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PubMed2000

Neoplastic diseases: Marek's disease, avian leukosis and reticuloendotheliosis.

The commercially important neoplastic diseases of poultry are Marek's disease, which is caused by a herpesvirus, and the avian leukoses and reticuloendotheliosis, which are caused by retroviruses. These diseases are responsible for economic loss due to both mortality and depressed performance. Marek's disease virus (MDV) and avian leukosis viruses (ALVs) are prevalent throughout the world, and new strains which arise in particular locations may spread across borders, thereby undermining national disease control measures. Reticuloendotheliosis virus (REV) is also present in many countries. Marek's disease virus is transmitted horizontally only, and international spread in hatching eggs and day-old chicks can be prevented by appropriate hygiene precautions. Transmission of ALV and REV occurs both horizontally and vertically (through the egg), and measures to prevent international spread are more demanding. Marek's disease is controlled by vaccination, whilst avian leukosis is controlled by virus eradication programmes, mainly at the primary breeding level. Similar virus control measures can be applied for reticuloendotheliosis if necessary. No strong evidence exists to suggest that these avian tumour viruses constitute a danger to public health.

Animals↗
PubMed1984

Extensive homology exists between Marek disease herpesvirus and its vaccine virus, herpesvirus of turkeys.

Marek disease is a lymphomatous disease of chickens caused by infection of a herpesvirus, Marek disease virus (MDV). Marek disease is the only neoplastic disease for which a successful vaccine has been developed. The vaccine virus, herpesvirus of turkeys (HVT), is non-oncogenic in chickens. Despite the strong antigenic relationship between these viruses, previous studies showed that the two viral DNAs share little or no homology. Using less stringent hybridization conditions and methods that greatly improve the reassociation kinetics, we have reexamined the sequence homology between MDV and HVT DNA. We report here that HVT and MDV are far more closely related than previously reported. The homology between these two viral DNAs ranges between 70% and 80% at the nucleotide level and appears to extend over 90-95% of the respective genomes. Under the low stringency conditions used, MDV DNA fails to cross-hybridize with DNA from feline rhinotracheitis virus, an antigenically unrelated herpesvirus with a G-C content identical to that of MDV and HVT.

Base Sequence↗
PubMed2004

Study of host-pathogen interactions to identify sustainable vaccine strategies to Marek's disease.

Marek's disease virus is a highly cell-associated, lymphotropic alpha-herpesvirus that causes paralysis and neoplastic disease in chickens. The disease has been contained by vaccination with attenuated viruses and provides the first evidence for a malignant cancer being controlled by an antiviral vaccine. Marek's disease pathogenesis is complex, involving cytolytic and latent infection of lymphoid cells and oncogenic transformation of CD4+ T cells in susceptible chickens. Innate and adaptive immune responses develop in response to infection, but infection of lymphocytes results in immunosuppressive effects. The remarkable ability of MDV to escape immune responses by interacting with, and down-regulating, some key aspects of the immune system will be discussed in the context of genetic resistance. Resistance conferred by vaccination and the implications of targeting replicative stages of the virus will also be examined.

Animals↗
PubMed1982

Inverted repeat nucleotide sequences in the genomes of Marek disease virus and the herpesvirus of the turkey.

The DNAs of two herpesvirus, the oncogenic Marek disease virus and the serologically related herpesvirus of the turkey, were studied by electron microscopy. On the basis of fold-back molecules observed in single-stranded DNA from both viruses, structures have been derived from the overall nucleotide sequence arrangement in their genomes. Although differing in molecular weight, the genomes of Marek disease virus and turkey herpesvirus are both constructed according to the same plan--two regions of unique nucleotide sequence, each enclosed by inverted repeat sequence. The genome structure of these viruses therefore closely resembles that of herpes simplex virus rather than the biologically more similar herpesvirus Epstein--Barr virus, H. saimiri, and H. ateles.

Animals↗
PubMed1975

Immunization against Marek's disease using Marek's disease virus-specific antigens free from infectious virus.

