes observed in the inoculated birds included neoplastic lesions such as cholangioma and testicular cell tumour, and non-neoplastic lesions such as lymphomyeloid hyperplasia. This report demonstrates that highly oncogenic ALV-J, capable of inducing a different spectrum of disease other than the widely reported myelocytomatosis, could be established in naturally infected flocks.
Marek's disease (MDV) virus is mainly known for the induction of visceral lymphomas and lymphoid infiltration of peripheral nerves. Recently, additional tropism for the central nervous system has been recognised as a distinct feature of disease induced by very virulent MDV isolates. During the analysis of changes in the peripheral blood leukocyte subpopulations in chickens infected with either a virulent (HPRS-16) or a very virulent (C12/130) strain of MDV, we observed a marked monocytosis in chickens infected with C12/130. Perivascular cuffing in brain and mononuclear cell infiltration into the meninges of chickens infected with C12/130 were associated with the appearance of the monocytosis from 6-10 days post-infection. Our results show that a peripheral blood monocytosis may be a contributory factor in establishing or accelerating the severity of mononuclear infiltration into the meninges and perivascular spaces in the brain during infection by very virulent C12/130 strain of MDV.
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