HLA-DQ Polymorphism Influences Progression of Demyelination and Neurologic Deficits in a Viral Model of Multiple Sclerosis

@article{Pavelko2000HLADQPI,
  title={HLA-DQ Polymorphism Influences Progression of Demyelination and Neurologic Deficits in a Viral Model of Multiple Sclerosis},
  author={Kevin D. Pavelko and Kristen M. Drescher and Dorian B. McGavern and Chella S. David and Moses Rodriguez},
  journal={Molecular and Cellular Neuroscience},
  year={2000},
  volume={15},
  pages={495-509}
}
The importance of genetic susceptibility in determining the progression of demyelination and neurologic deficits is a major focus in neuroscience. We studied the influence of human leukocyte antigen (HLA)-DQ polymorphisms on disease course and neurologic impairment in virus-induced demyelination. HLA-DQ6 or DQ8 was inserted as a transgene into mice lacking endogenous expression of MHC class I (beta(2)m) and class II (H2-A(beta)) molecules. Following Theiler's murine encephalomyelitis virus… 
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Human HLA-DR Transgenes Protect Mice from Fatal Virus-Induced Encephalomyelitis and Chronic Demyelination
TLDR
The hypothesis that the expression of a single human class II MHC molecule can, by itself, influence the control of an intracerebral pathogen in a host without a competent class I MHC immune response is supported.
Human class I major histocompatibility complex alleles determine central nervous system injury versus repair
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The hypothesis that the expression of a single human class I MHC molecule, independent of persistent virus infection, influences the extent of sub frequent chronic neuronal injury or repair in the absence of a class II MHC immune response is supported.
Periventricular Demyelination and Axonal Pathology Is Associated with Subependymal Virus Spread in a Murine Model for Multiple Sclerosis
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TLDR
Examination of a model of demyelination triggered by direct injection of Theiler s murine encephalomyelitis virus into the spinal cord suggests that animals that have been exogenously treated with glial growth factor have improved clinical function compared to animals receiving glia growth factor 2 or sensory motor derived factor.
Direct Comparison of Demyelinating Disease Induced by the Daniel's Strain and BeAn Strain of Theiler's Murine Encephalomyelitis Virus
TLDR
Findings indicate that the diseases induced by DA or BeAn are distinct, and functional deficits as measured by Rotarod were more severe in DA infected versus BeAn infected mice.
Untersuchung über die Virusausbreitung und -persistenz bei der murinen Theiler-Enzephalomyelitis von experimentell infizierten Mäusen mittels polyklonaler Antikörper und RNS-Sonden
TLDR
The aim of the study was to identify topographical differences of TMEV spread and demyelination in the CNS of experimentally infected susceptible SJL/J mice and resistant C57BL/6 mice.
Transgenic Expression of the 3D Polymerase Inhibits Theiler's Virus Infection and Demyelination
TLDR
It is found that 3D transgenic expression in genetically susceptible FVB mice led to substantially lower viral loads after infection with Theiler's murine encephalomyelitis virus (TMEV), which led to the preservation of large-diameter axons and motor function in these mice.
An Elite Controller of Picornavirus Infection Targets an Epitope That Is Resistant to Immune Escape
TLDR
The generated TMEV mutants that encode for mutations within the VP2121-130 peptide are generated, demonstrating that the virus is incapable of escaping the protective response and highlighting the importance of choosing appropriate vaccine antigens.
Immunogenetics, Resistance, and Susceptibility to Theiler’s Virus Infection
The genetic basis for differential susceptibility to Theiler’s virus-induced demyelinating disease is complex and often confusing, similar to the situation seen in analyzing the genetic risk for…
Factors directly affecting impulse transmission in inflammatory demyelinating disease: recent advances in our understanding
TLDR
Demyelination and inflammation both contribute to the neurological deficits characteristic of multiple sclerosis and Guillain-Barré syndrome, and factors such as nitric oxide, endocaine, cytokines, and antiganglioside antibodies also play significant roles.

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