Immunity against Marek's disease was conferred by the use of non-infectious materials extracted with non-ionic detergents from cells infected with the attenuated strain of Marek's disease virus (MDV). Antibody-free Rhode Island Red chicks were inoculated at 1 week of age with cell extracts emulsified in Freund's complete adjuvant and were given a second inoculation 1 week later without adjuvant. Protection against natural infection was obtained in groups inoculated with both soluble (not sedimented at 100,000 times g/2h) and insoluble antigens present in Nonidet P40 (NP40) extract, but only with the insoluble fraction of deoxycholate extract. The results suggest that the immunizing antigens can be partially solubilized with 0.5% NP40 and that the growth and spread of MDV are reduced in immunized chickens.

Animals↗
PubMedDate not supplied

The 132 bp repeats are present in RNA transcripts from 1.8 kb gene family of Marek disease virus-transformed cells.

Marek's disease virus (MDV) is an oncogenic, lymphotropic herpesvirus of chickens: Loss of its tumourigenic potential is believed to be associated with amplification of the 132 bp repeats from BamHI-D and BamHI-H fragments. We prepared cDNA libraries from RPL1 and MSB1 cell line and from the latter we identified a clone which spanned the 132 bp repeats within the BamHI-H fragment. By sequencing and Northern blot analysis we confirmed the presence of the 132 bp repeats. The analysis by PCR made on the total RNA revealed two 132 bp repeats in MDV transcripts from RPL1 and two to three repeats in transcripts from MSB1 cells. These results show that sequences within the 132 bp repeats are transcribed and are not spliced out as previously reported.

Base Sequence↗
PubMedDate not supplied

Comb lesions and mortality patterns in white leghorn layers affected by Marek's disease.

Marek's disease was diagnosed as the cause of prolonged high mortality in two commercial flocks of white leghorn layers by gross and microscopic examination of affected tissues and by immunofluorescent study of live tumor cells using anti-Marek's disease tumor-associated surface antigen, anti-immunoglobulin M, and monoclonal antibodies. The disease was characterized by swollen, necrotic, lymphomatous combs and mortality that rose above normal at 28 weeks of age, peaked at 35-36 weeks, and returned to normal by 45-46 weeks.

Animals↗
PubMed1999

High resolution mapping and identification of new quantitative trait loci (QTL) affecting susceptibility to Marek's disease.

Marek's disease (MD) is a lymphoproliferative disease of chickens that costs the poultry industry approximately $1 billion annually. Genetic resistance to MD is gaining increased attention to augment vaccinal control as disease outbreaks occur more frequently. Previously, analysis of a 272 F2 White Leghorn resource population measured for many MD traits and genotyped for 78 microsatellite markers revealed two and four quantitative trait loci (QTL) with significant and suggestive association, respectively, to one or more MD associated traits. Additional genetic markers have since been scored on the MD resource population to increase QTL resolution and genome coverage. Saturation of four of the QTL regions with 17 markers revealed five new QTL while 32 markers extended the genome coverage by 400 + CM and uncovered three more QTL. QTL analysis by single-point and interval mapping algorithms agreed well when marker saturation was approximately 20 CM or less. Currently 127 genetic markers cover approximately 68% of the genome that contain up to 14 MD QTL associated to one or more MD trait; seven at the significant level and seven at the suggestive level. Individually each QTL accounts for 2-10% of the variation and, in general, resistance was dominant although the resistant allele may come from either parental line. This study suggests that a limited number of genomic regions play a major role in the genetic control of MD resistance. Markers linked to these loci may be useful for selection of MD resistant stock by the poultry industry following verification of the association within their breeding populations.

Animals↗
PubMed1985

The structure of Marek disease virus DNA: the presence of unique expansion in nonpathogenic viral DNA.

