Marek's disease virus infection in the brain: virus replication, cellular infiltration, and major histocompatibility

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Assessing the Expression of Major Histocompatibility Complex Class I on Primary Murine Hippocampal Neurons by Flow Cytometry
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Published on: May 19, 2020

I M Gimeno1, R L Witter, H D Hunt

  • 1USDA-ARS Avian Disease and Oncology Laboratory, East Lansing, MI 48823, USA.

Veterinary Pathology
|September 27, 2001
PubMed

Insights

Marek's disease virus (MDV) brain infection causes distinct inflammatory and proliferative lesions, differing by viral pathotype. Highly virulent MDV strains induce more severe brain lesions and altered major histocompatibility complex (MHC) antigen expression.

Area of Science:

  • Veterinary Virology
  • Immunology
  • Pathology

Background:

  • Marek's disease virus (MDV) is a significant poultry pathogen.
  • Understanding MDV neurotropism is crucial for disease control.

Purpose of the Study:

  • To chronologically investigate Marek's disease virus (MDV) infection in chicken brains.
  • To differentiate the neuropathogenesis of virulent (v) and very virulent plus (vv+) MDV pathotypes.
  • To analyze viral replication, lesion development, and host immune responses in the brain.

Main Methods:

  • Inoculation of chickens with different MDV serotype I strains (v and vv+).
  • Chronological analysis of viral antigen expression (pp38, gB, meq) in brain tissue.
  • Histopathological examination of brain lesions and immune cell infiltration (macrophages, CD4+, CD8+ T cells).
  • Assessment of major histocompatibility complex (MHC) antigen expression on brain cells.

Main Results:

  • Viral replication correlated with brain lesion development.
  • vv+MDV caused both inflammatory and proliferative lesions, while vMDV induced only inflammatory lesions.
  • Inflammatory lesions (macrophages, CD4+, CD8+ T cells) were transient; proliferative lesions (CD4+CD8- T cells) persisted.
  • MDV infection altered MHC antigen expression; vv+MDV induced more severe MHC class II upregulation and MHC class I downregulation.

Conclusions:

  • MDV pathotype dictates the nature and timing of brain lesions.
  • vv+MDV exhibits greater neurovirulence, associated with persistent proliferative lesions and distinct MHC modulation.
  • Findings elucidate MDV neuroinvasion mechanisms and pathotype-specific neuropathogenesis.

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