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PubMed1997

Transformation of primary chick embryo fibroblasts by Marek's disease virus.

Marek's disease virus (MDV) is an alphaherpesvirus, which can mediate the malignant transformation of lymphocytes to form lymphomas in chickens. In this study, we demonstrate that MDV can transform primary chick embryo fibroblasts (CEF). The cell line derived from primary CEF infected with the GA strain of MDV was called CEM(MDV). The fibroblast nature of CEM(MDV) was verified by absence of cytokeratin type II. The CEM(MDV) phenotype differed from either primary CEF or MDV-infected CEF. CEM(MDV) were extensively vacuolated, with unusual multilamellar structures in the cytoplasm, The nuclei were considerably larger than those in primary CEF and were uniformly positive for proliferating cell nuclear antigen. The cell line was subcultured for more than 10 generations; however, CEM(MDV) did not support a fully productive MDV infection, because complete nucleocapsids were not detected and infectivity assays showed that cell line produced no infectious virus. PCR analyses demonstrated that this cell line carried both polypeptide 38 (pp38) and Meq DNA, MDV-specific genes associated with transformation. In addition, examination by laser scanning confocal microscopy revealed that CEM(MDV) constitutively produced MDV MEQ protein in nuclei and pp38 as well as glycoprotein B in the cytoplasm and on the plasma membrane. Growth in soft agar assay demonstrated that CEM(MDV) formed colonies, similar to HeLa and human melanoma cells. Retroviral insertion was not detected in DNA from the CEM(MDV) line.

Animals↗
PubMedDate not supplied

Comparison of a kinetic-based enzyme-linked immunosorbent assay (KELISA) and virus-neutralization test for infectious bursal disease virus. I. Quantitation of antibody in white Leghorn hens.

The kinetics of the enzyme-substrate reaction served to evaluate a single-serum-dilution indirect enzyme-linked immunosorbent assay (ELISA) for quantitating antibody in white leghorn hens inoculated with infectious bursal disease virus (IBDV) vaccines. The antibody profiles of primary and secondary responses induced by two IBDV immunization regimens were compared using a kinetic-based ELISA (KELISA) and the virus-neutralization (VN) test. KELISA was standardized with an IBDV-infected VERO cell suspension. Antigen was capable of binding minute quantities of sample (5 microliter) without requiring dilutions. Conjugate consisted of immunoglobulin G fraction of goat antiserum against chicken IgG bound to horseradish peroxidase. Neither test revealed a difference in antibody profiles between the two immunized groups. The KELISA was as efficient as the VN test in detecting antibody after vaccination and one log 2 unit more sensitive. The KELISA was suitable for testing large numbers of samples (n = 60) in a microplate compared with a conventional ELISA (n = 8).

Animals↗
PubMed2006

Interaction of MEQ protein and C-terminal-binding protein is critical for induction of lymphomas by Marek's disease virus.

Marek's disease virus (MDV) is an oncogenic herpesvirus that induces fatal T cell lymphomas in chickens. With more than 20 billion doses of vaccine used annually, vaccination constitutes the cornerstone of Marek's disease control. Despite the success of vaccination, evolution of virulence among MDV strains continues to threaten the effectiveness of the current Marek's disease vaccines. MDV-encoded protein MEQ (MDV EcoRI Q) probably acts as a transcription factor and is considered to be the major MDV oncoprotein. MEQ sequence shows a Pro-Leu-Asp-Leu-Ser (PLDLS) motif known to bind C-terminal-binding protein (CtBP), a highly conserved cellular transcriptional corepressor with roles in the regulation of development, proliferation, and apoptosis. Here we show that MEQ can physically and functionally interact with CtBP through this motif and that this interaction is critical for oncogenesis because mutations in the CtBP-interaction domain completely abolished oncogenicity. This direct role for MEQ-CtBP interaction in MDV oncogenicity highlights the convergent evolution of molecular mechanisms of neoplastic transformation by herpesviruses because Epstein-Barr virus oncoproteins EBNA 3A and 3C also interact with CtBP. We also demonstrate that the nononcogenic MDV generated by mutagenesis of the CtBP-interaction domain of MEQ has the potential to be an improved vaccine against virulent MDV infection. Engineering MDV with precisely defined attenuating mutations, therefore, represents an effective strategy for generating new vaccines against this major poultry disease.

Alcohol Oxidoreductases↗
PubMed1998

Fowl adenovirus recombinant expressing VP2 of infectious bursal disease virus induces protective immunity against bursal disease.

