Marek's disease: Genetic regulation of gallid herpesvirus 2 infection and latency

Gennart, Isabelle; Coupeau, Damien; Pejaković, Srđan; Laurent, Sylvie; Rasschaert, Denis; Muylkens, Benoît

doi:10.1016/j.tvjl.2015.04.038

Cited by 28 publications

(27 citation statements)

References 71 publications

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“…The oncogenic activities of the Meq protein are mediated by its dimerization, through the bZIP domain, with itself, as well as with c‐Jun‐like proteins, such as JunB, c‐Jun and c‐Fos. Meq also binds to cellular transcription factors such as ATF, CREB and C/EBP (Deng et al, ) and interacts with cellular proteins without a bZIP domain, such as the cellular tumour suppressors p53, the retinoblastoma protein (pRb) and the cyclin‐dependent kinase 2 (CDK‐2) or the heat shock protein Hsp70 (Deng et al, ; Gennart et al, ). The meq oncogene encodes a 339 amino acid unspliced open reading frame in vv and in vv + GaHV‐2 pathotypes and a larger form of 398 amino acids in low virulence strains, having amplifications in the C‐terminal proline‐rich repeat region (Shamblin, Greene, Arumugaswami, Dienglewicz, & Parcells, ).…”

Section: Introductionmentioning

confidence: 99%

Marek's disease viruses circulating in commercial poultry in Italy in the years 2015–2018 are closely related by their meq gene phylogeny

Mescolini

Lupini

Davidson³

et al. 2019

Transbound Emerg Dis

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Marek's disease (MD) is a lymphoproliferative disease important to the poultry industry worldwide; it is caused by Gallid alphaherpesvirus 2 (GaHV‐2). The virulence of GaHV‐2 isolates has shifted over the years from mild to virulent, very virulent and very virulent +. Nowadays the disease is controlled by vaccination, but field strains of increased virulence are emerging worldwide. Economic losses due to MD are mostly associated with its acute form, characterized by visceral lymphomas. The present study aimed to molecularly classify a group of 13 GaHV‐2 strains detected in vaccinated Italian commercial chicken flocks during acute MD outbreaks, and to scrutinize the ability of predicting GaHV‐2 virulence, according to the meq gene sequence. The full‐length meq genes were amplified, and the obtained amino acid (aa) sequences were analysed, focusing mainly on the number of stretches of four proline molecules (PPPP) within the transactivation domain. Phylogenetic analysis was carried out with the Maximum Likelihood method using the obtained aa sequences, and the sequences of Italian strains detected in backyard flocks and of selected strains retrieved from GenBank. All the analysed strains showed 100% sequence identity in the meq gene, which encodes a Meq protein of 339 aa. The Meq protein includes four PPPP motifs in the transactivation domain and an interruption of a PPPP motif due to a proline‐to‐serine substitution at position 218. These features are typically encountered in highly virulent isolates. Phylogenetic analysis revealed that the analysed strains belonged to a cluster that includes high‐virulence GaHV‐2 strains detected in Italian backyard flocks and a hypervirulent Polish strain. Our results support the hypothesis that the virulence of field isolates can be suggested by meq aa sequence analysis.

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Section: Introductionmentioning

confidence: 99%

Marek's disease viruses circulating in commercial poultry in Italy in the years 2015–2018 are closely related by their meq gene phylogeny

Mescolini

Lupini

Davidson³

et al. 2019

Transbound Emerg Dis

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“…The ability of MDV to replicate in the host is related to its pathogenicity, and the MDV genome load in infected chickens contributes to our understanding of the pathogenesis of MDV infection [4,5]. In addition, several MDV-encoded genes, including meq (MDV EcoRI-Q-encoded protein) [6,7,8], pp38 (MDV phosphoprotein 38) [9,10], vIL-8 (MDV-encoded CXC chemokine viral interleukin 8) [11,12], and ICP4 (MDV infected-cell peptide 4) [13,14,15], play important roles in MDV pathogenesis. Vaccination with MD vaccines is the primary approach used to protect chickens against MD.…”

Section: Introductionmentioning

confidence: 99%

Co-Infection with Marek’s Disease Virus and Reticuloendotheliosis Virus Increases Illness Severity and Reduces Marek’s Disease Vaccine Efficacy

Sun

Zhang

Zhou

et al. 2017

Viruses

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Marek’s disease virus (MDV) and reticuloendotheliosis virus (REV) cause Marek’s disease (MD) and reticuloendotheliosis (RE), respectively. Co-infection with MDV and REV is common in chickens, causing serious losses to the poultry industry. However, experimental studies of such co-infection are lacking. In this study, Chinese field strains of MDV (ZW/15) and REV (JLR1501) were used as challenge viruses to evaluate the pathogenicity of co-infection and the influence of MD vaccination in chickens. Compared to the MDV-challenged group, the mortality and tumor rates increased significantly by 20.0% (76.7 to 96.7%) and 26.7% (53.3 to 80.0%), in the co-challenged group, respectively. The protective index of the MD vaccines CVI988 and 814 decreased by 33.3 (80.0 to 47.7) and 13.3 (90.0 to 76.7), respectively. These results indicated that MDV and REV co-infection significantly increased disease severity and reduced the vaccine efficacy. The MDV genome load showed no difference in the feather pulps and spleen, and pathogenicity-related MDV gene expression (meq, pp38, vIL-8, and ICP4) in the spleen significantly increased at some time points in the co-challenged group. Clearly, synergistic pathogenicity occurred between MDV and REV, and the protective efficacy of existing MD vaccines was attenuated by co-infection with Chinese field MDV and REV strains.

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“…Several herpesviruses, like Marek’s Disease virus (MDV), gallid herpesvirus 2 (GaHV-2), and human herpesvirus 6 (HHV6), establish latent infections in CD4 + T cells with viral genomes integrated into host chromosomes (reviewed in Gennart et al, 2015). These viruses frequently integrate into telomere repeat tracts by homologous recombination (Kaufer et al, 2011; Robinson et al, 2010).…”

Section: Genome Maintenance Mechanismsmentioning

confidence: 99%

Epigenetics and Genetics of Viral Latency

Lieberman

2016

Cell Host & Microbe

126

118

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Viral latency can be considered a metastable, nonproductive infection state that is capable of subsequent reactivation to repeat the infection cycle. Viral latent infections have numerous associated pathologies, including cancer, birth defects, neuropathy, cardiovascular disease, chronic inflammation, and immunological dysfunctions. The mechanisms controlling the establishment, maintenance, and reactivation from latency are complex and diversified among virus families, species, and strains. Yet, as examined in this review, common properties of latent viral infections can be defined. Eradicating latent virus has become an important but elusive challenge and will require a more complete understanding of the mechanisms controlling these processes.

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Marek's disease: Genetic regulation of gallid herpesvirus 2 infection and latency

Cited by 28 publications

References 71 publications

Marek's disease viruses circulating in commercial poultry in Italy in the years 2015–2018 are closely related by their meq gene phylogeny

Marek's disease viruses circulating in commercial poultry in Italy in the years 2015–2018 are closely related by their meq gene phylogeny

Co-Infection with Marek’s Disease Virus and Reticuloendotheliosis Virus Increases Illness Severity and Reduces Marek’s Disease Vaccine Efficacy

Epigenetics and Genetics of Viral Latency

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