Immunization against Marek's Disease using a Live Attenuated Virus

Churchill, A. E.; Payne, L. N.; Chubb, R. C.

doi:10.1038/221744a0

Cited by 278 publications

(91 citation statements)

References 5 publications

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“…MD is the first virus-induced cancer in any species against which a live attenuated vaccine was used successfully, nearly 40 years ago (26). Despite the success of the vaccination strategy in reducing losses from MD, vaccines themselves are thought to be responsible for driving the virulence, and there is an urgent need to develop more effective vaccines to halt the pathogen race toward higher virulence (2).…”

Section: Discussionmentioning

confidence: 99%

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

Brown

Baigent

Smith

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

106

101

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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. viral oncogenesis ͉ vaccines ͉ transcriptional repression

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Section: Discussionmentioning

confidence: 99%

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

Brown

Baigent

Smith

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

106

101

View full text Add to dashboard Cite

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“…This resulted in widespread outbreaks and very high mortality rates around the world (Benton & Cover, 1957; Witter, 1997). There was an urgent need for human intervention to combat economic losses, and the solution came in the form of vaccination (Churchill, Payne, & Chubb, 1969; Okazaki, Purchase, & Burmester, 1970). Vaccination campaigns were so successful that deaths due to MD became almost nonexistent (Witter, 2001).…”

Section: Introductionmentioning

confidence: 99%

The industrialization of farming may be driving virulence evolution

Rozins

Day

2016

Evolutionary Applications

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Farming practices have changed dramatically over the years. The industrialization of farming has provided parasites with an abundance of hosts and is thought to have influenced parasite evolution. For example, the parasite that causes the highly contagious poultry disease, Marek's disease, has evolved over the past 60 years into a highly virulent pathogen. It is assumed that the industrialization of the industry and vaccination have selected for more virulent strains of the virus. Here, with the use of an impulsive differential equation model, we investigate how modern broiler farm practices could independently lead to virulence evolution. Our model suggests that longer cohort durations and more densely stocked barns both select for less virulent strains of the virus. Our model also suggests that if intensive cleaning between cohorts does not rid the barn of disease, it may drive evolution and cause the disease to become more virulent.

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“…The oncogenic MDV becomes attenuated after serial passage in vitro, and the attenuated MDV is successfully used to vaccinate chickens against Marek's disease [7]. Comparative analysis of the genomic DNA of oncogenic and attenuated MDV reveals expansion of the homologous BamHI-D and BamHI-H fragments of the attenuated MDV.…”

Section: Culture Of the Cells And Cell Growth Experimentsmentioning

confidence: 99%

Antisence Oligonucleotide Complementary to the BamHI-H Gene Family of Marek's Disease Virus Induced Growth Arrest of MDCC-MSB1 Cells in the S-Phase.

Hayashi

Kawamura

Akaike

et al. 1999

The Journal of Veterinary Medical Science

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ABSTRACT. DNA synthesis was effectively inhibited by antisense oligonucleotide A1 complementary to the BamHI-H gene family in Marek's disease virus (MDV)-derived lymphoblastoid MDCC-MSB1 cells. When a cell cycle distribution of a total cell population was analyzed by flow cytometry, the proportion of S-phase cells increased in the cell populations by treatment with oligonucleotide A1. Approximately 60-70% of the cells appeared in the S phase for 24 and 36 hr of incubation in the presence of oligonucleotide A1 (20-30% in the untreated control cells). The inhibition of cell cycle progression by treatment with oligonucleotide A1 was reversible. When the cells were treated with 5 µM aphidicolin for 12 hr, a similar pattern of cell cycle distribution was observed to that obtained after treatment with oligonucleotide A1. Aphidicolin is an inhibitor of cellular DNA polymerase α, and it halts progression of the cell cycle at the G1/S border or early S phase. When the cells were treated with aphidicolin for 12 hr and subsequently incubated with oligonucleotide A1, no significant difference was observed in the cycle phase distribution of cells in the presence and absence of oligonucleotide A1. In contrast, when the cells were treated with oligonucleotide A1 for 12 hr and subsequently incubated with aphidicolin, the cell cycle did not progress from the G1/S border or early S phase to the next phase.-KEY WORDS: BamHI-H gene family, cell cycle arrest, DNA synthesis, Marek's disease virus, MDCC-MSB1.

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Immunization against Marek's Disease using a Live Attenuated Virus

Cited by 278 publications

References 5 publications

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

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

The industrialization of farming may be driving virulence evolution

Antisence Oligonucleotide Complementary to the BamHI-H Gene Family of Marek's Disease Virus Induced Growth Arrest of MDCC-MSB1 Cells in the S-Phase.

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