Notes on the mechanism of postvaccination immunity in Marek's disease.
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Abstract:
The investigated 16th and 45th in vitro passages of non-pathogenic variant 83 of the Kekava strain Marek's disease virus have led in chickens to resistance to Marek's disease by introduction of the above-mentioned virus 14 days before application of pathogenic variant 55 of the Kekava strain Marek's disease virus. Simultaneous administration of both variants of the Kekava strains Marek's disease virus did not protect chickens from the disease. Presence in those variants of the Kekava strain Marek's disease virus of genetic markers manifesting themselves on passaging the virus in chicken fibroblast cultures created the possibility to investigate interrelations between them in the organism of chickens, utilizing in isolation of the virus the method of infecting cultures with chicken fibroblasts. The results of isolation of the virus from the blood cells of vaccinated chickens have shown that in their organism there is interference between those virus variants since the frequency of isolation of the pathogenic virus variant was 3-times lower than that of the apathogenic Kekava strain Marek's disease virus, and both virus variants persisted in various cells. After simultaneous administration of both virus variants to chickens equal amounts of the pathogenic and of the apathogenic Kekava strain Marek's disease virus were isolated from their blood cells. In that case also persistance of both virus variants in one cell may occur.Keywords:
Marek's disease
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A Marek's disease (MD) virus (MDV) strain was isolated in Jilin province from diseased chickens that had been vaccinated by turkey herpesvirus. The isolate was adapted to grow in chick embryo fibroblasts (CEF). Artificial infection of SPF chickens with the virus produced typical clinical symptoms of MD. The isolate was highly pathogenic and caused 76 % and 72 % morbidity in unvaccinated and HVT-vaccinated chickens, respectively. Analysis of 132 bp repeat sequence and meq gene sequences of the viral genome showed that the virus isolate belongs to the highly virulent MDV strains.
Marek's disease
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Isolation
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The investigated 16th and 45th in vitro passages of non-pathogenic variant 83 of the Kekava strain Marek's disease virus have led in chickens to resistance to Marek's disease by introduction of the above-mentioned virus 14 days before application of pathogenic variant 55 of the Kekava strain Marek's disease virus. Simultaneous administration of both variants of the Kekava strains Marek's disease virus did not protect chickens from the disease. Presence in those variants of the Kekava strain Marek's disease virus of genetic markers manifesting themselves on passaging the virus in chicken fibroblast cultures created the possibility to investigate interrelations between them in the organism of chickens, utilizing in isolation of the virus the method of infecting cultures with chicken fibroblasts. The results of isolation of the virus from the blood cells of vaccinated chickens have shown that in their organism there is interference between those virus variants since the frequency of isolation of the pathogenic virus variant was 3-times lower than that of the apathogenic Kekava strain Marek's disease virus, and both virus variants persisted in various cells. After simultaneous administration of both virus variants to chickens equal amounts of the pathogenic and of the apathogenic Kekava strain Marek's disease virus were isolated from their blood cells. In that case also persistance of both virus variants in one cell may occur.
Marek's disease
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The HPRS-24 strain of Marek's disease herpesvirus was selected for closer study from a group of virus isolates that appeared apathogenic under standard test conditons. Protection studies revealed an immunological relationship between this virus strain and acute Marek's disease herpesvirus. In chicken kidney cell cultures, the HPRS-24 strain caused small and slowly developing plaques, and the proportion of infected cells was less than with other strains. In chicken embryo fibroblast cultures, this virus multiplied rapidly, yielding a comparatively high proportion of infected cells. Electron microscopic studies revealed that infected fibroblasts contained more enveloped virus particles than those infected with other strains of Marek's disease herpesvirus. Infectious cell-free virus was extracted from cultured fibroblasts with titres high enough for use in neutralization studies. Cross-neutralization, immunofluorescence and precipitin tests served for serological comparison of the HPRS-24 strain with turkey herpesvirus and representatives of acute and classical Marek's disease herpesvirus. Antibody titres were 4-10 times higher against the homologous than against the heterologous virus strains. Qualitative differences between precipitating "A" antigens were characterized by spur line patterns of precipitation bands. These results suggest that the group of Marek's disease and turkey herpesviruses consists of at least three serological types. One of them is represented by the HPRS-24 strain of apathogenic Marek's disease virus. The other two types comprise pathogenic strains of Marek's disease virus and their attenuated variants, and turkey herpesvirus.
