Attenuated Marek's Disease Herpesvirus: Protection Conferred on Strains of Chickens Varying in Genetic Resistance

Jl, Spencer; Grunder, A. A.; Robertson, Alan; Gw, Speckmann

doi:10.2307/1588904

Cited by 41 publications

(17 citation statements)

References 12 publications

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“…However, this practice became widespread in several countries of Europe and Asia in the late 1990s (reviewed in Gimeno, 2004). The rationale is largely anecdotal as the few published reports have failed to provide support for the value of this practice (Spencer et al, 1972;Benda & Holzanek, 1975;Zanella et al, 1975;Cho et al, 1976;Ball & Lyman, 1977;Eleazer, 1978;Riddell et al, 1978;Lee & Witter, 1991). Recently, Wu et al (2009) evaluated the positive effect of revaccination in an outbreak of MD but they were not able to reproduce experimentally the benefits of revaccination.…”

Section: Discussionmentioning

confidence: 99%

“…Other attempts have been made in the past to reproduce revaccination benefits in the laboratory (Spencer et al, 1972;Benda & Holzanek, 1975;Zanella et al, 1975;Cho et al, 1976;Ball & Lyman, 1977;Eleazer, 1978;Riddell et al, 1978;Lee & Witter, 1991;Wu et al, 2009). Most of the previous studies used homologous revaccination (Spencer et al, 1972;Benda & Holzanek, 1975;Zanella et al, 1975;Cho et al, 1976;Ball & Lyman, 1977;Eleazer, 1978;Riddell et al, 1978) and that could explain the lack of positive results. Recently, Wu et al (2009) used various combinations of vaccines, some of which were heterologous protocols.…”

Section: Discussionmentioning

confidence: 99%

“…Because of the lack of written reports, it is difficult to determine when and where the poultry industry started MD revaccination. Sporadic use of revaccination against MD under field conditions has been reported since the 1970s (Spencer et al, 1972;Benda & Holzanek, 1975;Zanella et al, 1975;Cho et al, 1976;Ball & Lyman, 1977). However, this practice became widespread in several countries of Europe and Asia in the late 1990s (reviewed in Gimeno, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…The rationale behind this practice is unknown and there is no consensus on the timing or dose of the second vaccination. Despite the moderate success reported under field conditions, several attempts to demonstrate the benefit of MD revaccination under laboratory conditions have failed (Spencer et al, 1972;Benda & Holzanek, 1975;Zanella et al, 1975;Cho et al, 1976;Ball & Lyman, 1977;Eleazer, 1978;Riddell et al, 1978;Lee & Witter, 1991). A proper experimental model is crucial to better understand the seemingly sporadic successes associated with MD revaccination and to optimize it.…”

Section: Introductionmentioning

confidence: 99%

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Standardization of a model to study revaccination against Marek's disease under laboratory conditions

Gimeno

Witter²,

Cortes

et al. 2012

Avian Pathology

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Revaccination, the practice of administering Marek's disease (MD) vaccine a second time, has been used in commercial poultry flocks for many years. The rationale is largely anecdotal as the few published reports have failed to provide support for the value of the practice. In the present work, we have standardized a model to study MD revaccination under laboratory conditions. Nine bird experiments were conducted to evaluate homologous revaccination (same vaccine administered twice) and heterologous revaccination (administration of two different vaccines) with various challenge models. Our results demonstrated that heterologous revaccination (with a second vaccine more protective than the first vaccine) but not homologous revaccination provided a beneficial increase in protection. Administration of the first vaccine at 18 days of embryonation followed by a more protective second vaccine at hatch reproduced systematically the benefits of revaccination. In addition, our results show that revaccination protocols might aid in solving major drawbacks associated with various highly protective experimental MD vaccines; that is, lymphoid organ atrophy and residual virulence. Strain RM1 is one of the most protective vaccines against early challenge with highly virulent MD virus but it induces severe lymphoid atrophy in chickens lacking maternal antibodies against MD virus. In this study, strain RM1 did not induce lymphoid organ atrophy when administered as second vaccine in a revaccination protocol. Similarly, strain 648A100/BP5 maintains residual virulence in chickens lacking maternal antibodies against MD virus but did not induce any lesions when used as a second vaccine. Until now, arbitrary revaccination protocols have been occasionally proven useful to the poultry industry. The model developed in this study will allow for a better understanding of this phenomenon and its optimization. A more rational use of this practice will be of great help to control MD outbreaks until better vaccines are available.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Standardization of a model to study revaccination against Marek's disease under laboratory conditions

