Abstract
Cross‐protection tests were conducted using attenuated JMV (JMV‐A) Marek's disease‐derived lymphoblasts, glutaraldehyde‐treated JMV tumour cells, attenuated Marek's disease virus (MDV, strain HPRS‐16/att) and turkey herpesvirus (HVT, strain FC126) as vaccines, and virulent JMV and MDV (HPRS‐16) for challenge. The JMV and JMV‐A preparations were free of MDV, leukosis and reticuloendotheliosis viruses. Vaccination of chickens with attenuated MDV or with HVT provided good protection against both JMV lymphoblastosis and Marek's disease (MD). In one experiment HVT (cell‐free) caused a better resistance to JMV than to MD. Inoculation of JMV‐A always resulted in a 100% resistance to virulent JMV. However, JMV‐A did not induce any appreciable resistance to MD, even when the birds were challenged with MDV by contact exposure. Control experiments revealed that high doses of normal lymphocytes from uninfected chickens also had a protective effect against JMV. The 50% protective dose varied from 107 to 108 lymphocytes. JMV tumour cells inactivated by glutaraldehyde were used in different experiments but rarely caused a clear‐cut protection against virulent JMV. The results of this study suggested that a one‐way relationship exists in vivo between HVT or MDV and JMV lymphoblastic leukaemia. However, resistance induced against JMV tumour cells appeared to be related to his‐tocompatibility antigens at least as much as to tumour‐specific cell surface antigens. The results obtained failed to provide clear evidence for or against vaccinal resistance to MDV being dependent on the action of a common Marek's disease tumour‐associated surface antigen (MATSA) additional to the immune response to viral antigens.