Long-Term Studies of Marek's Disease Infection in Individual Chickens

Witter, R. L.; Jj, Solomon; Lr, Champion; Nazerian, K.

doi:10.2307/1588707

Cited by 78 publications

(47 citation statements)

References 19 publications

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“…However, all genotypes of chickens may be latently MDV-infected for life 62 and some difference (qualitative or quantitative) must exist in antigen expression between latently infected and neoplastically transformed (latently infected) cells, allowing the former to escape the immune response regardless of the particular genotype's MD resistance. In summary, host genotype-dependent MD resistance occurs at the cytolytic, latent, and tumor phases of MD.…”

Section: Few Cd8mentioning

confidence: 99%

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Resistance to Marek's Disease Herpesvirus-induced Lymphoma is Multiphasic and Dependent on Host Genotype

Burgess¹,

Başaran

Davison³

2001

Vet Pathol

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Abstract. Genotype-dependent differences in Marek's disease (MD) susceptibility were identified using 14-day-old line N and 6 1 (resistant) and 15I and 7 2 (susceptible) inbred chickens infected with HPRS-16 MD virus (MDV). All line 7 2 chickens developed progressive MD. Line 15I had fluctuating MD-specific clinical signs and individuals recovered. A novel histologic scoring system enabled indices to be calculated for lymphocyte infiltration into nonlymphoid organs. All genotypes had increased mean lesion scores (MLSs) and mean total lesion scores after MDV infection. These differed quantitatively and qualitatively between the genotypes. Lines 6 1 and 7 2 had a similar MLS distribution in the cytolytic phase, although scores were greater in line 7 2 . At the time lymphomas were visible in line 7 2 , histologic lesions in line 6 1 were regressing. AV37 ϩ cells were present in similar numbers in all genotypes in the cytolytic phase, suggesting that neoplastically transformed cells were present in all genotypes regardless of MD susceptibility. After the cytolytic phase, AV37ϩ cell numbers increased in lines 7 2 and 15I but decreased in lines 6 1 and N. In the cytolytic and latent phases, in all genotypes, most infiltrating cells were CD4 ϩ . After this time, line 7 2 and 15I lesions increased in size and most cells were CD4 ϩ ; line 6 1 and N lesions decreased in size and most cells were CD8ϩ . In all genotypes, AV37 immunostaining was weak in lesions with many CD8 ϩ cells, suggesting that AV37 antigen expression or AV37 ϩ cells were controlled by CD8 ϩ cells. The rank order, determined by clinical signs and pathology, for MD susceptibility (highest to lowest) was 7 2 Ͼ 15I Ͼ 6 1 Ͼ N.

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Section: Few Cd8mentioning

confidence: 99%

“…62 The MHC class I genes influence resistance to MD; chickens expressing the B21 allele (e.g., line N) are MD-resistant, although the mechanism is not known. 20 Additional, as yet unidentified, host genes also influence MD resistance and susceptibility.…”

mentioning

confidence: 99%

Resistance to Marek's Disease Herpesvirus-induced Lymphoma is Multiphasic and Dependent on Host Genotype

Burgess¹,

Başaran

Davison³

2001

Vet Pathol

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“…(Witter & Schat, 2003). In resistant chickens, latent infection may persist for the rest of the host's life (Witter et al, 1971;Baigent & Davison, 2004). 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).…”

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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“…A variety of vaccines and vaccination procedures can provide protection against the disease (Biggs et al, 1970;Mustaffa-Babjee & Spradbrow, 1973;Calnek et al, 1983;Sarma et al, 1995;Lee et al, 1999;Ricks et al, 1999;Islam et al, 2001b); however, vaccination does not preclude infection, and vaccinal and virulent viruses can co-exist together in the same host (Witter et al, , 1987Lee et al, 1999;Islam et al, 2001a). MDV infection can persist in resistant chickens without any clinical signs or pathological lesions (Witter et al ., 1971;Nair, 2005). Therefore, detection of the presence of MDV in chickens is not diagnostic for MD.…”

Section: Introductionmentioning

confidence: 99%

“…MD-resistant chickens proceed only to latent infection and may have a persistent infection for the rest of their life (Witter et al ., 1971).…”

Section: Introductionmentioning

confidence: 99%

Relationship between Marek's disease virus load in peripheral blood lymphocytes at various stages of infection and clinical Marek's disease in broiler chickens

Walkden‐Brown

Islam

Underwood³

et al. 2006

Avian Pathology

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Vaccination with herpesvirus of turkey (HVT) vaccine provides protection against clinical Marek's disease (MD) but does not preclude infection with wild-type MD virus (MDV). The quantity of MDV detected in circulating lymphocytes during the early period after infection may be a useful predictor of subsequent clinical MD later in the life. A study was designed to quantify MDV and HVT copy number in peripheral blood lymphocytes (PBL) using real-time polymerase chain reaction between days 5 and 35 post-challenge and to relate this to subsequent development of gross MD lesions. Female commercial broiler chickens were vaccinated with HVT or were sham-vaccinated at hatch, then challenged with MDV strain MPF-57 at day 2 post-vaccination and reared in positive-pressure isolators up to 56 days post-challenge, when all survivors were euthanized. All dead and euthanized chickens were examined post mortem for gross MD lesions. Birds were scored for MD lesions and mortality. MDV and HVT genome copy numbers were determined for each PBL sample. There was an increase in HVT load in PBL between days 7 and 37 post-vaccination, with marked increases between days 7 and 16 and again between days 30 and 37. There was a steady increase in MDV load to 35 days post-challenge. The mean MDV copy number (log 10 ) was greater in chickens subsequently exhibiting gross MD lesions (5.059/0.21) than in those that did not (2.889/0.223), with the largest difference at 14 and 21 days post-challenge (P B/0.001). Quantification of MDV during early infection is therefore a potential tool for monitoring MD in broiler flocks.

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Long-Term Studies of Marek's Disease Infection in Individual Chickens

Cited by 78 publications

References 19 publications

Resistance to Marek's Disease Herpesvirus-induced Lymphoma is Multiphasic and Dependent on Host Genotype

Resistance to Marek's Disease Herpesvirus-induced Lymphoma is Multiphasic and Dependent on Host Genotype

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

Relationship between Marek's disease virus load in peripheral blood lymphocytes at various stages of infection and clinical Marek's disease in broiler chickens

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