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

• Published in: Veterinary pathology Vol. 38; no. 2; pp. 129 - 142
• Main Authors: Burgess, S. C., Basaran, B. H., Davison, T. F.
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.03.2001
• Subjects: Animals; Antibodies, Monoclonal - immunology; Cell Transformation, Viral - genetics; Cell Transformation, Viral - immunology; Chickens - genetics; DNA, Viral - chemistry; Genetic Predisposition to Disease; Gonads - pathology; Herpesvirus 2, Gallid - pathogenicity; Immunohistochemistry - veterinary; Liver - pathology; Lymphoma - genetics; Lymphoma - immunology; Lymphoma - pathology; Lymphoma - virology; Marek Disease - complications; Marek Disease - genetics; Marek Disease - pathology; Polymerase Chain Reaction - veterinary; Poultry Diseases - genetics; Poultry Diseases - pathology; Poultry Diseases - virology; Proventriculus - pathology; Sciatic Neuropathy - pathology; Sciatic Neuropathy - veterinary; Skin - pathology; Specific Pathogen-Free Organisms; chickens; AV37; lymphoma; host genotype; tumor immunity; tumor regression; Marek's disease
• ISSN: 0300-9858; 1544-2217
• DOI: 10.1354/vp.38-2-129

Genotype-dependent differences in Marek's disease (MD) susceptibility were identified using 14-day-old line N and 61 (resistant) and 15I and 72 (susceptible) inbred chickens infected with HPRS-16 MD virus (MDV). All line 72 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 61 and 72 had a similar MLS distribution in the cytolytic phase, although scores were greater in line 72. At the time lymphomas were visible in line 72, histologic lesions in line 61 were regressing. AV37+ 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, AV37+ cell numbers increased in lines 72 and 15I but decreased in lines 61 and N. In the cytolytic and latent phases, in all genotypes, most infiltrating cells were CD4+. After this time, line 72 and 15I lesions increased in size and most cells were CD4+; line 61 and N lesions decreased in size and most cells were CD8+. In all genotypes, AV37 immunostaining was weak in lesions with many CD8+ cells, suggesting that AV37 antigen expression or AV37+ cells were controlled by CD8+ cells. The rank order, determined by clinical signs and pathology, for MD susceptibility (highest to lowest) was 72 > 15I > 61 > N.