| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Division of Immunopathology, Institute for Animal Health, Compton, Newbury, Berks, UK (SCB, TFD); and Department of Pathology and Infectious Diseases, Royal Veterinary College, Royal College Street, London, UK (BHB)
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.
Key words: AV37; chickens; host genotype; lymphoma; Marek's disease; tumor immunity; tumor regression.
Request reprints from Dr. S. C. Burgess, Division of Immunopathology, Institute for Animal Health, Compton, Newbury, Berkshire, RG20 7NN (UK). E-mail: shane.burgess{at}bbsrc.ac.uk.
This article has been cited by other articles:
 |
|
 |
|
  R. Dennis, H. M. Zhang, and H. W. Cheng Effect of Selection for Resistance and Susceptibility to Viral Diseases on Concentrations of Dopamine and Immunological Parameters in Six-Week-Old Chickens Poult. Sci., December 1, 2006; 85(12): 2135 - 2140. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Burgess, J. R. Young, B. J. G. Baaten, L. Hunt, L. N. J. Ross, M. S. Parcells, P. M. Kumar, C. A. Tregaskes, L. F. Lee, and T. F. Davison Marek's disease is a natural model for lymphomas overexpressing Hodgkin's disease antigen (CD30) PNAS, September 21, 2004; 101(38): 13879 - 13884. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Kaiser, G. Underwood, and F. Davison Differential Cytokine Responses following Marek's Disease Virus Infection of Chickens Differing in Resistance to Marek's Disease J. Virol., December 11, 2002; 77(1): 762 - 768. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. C. Burgess and T. F. Davison Identification of the Neoplastically Transformed Cells in Marek's Disease Herpesvirus-Induced Lymphomas: Recognition by the Monoclonal Antibody AV37 J. Virol., June 14, 2002; 76(14): 7276 - 7292. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