DNA of Marek disease virus (MDV) consists of two unique regions UL and US flanked by long inverted repeat regions TRL and IRL, and short inverted repeat regions TRS and IRS, respectively, similar to herpes simplex virus DNA. Comparison of restriction patterns between pathogenic and nonpathogenic MDV DNA was made to identify a region of viral DNA different between these two types of MDV, as it may be responsible for the tumorigenicity of MDV in chickens. The results indicated that BamHI-D and -H, located at the long inverted repeat regions TRL and IRL, were specifically expanded in nonpathogenic viral DNA. The location of the expanded region has been determined within 1.5 kilobase pairs of the Bgl I/Pst I fragment of BamHI-D and -H, close to the junction between the inverted repeat and the unique region. The possibility that a gene responsible for tumor induction may be disrupted by such expansion has been discussed.

Animals↗
PubMed1976

Cyclophosphamide-induced amelioration of Marek's disease in Marek's disease-susceptible chickens.

Bursa- and thymus-dependent functions were examined in Marek's disease (MD)-susceptible normal chickens and in chickens treated with 5 and 16 mg of cyclophosphamide (CY) at the time of hatching. Chickens not exposed to Marek's disease virus (MDV) and treated with CY temporarily lost mitogenic response to concanavalin A but regained full response after 5 weeks. Bursa-dependent functions, such as presence of germinal centers in spleen and cecal tonsils, morphologic features of bursa, and sheep red blood cell antibody response were completely lost in chickens treated with 16 mg of CY and only partly retained in chickens treated with 5 mg of CY. In chickens exposed to MDV, the degree of thymus-dependent spleen cell mitogenic response was directly related to frequency and severity of MD. Chickens treated with 16 mg of CY had a mild mitogenic depression and low frequency and severity of MD lesions, whereas those treated with 5 mg of CY and those not treated had marked mitogenic depression and high frequency and severity of MD. Suppressions of bursa- and thymus-dependent functions by MDV alone were also evident when comparing MDV-exposed and nonexposed chickens. The results also indicate that presence of small, residual amounts of humoral factor(s) may enhance MDV oncogenesis.

Animals↗
PubMed1981

Influence of oncogenicity of Marek' disease virus on evaluation of genetic resistance.

Resistance to Marek's disease ( MD) is, in part, genetically determined and linked to the major histocompatability complex. The genetic resistance of 9 previously characterized lines of chickens and also of the inbred UCD-003 and 4 congenic lines was evaluated by challenge with JM-10. Five lines were highly resistant. These included the N-line and two derivatives from N-line (N-2 and N-5), PDRC strain, and one of the congenic UCD lines. The PDRC genotype is unknown, but the 3 related lines carry the B21 allele and the UCD line carries the BQ allele, which appears to be similar to B21. The UCD-003 and the other 3 congenic lines were moderately resistant while S-strain, P-2 and P-5 lines were highly susceptible to JM-10. The total MD incidence varied from 0 to 100% among the lines. Challenge with highly oncogenic virus isolates like GA-5, and especially the recently isolated RB-1B, caused high incidences of MD in all lines and, thus, did not permit differentiation of genetic resistance levels as was possible with the less oncogenic JM-10.

Animals↗
PubMed1992

Marek disease virus encodes a basic-leucine zipper gene resembling the fos/jun oncogenes that is highly expressed in lymphoblastoid tumors.

Marek disease virus (MDV) is a herpesvirus of chickens that induces T lymphomas within 3 weeks of infection. The short latency and polyclonal nature of MDV-induced tumors have suggested that the virus may encode one or more direct-acting oncogenes. To date, however, no MDV-specific tumor antigens or candidate transforming genes have been demonstrated. In this paper, we report the identification of a MDV gene encoding a protein with homology to the leucine-zipper class of nuclear oncogenes. It also contains a proline-rich domain characteristic of another class of transcription factors. This gene, designated meq, maps to the long repeat of MDV and is one of the few genes that are highly expressed in MDV-induced T-cell tumors. To our knowledge, a herpesvirus gene closely related to the fos/jun family of oncogenes has not been reported previously.

Amino Acid Sequence↗
PubMed1978

A comparative pathogenesis of two Mareks disease virus isolates.

