ArticleBrain pathology (Zurich, Switzerland)2011
Transgenic expression of viral capsid proteins predisposes to axonal injury in a murine model of multiple sclerosis.
Article in Brain pathology (Zurich, Switzerland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Comparison of Reported Spinal Cord Lesions in Progressive Multiple Sclerosis with Theiler's Murine Encephalomyelitis Virus Induced Demyelinating Disease.International journal of molecular sciences · 2019Article
- Therapeutic potential of extracellular vesicles derived from human mesenchymal stem cells in a model of progressive multiple sclerosis.PloS one · 2018Article
- A single dose of a neuron-binding human monoclonal antibody improves brainstem NAA concentrations, a biomarker for density of spinal cord axons, in a model of progressive multiple sclerosis.Journal of neuroinflammation · 2015Article
- A CD8 T-cell epitope variant enhances immune targeting to a recombinant picornavirus vaccine antigen.Viral immunology · 2014Article
- Differential expression of multiple kallikreins in a viral model of multiple sclerosis points to unique roles in the innate and adaptive immune response.Biological chemistry · 2014Article
- Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.Journal of neurology & translational neuroscience · 2014Article
- Kallikrein 6 regulates early CNS demyelination in a viral model of multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2012Article
- Viral models of multiple sclerosis: neurodegeneration and demyelination in mice infected with Theiler's virus.Progress in neurobiologyArticle
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
We used transgenic expression of capsid antigens to Theiler's murine encephalomyelitis virus (TMEV) to study the influence of VP1, VP2 or VP2(121-130) to either protection or pathogenesis to chronic spinal cord demyelination, axonal loss and functional deficits during the acute and chronic phases of infection. We used both mice that are normally susceptible (FVB) and mice normally resistant (FVB.D(b) ) to demyelination. Transgenic expression of VP2(121-130) epitope in resistant FVB.D(b) mice caused spinal cord pathology and virus persistence because the VP2(121-130) epitope is the dominant peptide recognized by D(b) , which is critical for virus clearance. In contrast, all three FVB TMEV transgenic mice showed more demyelination, inflammation and axonal loss as compared with wild-type FVB mice, even though virus load was not increased. Motor function measured by rotarod showed weak correlation with total number of midthoracic axons, but a strong correlation with large-caliber axons (>10µm(2) ). This study supports the hypothesis that expression of viral capsid proteins as self influences the extent of axonal pathology following Theiler's virus-induced demyelination. The findings provide insight into the role of axonal injury in the development of functional deficits that may have relevance to human demyelinating disease.
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