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Journal of the neurological sciences1981; 49(3); 397-418; doi: 10.1016/0022-510x(81)90030-7

Central nervous system demyelination in Venezuelan equine encephalomyelitis infection.

Abstract: Arboviruses are important pathogens for both animals and humans. Venezuelan equine encephalomyelitis virus (VEEV) is an arbovirus whose pathogenicity for grey matter structures has been previously studied. To our knowledge, the present study is the first to describe extensive inflammation and demyelination in spinal cord white matter of mice infected with VEEV. To probe a possible immunepathogenesis of white matter alterations in this infection, nude mice and heterozygous controls were similarly infected. Whereas controls still showed inflammatory demyelination, nude mice showed no white matter changes in the absence of a mononuclear inflammatory response. These results suggest that white matter changes in VEEV infection are dependent upon the host immune-response, rather than produced by primary viral cytolytic activity. Such findings are similar to those we and others obtained in a number of different viral infections and support the possibility that the host immune response may be the common denominator leading to myelin injury in a variety of viral diseases. The hypothesis of "by-stander killing" of myelin is discussed as a possible host-mediated mechanism of demyelination in viral infections.
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Publication Date: 1981-03-01 PubMed ID: 7217991DOI: 10.1016/0022-510x(81)90030-7Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article discusses a study that reveals the contribution of the immune response, rather than direct viral activity, to the degeneration of myelin (demyelination) in the white matter of the spinal cord in mice infected with the Venezuelan equine encephalomyelitis virus (VEEV).

Understanding the Research

The article breaks down several areas of understanding:

  • Background: Arboviruses, the key pathogens for animals and humans, cause a variety of diseases. The pathogenicity of VEEV, an arbovirus, for grey matter had been previously studied, but its impact on spinal cord white matter had not been explored until this research.
  • Study Objective: The researchers sought to highlight the potentially damaging impact of VEEV on the white matter of the spinal cord, focusing specifically on inflammation and demyelination.
  • Research Methods: Mice were infected with VEEV to study the white matter changes. The study utilized both ‘nude mice’ and ‘heterozygous controls’, i.e., ‘naked’ mice with a compromised immune system and ‘normal’ mice respectively.
  • Findings: The study discovered extensive inflammation and demyelination in the white matter of normal mice. However, nude mice, with a deficient immune response, showed no white matter changes. These findings suggest that the host immune response causes white matter changes in VEEV infection, not the direct viral activity.
  • Comparisons with Other Viral Infections: The researchers compare these findings with other viral infections and propose that the host’s immune response may be a common factor causing myelin injury in various viral diseases, supporting the concept of “by-stander killing” of myelin in viral infections.

Implications and Hypothesis

The research essentially reveals that the degeneration of myelin in the white matter of the spinal cord in VEEV-infected mice is dependent on the host’s immune response rather than the direct impact of the virus. This could potentially change the way medical professionals approach treatment.

The ‘by-stander killing’ hypothesis suggests that in viral infections, the immune system inadvertently injures and destroys the myelin while trying to combat the virus. This could explain the inflammation and demyelination observed in the study and can potentially help understand and manage viral diseases better.

Cite This Article

APA
Dal Canto MC, Rabinowitz SG. (1981). Central nervous system demyelination in Venezuelan equine encephalomyelitis infection. J Neurol Sci, 49(3), 397-418. https://doi.org/10.1016/0022-510x(81)90030-7

Publication

Journal of the neurological sciences
ISSN: 0022-510X
NlmUniqueID: 0375403
Country: Netherlands
Language: English
Volume: 49
Issue: 3
Pages: 397-418

Researcher Affiliations

Dal Canto, M C
    Rabinowitz, S G

      MeSH Terms

      • Animals
      • Axons / ultrastructure
      • Brain / pathology
      • Demyelinating Diseases / pathology
      • Disease Models, Animal
      • Encephalomyelitis, Equine / pathology
      • Encephalomyelitis, Venezuelan Equine / pathology
      • Heterozygote
      • Mice
      • Mice, Inbred BALB C
      • Mice, Nude
      • Microscopy, Electron
      • Nerve Fibers, Myelinated / ultrastructure
      • Spinal Cord / pathology

      Grant Funding

      • NS-13011 / NINDS NIH HHS
      • NS-13045 / NINDS NIH HHS

      Citations

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