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Measles virus in the brain

E Norrby1, K Kristensson

  • 1Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden.

Brain Research Bulletin
|January 1, 1997
PubMed

Insights

Measles virus causes three central nervous system infections: autoimmune encephalitis, direct viral attack encephalitis, and subacute sclerosing panencephalitis (SSPE). Molecular studies reveal viral persistence mechanisms in SSPE, impacting immune surveillance.

Area of Science:

  • Neurovirology
  • Immunology
  • Molecular Genetics

Background:

  • Measles virus (MeV) infections manifest in the central nervous system (CNS) as acute postinfectious encephalitis, acute progressive encephalitis (inclusion body encephalitis), and subacute sclerosing panencephalitis (SSPE).
  • Postinfectious encephalitis is linked to autoimmune responses, while acute progressive encephalitis involves direct viral attack with compromised cell-mediated immunity.
  • SSPE is a late-onset, persistent measles infection with complex viral mechanisms.

Purpose of the Study:

  • To review and discuss mechanisms of measles virus persistence in the brain.
  • To explore virus-cell interactions in CNS infections using explant cultures and experimental animal models.
  • To investigate the role of immune function defects in measles virus brain infection initiation and spread.

Main Methods:

  • Analysis of molecular genetic studies on MeV protein expression (matrix, fusion, hemagglutinin) and viral persistence.
  • Examination of virus-cell interactions using explant cultures of human and animal neuronal cells.
  • In vivo studies using experimental animals, including immunodeficient mice, to model CNS infections.

Main Results:

  • Molecular genetic studies identified mechanisms of viral persistence due to defective MeV protein expression, evading immune surveillance.
  • Explant cultures provided insights into virus-cell interactions in neuronal cells.
  • Animal models, particularly immunodeficient mice, facilitated the study of MeV infection initiation and dissemination in the brain.

Conclusions:

  • Defective measles virus protein expression is a key mechanism for viral persistence in the CNS, enabling immune evasion.
  • Virus-cell interactions and host immune status critically influence the pathogenesis of measles virus-induced encephalitis.
  • Experimental models are crucial for understanding the complex interplay between measles virus and the brain, leading to diverse neurological outcomes.

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