Marek's disease
Precipitin
Immunofluorescence
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Pseudorabies
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Marek's disease
Replication
Herpes virus
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Abstract A chicken lymphoblastoid cell line (TLT)‐6855 originally established from an avian oncornavirus‐induced lymphoma (Siegfried and Olson, 1972) was studied for the presence and expression of Marek's disease virus (MDV) genome. By nucleic acid hybridization a significant amount of MDV DNA was found in this cell line. This virus DNA, however, was not expressed in either virus‐specific intracellular or membrane antigens or the MD‐associated tumour‐specific surface antigen (MATSA). Moreover, MDV‐specific antigens could not be activated in this cell line by treatment with 5‐IdUrd. In several experiments, when chickens were inoculated with the cell line a herpesvirus was repeatedly isolated from the kidneys. This herpesvirus was antigenically similar to MDV but was low in oncogenicity for chickens.
Marek's disease
Lymphoblast
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Marek's disease is the most commonly occurring neoplasm of any animal population and until recently it has caused extensive economic loss globally. Marek's virus, an actively evolving virus is the causative agent. Now with the virus's genetic code in hand we could easily characterise the immunogenic proteins of the closest relative of the virus, the Herpes virus of Turkey's.The important glycoprotein genes gC, gD,and gI of an isolated strain of Herpes virus of Turkey's were amplified, cloned in pGEM T-Easy vector and sequenced as an initial step in developing a recombinant vaccine against Marek's Disease. The recombinant genes were analysed and sequence data confirmed that the isolated strain was HVT (FC126), a vaccine strain.
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More than 200 cells were cloned from populations of mammalian cells persistently infected with Japanese encephalitis virus. Only four cloned cultures contained cells that had viral antigen measurable by immunofluorescence and that released infectious virus, yet all clones harbored virus-specific RNA. Superinfection of cloned cells with wild-type Japanese encephalitis virus did not produce cytopathic effects, but resulted in production of viral antigen and infectious virus in formerly nonproducing clones. Cocultivation of nonproducer clone cells with normally permissive cells did not induce virus production, nor did treatment of nonproducer clones with various inhibitors of DNA, RNA, or protein synthesis. It is suggested that the cloning procedure may have selected for a particular subpopulation of cells and that defective virus is also involved in establishment and maintenance of persistent infection.
clone (Java method)
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Precipitating antigens associated with a number of Marek's disease virus strains and with a turkey herpesvirus have been analyzed. The 'A' antigen has been defined as the major soluble antigen in feather follicles of infected chickens, which is identical with the major antigen usually present in supernatants of chicken kidney cell cultures infected with strains of Marek's disease virus. 'BC' antigens are 2 or more antigens which are usually not noted in skin extracts but present in cultured cells infected with Marek's disease virus or turkey herpesvirus, in addition to the 'A' antigen. Some of the virus strains examined were positive and others negative for 'A' antigen, but all contained the 'BC' antigens. Results of agar-gel precipitin tests suggested a serological classification of the group of avian herpesviruses formed by Marek's disease viruses and turkey herpesvirus into 3 types. Pathogenic strains of Marek's disease virus and their attenuated A- variants, represented by the HPRS-16 strain (HPRS-16, JM, GA, VC, Oldenburg). Apathogenic Marek's disease virus, represented by the HPRS-24 strain. Turkey herpesvirus and its A- variants, represented by the FC126 strain. A serological subdivision corresponding to the different grades of pathogenicity of virus strains of the first type was not possible. Differences between antigens associated with the 3 types of virus were apparent from the antigen and antibody titres against homologous and heterologous reagents. Precipitin bands produced by homologous antigen and antibody were stronger than those produced by heterologous reagents. Differences between 'A' antigens of the 3 virus types were characterized by spur patterns of precipitin bands indicating a partial identity. At least 3 'BC' precipitin bands were noted; at least one was group-specific and one appeared to be type-specific.
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Precipitin
Heterologous
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Abstract Four lymphoblastoid cell lines were established from tumors of turkeys inoculated with high doses of the GA strain of Marek's disease virus (MDV). Unlike other MD lymphoblastoid cell lines of chicken origin, these MDV transformed turkey lines appear to be B lymphocytes and produce immunoglobulin. Growth characteristics of these cell lines are slightly different; however, they all produce low levels of MDV‐specific antigen and carry the complete genome of the virus as determined by virus rescue in the chicken or in duck embryo fibroblast cultures. These cell lines are pathogenic for chickens and produce virus‐induced MD lesions. All four lines are free of the herpesvirus of turkeys, reticuloendotheliosis virus, and three lines are also free of avian leukosis virus. They all have typical normal turkey chromosomes and are positive for Marek's disease tumor‐associated surface antigen.
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Lymphoblast
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