The right hand end Nde I fragment 3 (90.8-100 map units) of the fowl adenovirus serotype 10 (FAV-10) was characterised so as to allow the location of an insertion site for recombinant vector construction. Infectious bursal disease virus (IBDV) VP2 gene from the Australian classical strain 002/73, under the control of the FAV-10 major late promoter/leader sequence (MLP/LS) was inserted into a unique Not I site that was generated at 99.5 map units. This recombinant virus was produced without deletion of any portion of the FAV-10 genome. When administered to specific pathogen free (SPF) chickens intravenously, intraperitoneally, subcutaneously or intramuscularly, it was shown that the FAV-10/VP2 recombinant induced a serum VP2 antibody response and protected chickens against challenge with IBDV V877, an intermediate virulent classical strain. Birds were not protected when the recombinant was delivered via the conjunctival sac.

Animals↗
PubMed2006

Spread of plant virus disease to new plantings: a case study of rice tungro disease.

The spread of plant virus disease between fields is reviewed for several horticultural and agricultural crops. Previous studies have focused on cropping systems where there is scope for using separation in time and space to reduce the potential for virus spread between plantings. In our study, data are presented on virus disease spread between fields in an irrigated rice area in the tropics where crops are grown continuously throughout the year. An intensive survey was conducted in rice fields planted from November 1992 to October 1994 in which the occurrence of new infections of rice tungro virus disease was recorded. The effect of a number of variables on disease incidence, including the proximity of a field to inoculum sources, was examined using ordinal regression analysis. Primary infection showed large seasonal fluctuation. In addition, the number of leafhopper vectors had a significant effect, as did the tungro vector resistance of the rice variety grown. The distance to nearest inoculum source and the tungro incidence of this source significantly affected the level of infection occurring in a vulnerable field. The results are discussed in relation to management strategies to reduce the spread of tungro disease between fields in irrigated lowland rice cropping systems.

Crops, Agricultural↗
PubMed2004

Avian adenovirus CELO recombinants expressing VP2 of infectious bursal disease virus induce protection against bursal disease in chickens.

To develop a CELO virus vector that can induce protection against infectious bursal disease, CELO viruses expressing the host-protective antigen VP2 of infectious bursal disease virus (IBDV) were constructed. In the engineered recombinants, the VP2 gene (the 441-first codons of the IBDA polyprotein) was placed under the control of the CMV promoter. Two positions in the CELO genome were chosen to insert the VP2 expression cassette. The recombinants were found apathogenic, when inoculated by different routes and even at high doses (up to 10(8) per animal). Chickens vaccinated oro-nasally with these different recombinants and challenged with very virulent IBDV were found to be poorly protected. In contrast, when inoculated with one or two (subcutaneous or intradermic) injections of CELOa-VP2, the chickens showed no clinical signs and no mortality after challenge. In the vaccinated chickens, the titers of neutralization antibody reached 7-9 values, showing that protection could be explained by the induction of a sufficient humoral response. After challenge, the weight ratio Bursa of Fabricius/body was about 2.5 per thousand, a value similar to that obtained with the commercial Bur706 vaccine. However, histological lesions in the Bursa of Fabricius were observed, showing that a complete protection was not totally achieved. Contact transmission was evidenced. Protection was also obtained when inoculation of CELOa-VP2 was carried out in ovo. Prime-boost strategies were also tested with the CELOa-VP2 vector used in association with the purified VP2 antigen, or DNA encoding VP2 or a CELO vector expressing chicken myeloid growth factor (cMGF). None of these regimens were shown to substantially increase the level of protection when compared to double CELOa-VP2 inoculations. These results indicate that CELO-based vectors are useful to safely induce a strong protective immunity against vvIBDV in chickens.

Animals↗
PubMed2002

Protective effect of avian myelomonocytic growth factor in infection with Marek's disease virus.

