Lymphomagenesis in Marek's disease

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Abstract
Lymphomagenesis in Marek's disease (MD) has been studied from the pathological, virological, biological, immunological and molecular viewpoints, but certain aspects remain enigmatic, including the molecular basis to neoplastic transformation by the causative herpes virus. Questions include: what factors determine why only certain cells are transformation targets, what influences the frequency of their infection and the progression of infection to transformation, how is transformation effected, and how do transformed cells escape immunosurveillance? Certain subsets of T‐cells are targets for transformation because they are the ones available at the site of early cytolytic infection, they can sustain a latent infection, and they can respond to viral genes involved in oncogenicity, all prerequisites to transformation. Little is known about differences in virus infection and spread in T‐cell targets that might relate to host genotype or age, or virus pathotype, nor why virus pathotypes differ in oncogenicity. Several candidate oncogenes have been proposed; of these, meq, a basic‐Ieucine zipper gene, appears to be the most promising. Tumour cells appear to have little or no antigenic distinctness to permit immune detection, and the problem with immunosurveillance is further complicated by the immunodepression associated with the disease.