Gimeno

Witter²,

Cortes

et al. 2012

Avian Pathology

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“…The virus strains used were the oncogenic strains BC1 (Spencer et al, 1972), JM (Sevoian et al, 1962) and Md5 (Witter et aL, 1980) of MDV1, the non-oncogenic strains C2 (Kato et al, 1970) and CVI988 (Rispens et al, 1972) of MDV2, strains HPRS24 (Biggs & M ilne, 1972) and SB 1 (Schat & Calnek, 1978) of MDV2 and vaccine strains O1 (Ono et al, 1974) and FC126 (Witter et al, 1970) of HVT. These viruses were propagated in primary chicken embryo fibroblasts (CEF) as described previously (Ikuta et al, 1981).…”

Section: Methodsmentioning

confidence: 99%

Identification of Virus-specific Polypeptides by Monoclonal Antibodies against Serotype 2 Marek's Disease Virus

Nakajima

Shibayama²,

Ikuta³

et al. 1989

Journal of General Virology

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SUMMARYA total of 41 antibody-secreting hybridoma cells against the HPRS24 strain of Marek's disease virus (MDV) type 2 (MDV2) have been isolated. Of these monoclonal antibodies (MAbs), 24 were found by immunofluorescence tests to react specifically with MDV2-infected cells, but not MDV type 1 (MDV1)-or herpesvirus of turkeys (HVT)-infected cells, while eight reacted with MDV1-or MDV2-infected cells and nine with MDVI-, MDV2-or HVT-infected cells. By using these MAbs, seven classes of MDV type-specific or cross-reactive polypeptides were characterized by immunoprecipitation followed by SDS-PAGE. Among them, a 28K/32K glycoprotein differed from the previously identified gA and gB. The 28K/32K glycoprotein was found on the surface of MDV2-infected cells and in the cytoplasm by an immunofluorescence test with MAbs. In addition, a cross-reactive polypeptide of 25K/29K was also detected in MDVl-infected cells with MAbs reactive with the 28K/32K glycoprotein of MDV2.

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Genetic resistance to herpesvirus‐induced lymphoma at the level of the target cell determined by the thymic microenvironment

Gallatin

Longenecker

1981

Intl Journal of Cancer

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The mechanisms responsible for non‐major‐histocompatibility‐complex (MHC)‐associated genetic resistance to Marek's disease (MD) were studied in resistant line 6 and susceptible line 7 chickens. Adoptive transfer of specific‐pathogen‐free (SPF) adult spleen cells from the susceptible line into irradiated 8‐day‐old resistant recipients significantly increased MD mortality following contact exposure to Marek's disease virus (MDV). No protective effect was observed following transfer of spleen cells from line 6 donors into susceptible line 7 recipients. Lymphocytes from the susceptible line 7 were shown by earlier experiments to have a higher capacity to adsorb the herpesvirus of turkeys (HVT). Fragments of thymic stroma from line 6 and line 7 were grafted onto the chorioallantoic membrane (CAM) of line 6 embryos. Following revascularization and repopulation of the grafts with lymphocytes of resistant host origin, the virus adsorption capacity of the non‐lymphoid stromal and lymphoid portions of the grafts was assayed in vitro by focus inhibition. While no difference in adsorption was observed between the line 6 and line 7 donor origin stromal cells, significantly more virus was adsorbed by the repopulating line 6 lymphoid cells harvested from the susceptible line 7 grafts than by line 6 lymphocytes from syngeneic line 6 grafts. The genotype of the thymic microenvironment was, therefore, found to be a determining factor in the expression of the high virus‐binding phenotype. Virus neutralizing monoclonal antibodies against HVT were prepared and used in the new in vitro antibody‐directed rosetting assay (ADRA) to determine the frequency of virus‐binding cells in the lymphoid organs of these two lines. Virus‐binding leukocytes were more frequent in the line 7 susceptible birds. In a time‐course study, following reconstitution of irradiated, third‐party, histocompatible recipients with SPF line 7 spleen cells, a sharp increase in MDV‐infectious centres was observed in peripheral blood at day 17 post exposure. A decrease in infectious centres was observed, however, at the same time point in recipients of line 6 spleen cells. The explanation for the difference in MD mortality seen in line 6 and line 7 is, thus, complex and may reflect separate resistance mechanisms which operate at more than one level. First, resistance is manifested at the level of a direct interaction between MDV and its target T lymphocyte with the thymic microenvironment playing a key role in the event. Second, and later during the course of infection, genetic variation in the capacity for immune surveillance against MDV‐infected and/or transformed cells may come into play. Whether these two properties segregate independently or not has yet to be determined.

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Attenuated Marek's Disease Herpesvirus: Protection Conferred on Strains of Chickens Varying in Genetic Resistance

Cited by 41 publications

References 12 publications

Standardization of a model to study revaccination against Marek's disease under laboratory conditions

Standardization of a model to study revaccination against Marek's disease under laboratory conditions

Identification of Virus-specific Polypeptides by Monoclonal Antibodies against Serotype 2 Marek's Disease Virus

Genetic resistance to herpesvirus‐induced lymphoma at the level of the target cell determined by the thymic microenvironment

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