Marek's disease virus (MDV) is a herpesvirus that induces T lymphomas in chickens. The aim of this study was to assess the role of the macrophage activator chicken myelomonocytic growth factor (cMGF) in controlling MDV infection. B13/B13 chickens, which are highly susceptible to MD, were either treated with cMGF delivered via a live fowlpox virus (fp/cMGF) or treated with the parent vector (fp/M3) or were left as untreated controls. Seven days later, when challenged with the very virulent RB-1B strain of MDV, the spleens of chickens treated with fp/cMGF showed increased expression of the inducible nitric oxide synthase (iNOS) gene compared to those of control chickens and fp/M3-treated chickens. Increased iNOS gene expression was also accompanied by greater induction of gamma interferon and macrophage inflammatory protein (K203) gene expression, both possible activators of iNOS. fp/cMGF treatment also increased the number of monocytes and systemic NO production in contrast to fp/M3 treatment. Even though cMGF treatment was unable to prevent death for the chickens, it did prolong their survival time, and viremia and tumor incidence were greatly reduced. In addition, cMGF treatment improved the partial protection induced by vaccination with HVT (herpesvirus isolated from turkeys) against RB-1B, preventing 100% mortality (versus 66% with vaccination alone) and greatly reducing tumor development. Treatment with fp/M3 did not have such effects. These results suggest that cMGF may play multiple roles in protection against MD. First, it may enhance the innate immune response by increasing the number and activity of monocytes and macrophages, resulting in increased NO production. Second, it may enhance the acquired immune response, indicated by its ability to enhance vaccine efficacy.

Animals↗
PubMed1977

Restitution of hemagglutinating activity to spikeless particles of HVJ (Sendai virus) by glycoprotein components of Newcastle disease virus.

Spikeless particles of HVJ (Sendai virus) lacking in hemagglutinating (HA) activity were obtained by enzymatic digestion of virions with trypsin followed by centrifugation through a sucrose gradient. When they were mixed with glycoprotein components of Newcastle disease virus (NDV) obtained by treatment of purified virions with deoxycholate (DOC), the mixture showed hemagglutination reaction, which was inhibited by anti-NDV serum, but not by anti-HVJ serum. Sedimentation profile of the HA active agents was then examined by centrifugation of the mixture of spikeless particles of HVJ (labeled with 3H-uridine) and glycoproteins of NDV (labeled with 14C-amino acid mixture). The results showed that the peak of HA activity had both of the radioactivities, and that the sedimentation rate of the HA was faster than that of spikeless HVJ but slower than that of intact HVJ. Electron micrographs of such HA active structures showed that they were morphologically closely similar to intact virion of HVJ, although they had neither hemolytic activity nor infectivity. The mixture of spikeless HVJ and glycoproteins of HVJ or NDV which were removed from virions by proteolytic enzymes, on the other hand, did not show any detectable hemagglutinating activity.

Deoxycholic Acid↗
PubMedDate not supplied

Comparison of a kinetic-based enzyme-linked immunosorbent assay (KELISA) and virus-neutralization test for infectious bursal disease virus. II. Decay of maternal antibody in progeny from white Leghorns receiving various vaccination regimens.

A computer-assisted single-serum-dilution indirect kinetic-based enzyme-linked immunosorbent assay (KELISA) was used for quantitating the natural decay rate of infectious bursal disease virus (IBDV) maternal antibody in progeny obtained from white leghorn breeders. The KELISA results were compared with those of a standard virus-neutralization (VN) test. Pullets were subjected to two IBDV immunization regimens. Group 1 was vaccinated at weeks 0, 2, and 10 with two live vaccines in drinking water and at week 20 with an oil-emulsified (SC) IBDV vaccine, group 2 received only the first and last immunizations, and group 3 served as the unvaccinated control. Pullets were artificially inseminated at 28 weeks of age. Progeny chicks from each group were bled every other day for 47 days. Both KELISA and VN test detected linear relationship in the decay of maternal antibodies. The VN test detected no significant differences (P greater than 0.05) in the IBDV maternal antibody titers at day 1 or in the rate of decay between the progeny from groups 1 and 2. The VN maternal antibody titers decreased at a rate of 0.16 log2 titer per day. In contrast, KELISA revealed higher IBDV maternal antibody titers in day-old progeny from pullets vaccinated 4 times (log2 = 14.3). However, KELISA titers of progeny from this group decreased at a faster rate than titers of progeny from pullets vaccinated twice (0.20 vs. 0.13 log2 titer per day).

Animals↗
PubMed1996

Apoptosis and CD8-down-regulation in the thymus of chickens infected with Marek's disease virus.

Marek's disease virus (MDV)-infected chickens show thymic atrophy during the acute phase of infection. We examined whether the thymic atrophy by MDV-infection was mediated by apoptosis. Apoptosis-specific DNA ladderings were clearly observed in thymocytes one week after MDV-infection. Histological and flow cytometry studies revealed that immature CD4+ CD8+ thymocytes underwent apototic cell death. In addition, the expression level of CD8 molecules on both CD4(-)CD8+ and CD4+ CD8+ thymocyte populations was down-regulated in the infected chickens. These thymic changes might be involved in the pathogenesis of Marek's disease.

