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Measles virus in the brain
1Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden.
Brain Research Bulletin
|January 1, 1997
Summary
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.