Differentiation between strains of Marek's disease virus and turkey herpesvirus by immunofluorescence assays

Bülow, Vicco von; Biggs, P. M.

doi:10.1080/03079457509353859

Cited by 134 publications

(23 citation statements)

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“…The three serotypes of MDV are serotype 1, oncogenic viruses that include RB1B and GA strains; serotype 2, nononcogenic MDV including SB-1; and serotype 3, consisting of the nononcogenic herpesvirus of turkeys (8,9,21,40). Although the three serotypes share many antigens (8,9,21,24,40), they can be distinguished from each other by serologic methods and by their genomic sequences (3,25,46).…”

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confidence: 98%

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Pathogenesis of a Marek's Disease Virus Mutant Lacking vIL-8 in Resistant and Susceptible Chickens

Cortes

Cardona

2004

Avian Diseases

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A homologue of interleukin-8, viral interleukin-8 (vIL-8) has been identified in the genome of Marek's disease virus (MDV). This protein attracts peripheral blood mononuclear cells in vitro although its role in the pathogenesis of Marek's disease (MD) is not known. P chickens, genetically susceptible to MD, and N chickens, genetically resistant to the disease, were inoculated with either RB1B MDVor RB1BvIL-8smGFP, a vIL8 knockout RB1B MDV, to assess the role of vIL8 in the pathogenesis of MD. The tumor incidence was highest in the P birds given the RBIB virus, where the incidence was 100%. Tumor incidence in N birds given RB1B was 41.5%. Thirty-one percent of the P birds given RB1BvIL-8smGFP developed tumors, and no N bird given RB1BvIL-8smGFP developed tumors. Histologically, the tumors from RB1B-inoculated birds were larger and more invasive and had a more homogeneous cellular composition than those from RB1BvIL-8smGFP-inoculated birds, which were best described as microtumors. These microtumors did not obliterate the normal architecture of the tissues, and in contrast to the RBIB tumors, moderate numbers of heterophils were admixed with the proliferating lymphocytes. Susceptible birds receiving RB1B had the highest viral titers throughout the study, followed by the resistant birds inoculated with RB1B. P and N birds receiving RB1BvIL-8smGFP virus had consistently lower levels of viremia than their RB1B-inoculated counterparts although virus could be recovered from the birds during all stages of MD. In addition, the RB1BvIL-8smGFP virus was detected in birds held in contact with the inoculated group, although no tumors developed in contact control birds. This result indicates that RB1BvIL-8smGFP replicates in vivo but not as well as RB1B and that vIL8 is not essential for the completion of the pathogenesis of MD.

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“…Although the three serotypes share many antigens (8,9,21,24,40), they can be distinguished from each other by serologic methods and by their genomic sequences (3,25,46). Serotype 1 MDVs have several unique open reading frames such as meq and viral interleukin 8 (vIL-8) (3,44).…”

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Pathogenesis of a Marek's Disease Virus Mutant Lacking vIL-8 in Resistant and Susceptible Chickens

Cortes

Cardona

2004

Avian Diseases

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“…The causative agent of MD is an avidly cell-associated alphaherpesvirus called gallid herpesvirus type 2 (GaHV-2), commonly called Marek's disease virus type 1 (MDV-1) [2]. Based on data obtained by indirect immunofluorescence, agar gel precipitin and neutralization tests, three socalled serotypes of MDV have historically been described [3,4]. Serotype 1 (MDV-1) is the oncogenic virus that causes MD.…”

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confidence: 99%

Comparative genomic sequence analysis of the Marek’s disease vaccine strain SB-1

Spatz

Schat

2011

Virus Genes

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Marek's disease virus (MDV), an oncogenic alphaherpesvirus, induces a rapid onset T-cell lymphoma and demyelinating disease in chickens. Since the 1970s the disease has been controlled through mass vaccination with herpesvirus of turkeys [meleagrid herpesvirus type 1 (MeHV-1)]. Over time this vaccine's efficacy decreased, and in the 1980s a bivalent vaccine consisting of MeHV-1 and a non-oncogenic gallid herpesvirus type 3 (GaHV-3) strain known as SB-1 was introduced. The complete DNA sequence (165,994 bp) of this GaHV-3 strain was determined using 454 pyrosequencing. A total of 524 open reading frames (ORFs) were examined for homology to protein sequences present in GenBank using BLAST (E-values <0.9). Of the 128 ORF hits, 75 ORFs showed homology to well-characterized alphaherpesviral proteins. Phylogenetically, this strain partitions in its own branch along with the GaHV-3 strain HPRS24 and shows more relatedness to MeHV-1 than gallid herpesvirus type 2 (GaHV-2, Marek's disease virus). When comparing the GaHV-3 ORFs to their homologues in MeHV-1 and GaHV-2, a greater percentage of amino acid similarity was found with homologous ORFs in the genome of SB-1 than with those in the HPRS24 genome. Overall, twice as many of the 75 ORFs within the SB-1 genome showed greater sequence identities and similarities to homologous ORFs in the Marek's disease genome than those within the HPRS24 genome. This paper describes the sequence difference between the two GaHV-3 genomes. Overall 19 ORFs differ in the number of predicted amino acids; of these, eight (U(L)3.5, U(L)5, U(L)9, U(L)28, U(L)30, U(L)36, U(L)37, and U(L)50) encode well-characterized alphaherpesviral proteins A sequence within the unique short region of the SB-1 genome exhibited significant sequence homology to long terminal repeat (LTR) sequences of avian retroviruses. This sequence was only found in the SB-1 genome and not the HPRS24 genome.

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“…MDV has been divided into three serotypes based upon common and unique antigenic epitopes [1,2]. Serotype 1 MDVs are the pathogenic strains commonly found in the field.…”

Section: Introductionmentioning

confidence: 99%

Oncogenic Marek’s disease viruses lacking the 132 base pair repeats can still be attenuated by serial in vitro cell culture passages

Silva

Gimeno

2007

Virus Genes

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Marek's disease virus (MDV) can be attenuated by serially passing the virus in cell culture. During cell culture passage, two copies of a 132 bp repeat are expanded to over 30 copies. We deleted the two copies of the 132 bp repeat region in a pathogenic MDV and demonstrated that the virus was still pathogenic. The pattern and frequency of tumors in the parental and mutant virus were the same. Early virus replication, and the appearance of persistent neurological disease were also similar between the parental and deleted virus. Nevertheless, wild-type MDV and the deletion virus could be attenuated by serial in vitro cell culture passages. Based upon analyzing the passage 40 viruses, attenuation of the MDV lacking the 132 bp repeats appears to occur in a manner that is analogous to the process occurring wild-type MDV attenuation. Whatever process is involved in the cell culture attenuation of MDV, the mechanism does not involve the 132 bp repeat region.

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Differentiation between strains of Marek's disease virus and turkey herpesvirus by immunofluorescence assays

Cited by 134 publications

References 13 publications

Pathogenesis of a Marek's Disease Virus Mutant Lacking vIL-8 in Resistant and Susceptible Chickens

Pathogenesis of a Marek's Disease Virus Mutant Lacking vIL-8 in Resistant and Susceptible Chickens

Comparative genomic sequence analysis of the Marek’s disease vaccine strain SB-1

Oncogenic Marek’s disease viruses lacking the 132 base pair repeats can still be attenuated by serial in vitro cell culture passages

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