Animals↗
PubMed1996

Susceptibility of hares and rabbits to the European brown hare syndrome virus (EBHSV) and rabbit haemorrhagic disease virus (RHDV) under experimental conditions.

The European brown hare syndrome virus (EBHSV) and the rabbit haemorrhagic disease (RHDV) virus were inoculated in hares and rabbits to discover whether the homologous and heterologous host could be infected. The aims were to confirm the results of previous studies that showed the existence of antigenic differences between these two viruses, and also to define the role attributed to the hare in transmission to rabbits of a disease, EBHS, initially mistaken for RHD. During the trials, clinical symptoms and pathological lesions were noted, and virological and serological analysis were conducted, using specific tests set up for both diseases. The hares infected with EBHSV died of an acute form of EBHS, whereas the rabbits remained healthy. The low serological response in these rabbits towards the EBHSV did not protect them against RHDV. Similarly, hares inoculated with RHDV remained healthy and showed a low anti-RHDV antibody titre but died when challenged with EBHSV.

Animals↗
PubMed1999

T-cell transformation by Marek's disease virus.

Marek's disease virus (MDV) is an avian herpesvirus that causes rapid development of T-cell lymphomas in chickens. The MDV genes currently thought to be involved in lymphomagenesis include a bZIP transactivator that is homologous to fos and jun oncogenes but do not appear to have counterparts in other oncogenic herpesviruses.

Animals↗
PubMed1995

Development of a sustainable chick cell line infected with Marek's disease virus.

Marek's disease virus (MDV) is a highly infectious and cell-associated avian herpesvirus. Fully productive infections with MDV are restricted to feather follicle epithelium of afflicted birds. In culture, MDV infection of primary chick (CEF) and duck embryo fibroblast cells is semiproductive. Passage of MDV and production of MDV vaccines is limited to these primary cell-associated systems. The finite life span of primary avian cell cultures has hampered efforts to use positive selection in generation of recombinant MDV and complicates studies of temporal gene regulation. In this report, we describe continuous chick fibroblast cell lines (MDV OU2.2 and MDV OU2.1) which support MDV replication. Southern blot and PCR analyses demonstrate that these cell lines harbor MDV DNA. Western blot analyses indicate that MDV OU2.2 cells express at least a limited set of viral proteins, pp38 and pp14, similar to that seen in MDV-lymphoblastoid cells. Presence of distinct plaques in confluent MDV OU2.2 cell monolayers is consistent with cytolytic semiproductive infection, similar to that observed in primary CEF. MDV OU2.2 cells are capable of transferring MDV infection to primary CEF cultures and inducing clinical signs of Marek's disease in susceptible birds. MDV OU2.2 cells have maintained a MDV-positive phenotype for over 16 months of active culture. Southern blot hybridization of MDV OU2.2 cell DNA reveals a distinct expansion of the MDV BamHI H fragment in a subset of viral genomes following long-term cultivation.

Animals↗
PubMed2003

Infection of macrophages by a lymphotropic herpesvirus: a new tropism for Marek's disease virus.

Marek's disease virus (MDV) is classified as an oncogenic lymphotropic herpesvirus of chickens. MDV productively and cytolytically infects B, alphabetaT and gammadeltaT lymphocytes and latently infects T-helper lymphocytes. The aims of this study were to identify whether MDV infects macrophages in vivo and, if so, whether quantitative differences in macrophage infection are associated with MDV strain virulence. Chickens were infected with either virulent MDV (HPRS-16) or 'hypervirulent' MDV (C12/130). Flow cytometry with monoclonal antibodies recognizing MDV pp38 antigen and leukocyte antigens was used to identify MDV lytically infected cells. Macrophages from HPRS-16- and C12/130-infected chickens were pp38(+). It is demonstrated that macrophages are pp38(+) because they are infected and not because they have phagocytosed MDV antigens, as assessed by confocal microscopy using antibodies recognizing MDV antigens of the three herpesvirus kinetic classes: infected cell protein 4 (ICP4, immediate early), pp38 (early) and glycoprotein B (gB, late). Spleen macrophages from MDV-infected chickens were ICP4(+), pp38(+) and gB(+), and ICP4 had nuclear localization denoting infection. Finally, MDV pp38(+) macrophages had high inherent death rates, confirming cytolytic MDV infection, although production of virus particles has not been detected yet. These results have two fundamental implications for understanding MDV pathogenesis: (i) MDV evolved to perturb innate, in addition to acquired, immunity and (ii) macrophages are excellent candidates for transporting MDV to primary lymphoid organs during the earliest stages of pathogenesis.

Animals↗
PubMed2000

Biochemical characterization of salmon pancreas disease virus.