The pathogenesis of the JM and GA isolates of Marek's disease virus (MDV) infection was compared by studying the sequential tissue distribution of MDV associated antigens with gross and microscopic lesions in infected chickens. With both MDV isolates the initial sites of viral replication were the lymphoid organs, skin, and featers. Both the GA and JM isolates were viscerotropic as demonstrated by the presence of MDV antigens with gross and microscopic changes occurring in several visceral organs. The JM isolate was more neurotropic and had a greater affinity for the gonads than the GA isolates as evidenced by an early detection of MDV antigens and severe pathology in the peripheral nerves and gonads.

Animals↗
PubMedDate not supplied

[Cloning and sequencing of genes coding the glycoproteins of antigens A and B of oncogenic strain JM of Marek disease virus (MDV)].

The genes encoding the precursors of secretory glycoprotein gp57-65 (A antigen) and glycoprotein complex gp100, gp60, gp48 (B antigen) of virulent strain JM of Marek's disease virus (MDV) have been cloned using PCR of viral DNA. Nucleotide sequences of both genes have been determined and amino acid sequence of the precursor peptides predicted, and compared with the corresponding sequences of other MDV strains. The results will be used for developing methods for the diagnosis of Marek's disease and vaccination against it.

Amino Acid Sequence↗
PubMedDate not supplied

Effect of infectious bursal agent on the response of chickens to Newcastle disease and Marek's disease vaccination.

White Leghorn chickens raised from one day old in an environment contaminated by the infectious bursal agent (IBA) had lower geometric mean titers (GMT) as measured by the hemagglutination-inhibition (HI) test to the Newcastle disease virus (NDV), than control Leghorns reared in an uncontaminated environment. Immunosuppression, defined as a reduction in GMT, was most pronounced at 35-56 days old for Leghorns vaccinated with NDV at 1 and 28 days or at 28 days. In a separate trial with broilers, immunosuppression was similar at 42-56 days old. This study also demonstrated that IBA infection in chickens increased susceptibility to Marek's disease (MD). The unvaccinated control chickens infected with IBA averaged 56.3% MD lesions, whereas unvaccinated controls not exposed to IBA averaged only 18.1% macroscopic lesions. It was also found that 20.7% of the HVT-vaccinated chickens exposed to IBA had gross MD lesions, whereas those HVT-vaccinated chickens reared in an environment free of IBA had 2.99% gross MD lesions.

Animals↗
PubMedDate not supplied

Effects of infectious bursal disease on Marek's disease vaccination: suppression of antiviral immune response.

Studies were made to determine whether infectious bursal disease virus (IBDV) infection would affect the response of chickens to turkey herpesvirus (HVT) vaccination in the development and level of HVT viremia and virus-neutralizing (VN) antibodies to HVT. The HVT viremia in the vaccinated chickens was not affected by IBDV, whether IBDV was inoculated simultaneously with HVT vaccination at one day of age or whether it was inoculated 3 weeks postvaccination with HVT. However, VN antibody response to HVT was significantly suppressed (P less than 0.001) when vaccinated chickens were exposed to IBDV either at the time of vaccination or at 3 weeks postvaccination. Such immunosuppression by IBDV of VN antibody response to HVT vaccination may result in a reduced antiviral immunity against Marek's disease virus.

Animals↗
PubMed1976

[Heterogeneity of a population of the Kekaya strain of Marek disease virus].

While infecting VMD-Kekava chick fibroblasts cultures two plaque-forming variants of the virus were isolated. Both variants are cell-associated viruses; during a prolonged period these are circulating in the blood of infected chicks, including also healthy ones. The cultures infected contain a common precipitating antigen; sera from the infected chicks have antibodies to VMD feather antigen, both viruses produced, although in a different degree, in the infected chicks lymphoid infiltration of nerve trunks typical for Marek's disease. These variants differ one from the other in the type of plaques formed by them in the tissue culture, and in their pathogenicity for chicks. Variant 83 is likely to be naturally attenuated virus, and further on it may be investigated as a vaccine strain.

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