Immune responses against Marek's disease virus

It is more than a century since Marek's disease (MD) was first reported in chickens and since then there have been concerted efforts to better understand this disease, its causative agent and various approaches for control of this disease. Recently, there have been several outbreaks of the disease in various regions, due to the evolving nature of MD virus (MDV), which necessitates the implementation of improved prophylactic approaches. It is therefore essential to better understand the interactions between chickens and the virus. The chicken immune system is directly involved in controlling the entry and the spread of the virus. It employs two distinct but interrelated mechanisms to tackle viral invasion. Innate defense mechanisms comprise secretion of soluble factors as well as cells such as macrophages and natural killer cells as the first line of defense. These innate responses provide the adaptive arm of the immune system including antibody- and cell-mediated immune responses to be tailored more specifically against MDV. In addition to the immune system, genetic and epigenetic mechanisms contribute to the outcome of MDV infection in chickens. This review discusses our current understanding of immune responses elicited against MDV and genetic factors that contribute to the nature of the response.     

A standard vaccine against Marek's disease

HVT-7, the standard vaccine against MD, was prepared from HVT strain FC126 grown in fibroblast cultures from SPF embryos. Ampoules of freeze dried material were prepared from a cell free suspension of virus in a solution of SPGA. The vaccine is stored at −20°C.The primary purpose of the standard vaccine was to control the variation encountered in the assay of virus content of HVT vaccines. The virus content of the standard vaccine was determined under a range of assay conditions, and the method in current use was shown to be satisfactory.A mean value for the virus content of the standard vaccine was determined using a constant assay method, by titrating 27 ampoules over a period of time. A further series of assays performed after one year's storage showed there to be no significant loss of titre.When several ampoules were titrated at the same time, some vial to vial variation was detected, but this was less than normal assay to assay variation.During routine determinations of the virus content of commercial HVT vaccines, an assay of the standard vaccine was carried out simultaneously to determine whether the assay conditions were acceptable. Assays where the value for the virus content of standard vaccine fell outside the expected range were considered invalid.The stability of the standard vaccine after reconstitution in SPGA was considered satisfactory: when reconstituted in phosphate-buffered saline, the rate of decrease in virus content was significantly greater. The vaccine could therefore be used as a control preparation in stability tests.Preliminary investigations showed that the behaviour of the standard vaccine in vivo was similar to that of satisfactory commercial vaccines, so that the preparation may also be of value in tests of vaccines for their ability to produce viraemia and confer protection.     

Immunoprophylaxis against Marek's disease and its perspectives

An account is given of the present international position in immunoprophylactic control of Marek's disease. An assessment is made of the method used for immunisation in the GDR. In that context, reference is made to problems for which solutions will have to be found in the long run.     

Immunization against Marek's disease transplantable cell lines

Continuous passage of MDCC-RP1, a highly tumorigenic Marek's disease (MD) lymphoblastoid cell line, in cell culture resulted in a gradual loss in ability of the cell line to cause progressive tumors in susceptible day-old chicks. Inoculation of day-old chicks with high-cell-culture-passaged (187th to 417th) nontumorigenic MDCC-RP1 cells gave excellent protection against challenge at 8 days with low-passaged tumorigenic MDCC-RP1 cells but failed to protect against primary tumors caused by inoculation with MD virus. Vaccination with the herpesvirus of turkeys, on the other hand, protected the chickens well against primary tumors caused by MD virus and against transplantable tumors caused by tumorigenic MDCC-RP1 cells, but it did not protect as well against another MD lymphoblastoid cell line, MDCC-RP4. It is unlikely, therefore, that vaccines prepared from passaged MDCC-RP1 cell lines will have value for protecting chickens against MD in the field.     

Efficacy of a bivalent vaccine against Marek's disease

A bivalent vaccine was prepared by combining inactivated Marek's disease virus and turkey herpesvirus. The efficacy of this vaccine, compared to turkey herpesvirus and inactivated Marek's disease virus separately, was studied in unsexed White Leghorn chicks which were vaccinated at one day old and then challenged at 21 days old with fowl blood infected with virulent Marek's disease virus. The bivalent vaccine appreciably delayed mortality resulting from Marek's disease and elicited the highest protective efficacy as judged on the basis of Marek's disease-specific mortality and percentage occurrence of lesions. The occurrence, extent and severity of gross lymphomas and microscopic lymphoproliferative lesions in various organs of the bivalent vaccinated birds were less than in the other challenged groups. In addition, the level of viraemia remained consistently and significantly lower in the bivalent vaccinated birds.