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Electron microscopic and immunohistochemical localization of Marek's disease (MD) herpesvirus particles in MD skin

K O Cho1, K Ohashi, M Onuma

  • 1Department of Disease Control, School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.

Veterinary Pathology
|July 27, 1999
PubMed

Insights

Marek's disease virus (MDV) can cause skin lymphomas in chickens. Abortive MDV replication was observed in necrotic lymphoblasts within necrotizing lymphomas, suggesting ischemia may play a role.

Area of Science:

  • Veterinary Pathology
  • Virology
  • Oncology

Background:

  • Marek's disease virus (MDV) is a herpesvirus known to cause lymphomas in chickens.
  • Understanding the pathogenesis of MDV-induced lymphomas, particularly skin lymphomas, is crucial for disease control.

Purpose of the Study:

  • To investigate the viral and cellular events occurring in Marek's disease virus-induced skin lymphomas in chickens.
  • To differentiate between necrotizing and non-necrotizing lymphoma types based on viral replication and vascular changes.

Main Methods:

  • Induction of skin lymphomas in specific-pathogen-free chickens using MDV.
  • Weekly biopsies of lymphomas for examination via electron microscopy and immunohistochemistry.
  • Detection of MDV antigens (early pp38, late glycoproteins B and C).

Main Results:

  • Abortive MDV replication (immature particles) was identified in the nuclei of necrotic lymphoblasts within necrotizing lymphomas.
  • Necrotizing lymphomas in two birds showed vascular endothelial cell injury and fibrinoid necrosis of blood vessels.
  • Non-necrotizing lymphomas lacked detectable virus particles and distinct vascular lesions.
  • MDV early antigen (pp38) was present only in necrotizing lymphomas, while late antigens were not detected.

Conclusions:

  • Abortive MDV replication appears primarily associated with necrotic lymphoblasts in necrotizing lymphomas.
  • Vascular injury, potentially induced by ischemia, may contribute to the development of necrotizing lymphomas.
  • The absence of late viral antigens in necrotizing lymphomas suggests a role for early viral events or host responses in pathogenesis.

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