Salmon pancreas disease virus (SPDV) has been shown to cause severe economic losses in farmed Atlantic salmon (Salmo salar) and has been reported to occur in Europe, Scandinavia and the United States. This paper describes the biochemical characterization of SPDV in terms of its RNA and protein composition. SPDV was purified by precipitation from infected Chinook salmon embryo (CHSE-214) cell-culture supernatant and sucrose density-gradient centrifugation. Fractions containing virus were identified by an immunodot blot assay using an SPDV-specific MAb. Two major proteins with molecular masses of approximately 55 and 50 kDa, putatively identified as the E1 and E2 alphavirus glycoproteins respectively, were detected when purified virus preparations were analysed by PAGE. Radiolabelling experiments indicated that SPDV infection of CHSE-214 cells did not shut-off host-cell protein synthesis, making attempts to identify virus-specific proteins unsuccessful. However, radioimmunoprecipitation assay (RIPA) experiments showed that two SPDV-specific MAbs reacted with a protein in the 50-55 kDa range. Northern blot hybridization with cloned cDNA probes indicated that infected cells contained RNA species of approximately 11.4 and 4 kb, which correspond to the genomic and subgenomic RNAs specified by SPDV. The results described are consistent with SPDV being characterized as an alphavirus.

Alphavirus↗
PubMed2003

The RNA subunit of telomerase is encoded by Marek's disease virus.

Marek's disease virus (MDV) is a herpesvirus of chickens that induces T lymphomas and tumors within 4 to 5 weeks of infection. Although the ability of MDV to induce tumors was demonstrated many years ago and although a number of viral oncogenic proteins have been identified, the mechanism by which the MDV is implicated in tumorigenesis is still unknown. We report the identification of a virus-encoded RNA telomerase subunit (vTR) within the genome of MDV. This gene is found in the genomic DNA of the oncogenic MDV strains, whereas it is not carried by the nononcogenic MDV strains. The vTR sequence exhibits 88% sequence identity with the chicken gene (cTR). Our functional analysis suggests that this telomerase RNA can reconstitute telomerase activity in a heterologous system (the knockout murine TR(-/-) cell line) by interacting with the telomerase protein component encoded by the host cell. We have also demonstrated that the vTR promoter region is efficient whatever the species of cell line considered and that vTR is expressed in vivo in peripheral blood leukocytes from chickens infected with the oncogenic MDV-RB1B and the vaccine MDV-Rispens strains. The functionality of the vTR gene and the potential implication of vTR in the oncogenesis induced by MDV is discussed.

Animals↗
PubMedDate not supplied

Serological characteristics of a membrane glycoprotein gp82 of Marek's disease virus.

Marek's disease virus (MDV) is a cell-associated herpesvirus of gallinaceous fowl. Glycoproteins of herpesviruses have been reported to be important in stimulating humoral and cell-mediated immune responses against viral infection. At least eight glycoproteins of MDV have been identified, and glycoprotein B (gB) has been reported to produce protective immunity. In addition to glycoproteins, other cell membrane proteins may also be important for engendering immunity. In an attempt to determine whether the protein is involved in immune responses, we developed three monoclonal antibodies (Mabs) and rabbit polyclonal antibodies specific for MDV membrane protein gp82. Three Mabs (Mab2.1, 3.7, and 5.7) were produced by using TrpEgp82 fusion protein as the immunogen that was expressed by recombinant pATH expression vector pATHgp82 in Escherichia coli. Indirect immunofluorescence assay (IFA), immunoprecipitation, and Western blot analysis were used to determine the characteristics of gp82. All of the Mabs reacted with gp82 protein irrespective of its conformation. The gp82 protein was predominantly anchored on the surface membrane of a chicken embryo fibroblast (CEF) infected with serotype 1 MDV (MDV-1). There was no detectable immunofluorescence staining in the cytoplasm or nucleus in the MDV-1-infected CEFs. These results indicate that gp82 is a membrane protein. The distribution pattern of immunofluorescence staining of gp82 varies between CEFs infected with the low passage MDV-1 isolate Md11, and those infected with a high passage derivative, Md11/75c. In SB-1 (Serotype 2 MDV [MDV-2]) and Turkey herpesvirus (HVT) (serotype 3 MDV [MDV-3]) infected CEFs, gp82 was not detected by immunoprecipitation, Western blot, or IFA using both monoclonal and polyclonal antibodies. These results suggest that gp82 in serotype 2 or 3 has a modified epitope, or that the gene is permanently repressed.

Animals↗