CAN VIRAL ENVELOPE GLYCOLIPIDS PRODUCE AUTO‐IMMUNITY, WITH REFERENCE TO THE CNS AND MULTIPLE SCLEROSIS?
Identifieur interne : 001656 ( Main/Exploration ); précédent : 001655; suivant : 001657CAN VIRAL ENVELOPE GLYCOLIPIDS PRODUCE AUTO‐IMMUNITY, WITH REFERENCE TO THE CNS AND MULTIPLE SCLEROSIS?
Auteurs : H. E. Webb ; J. K. FazakerleySource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 1984-01.
English descriptors
- Teeft :
- Acta pathologica, Almeida waterson, Alphavirus, Avirulent semliki forest virus, Basement membrane, Blocks receptors, Brain cell cultures, Canine distemper, Canine distemper virus, Carrier effect, Cell membranes, Demyelination, Dowling russell, Fazakerley, Gangliosides, General virology, Glycolipids, Hirschberg robbins, Host cell, Host cell membranes, Illavia webb, Ilyas davison, Immune, Immune reaction, Immune response, Immune serum, Immune system, Influenza virus, Langat, Langat virus, Leibowitz gregson, Lipid, Lymphocyte, Many viruses, Marcus schwarting, Measles, Measles virus, Membrane, Microbios letters, Mouse brain, Multiple sclerosis, Multiple sclerosis patients, Mumps virus, Myelin, National academy, Neurological, Neurological sciences, Neurotropic, Neurotropic viruses, Neurovirology unit, Pathak, Pathak webb, Peripheral blood lymphocytes, Peripheral circulation, Phospholipid composition, Possible role, Powerful stimulators, Rapport graf, Sclerosis, Semliki, Semliki forest virus, Several viruses, Sindbis, Sindbis virus, Such diseases, Susceptible individuals, Tissue culture, Tschannen schaefer, Ultrastructural study, Vaccinia virus, Venezuelan equine encephalomyelitis virus, Viral, Viral envelope, Viral envelope glycolipids, Viral protein spikes, Viral proteins, