Morphogenesis of Marek's Disease Virus in Feather Follicle Epithelium2

Johnson, Elizabeth A.; Burke, C. N.; Fredrickson, T. N.; DiCapua, Richard A.

doi:10.1093/jnci/55.1.89

Cited by 30 publications

(12 citation statements)

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“…It is the same in the tissues of infected chickens, except skin (see review [85]). The skin has been shown to contain many MDV infectious particles in the epidermis of feather follicles in the transitional layer [42,86,87]. In these cells, particles are often within cytoplasmic inclusions constituted of electron-dense amorphous material and lacking visible peripheral lipid membranes.…”

Section: Atypical Morphogenesis Of MDV In the Skinmentioning

confidence: 99%

Marek’s disease virus and skin interactions

Couteaudier¹,

Denesvre²

2014

Vet Res

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Marek’s disease virus (MDV) is a highly contagious herpesvirus which induces T-cell lymphoma in the chicken. This virus is still spreading in flocks despite forty years of vaccination, with important economical losses worldwide. The feather follicles, which anchor feathers into the skin and allow their morphogenesis, are considered as the unique source of MDV excretion, causing environmental contamination and disease transmission. Epithelial cells from the feather follicles are the only known cells in which high levels of infectious mature virions have been observed by transmission electron microscopy and from which cell-free infectious virions have been purified. Finally, feathers harvested on animals and dust are today considered excellent materials to monitor vaccination, spread of pathogenic viruses, and environmental contamination. This article reviews the current knowledge on MDV-skin interactions and discusses new approaches that could solve important issues in the future.

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Section: Atypical Morphogenesis Of MDV In the Skinmentioning

confidence: 99%

Marek’s disease virus and skin interactions

Couteaudier¹,

Denesvre²

2014

Vet Res

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“…After about 7 d p.i., the virus enters latency. Infected lymphocytes, mostly active T lymphocytes, migrate through the bloodstream to various tissues including the feather follicle epithelium, which is the sole source of the enveloped fully infectious virus (Calnek et al, 1970;Johnson et al, 1975;Calnek, 2001). After 21 d p.i., infected lymphocytes become neoplastically transformed and, in susceptible chickens, proliferate to form gross lymphomas (Calnek, 2001).…”

Section: Introductionmentioning

confidence: 99%

Expression profiles of genes within a subregion of chicken major histocompatibility complex B in spleen after Marek’s disease virus infection

Lian

Zheng

et al. 2010

Poultry Science

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Major histocompatibility complex has previously been shown to influence the resistance of chicken to Marek's disease virus (MDV). However, little is known about expression of other genes in the MHC-I and II pathway after MDV infection. This study aimed at investigating 8 immune-related genes in the MHC core region that affects host responses to MDV. Spleens of infected and age-matched uninfected chickens were removed at 4, 7, 14, 21, and 28 d postinfection for gene expression detection using real-time PCR. Different expression patterns of MHC-I and II pathway genes were observed in the spleen. In the MHC-I pathway, the expression of transporter of antigen protein 1 (TAP1), transporter of antigen protein 2 (TAP2), and transporter of antigen protein-binding protein (TAPBP) genes was significantly increased in the spleen of MDV-infected than that of uninfected chickens. It indicated that host antivirus responses were generated to enhance antigen presentation. However, MHC-II pathway genes showed contrary trends. Classical MHC-II β chain major gene (BLB2) and nonclassical class II genes [DM α chain gene (DMA), DM β chain gene-1 (DMB1), and DM β chain gene-2 (DMB2)] had consistent lower transcripts in spleens of MDV-infected than that of uninfected chickens, which reflected that MDV interfered with multiple components of the MHC-II pathway. Overall, expression of most genes in the MHC core region was altered; moreover, the genes in endogenous and exogenous antigen presentation pathways had different expression patterns in the spleen after MDV infection.

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“…At about 7 d.p.i., MDV also commences productive replication in the feather follicle epithelium, with highlevel expression of MDV antigens (Gilka & Spencer, 1993). At about 14 d.p.i., cell-free virus is shed in feather dander to the environment (Beasley et al, 1970;Carrozza et al, 1973;Johnson et al, 1975), which is the main source of infection for other chickens. Latently infected resistant chickens as well as vaccinated chickens can shed virus throughout their life without showing any clinical MD (Witter et al, 1971).…”

Section: Introductionmentioning

confidence: 99%

Kinetics of Marek's disease virus (MDV) infection in broiler chickens 1: effect of varying vaccination to challenge interval on vaccinal protection and load of MDV and herpesvirus of turkey in the spleen and feather dander over time

et al. 2008

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Two experiments in commercial broiler chickens vaccinated with herpesvirus of turkeys (HVT) and challenged with Marek's disease virus (MDV) investigated the effects of the vaccination-to-challenge interval (VCI) on vaccinal protection against Marek's disease, and the kinetics of MDV and HVT load in the spleen and feather dander determined using real-time quantitative polymerase chain reaction. Experiment 1 in isolators tested VCI of 2, 4 and 7 days, while Experiment 2 in floor pens tested VCI of 0, 2, 4, 7 and 10 days. MDV challenge induced gross Marek's disease lesions in 14% to 74% of chickens by 56 days post-challenge. Vaccinal protection increased from approximately 40% to approximately 80% with increasing VCI between days 2 and 7 in both experiments, but not thereafter. MDV was detected in both the spleen and dander at 7 days post-challenge and increased rapidly to approximately 21 days post-challenge, after which levels plateaued, rose or fell gradually depending on treatment. HVT was also shed in significant amounts, 1 to 2 logs lower than for MDV, with a clear peak around 14 to 21 days post-vaccination. Vaccination significantly reduced the log(10)MDV load in the spleen (vaccinated, 2.99+/-0.20/10(6) spleen cells; unvaccinated, 4.60+/-0.23/10(6) spleen cells) and dander (vaccinated, 5.28+/-0.13/mg; unvaccinated, 6.00+/-0.18/mg) from infected chickens. The MDV load had a significant negative association with the VCI and the level of vaccinal protection. Measurement of dander production in Experiment 1 and the dust content of air in Experiment 2, combined with determination of the MDV load in these, enabled estimation of total daily shedding rates of MDV per chicken and of the MDV load in air for the first time.

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Morphogenesis of Marek's Disease Virus in Feather Follicle Epithelium2

Cited by 30 publications

References 0 publications

Marek’s disease virus and skin interactions

Marek’s disease virus and skin interactions

Expression profiles of genes within a subregion of chicken major histocompatibility complex B in spleen after Marek’s disease virus infection

Kinetics of Marek's disease virus (MDV) infection in broiler chickens 1: effect of varying vaccination to challenge interval on vaccinal protection and load of MDV and herpesvirus of turkey in the spleen and feather dander over time

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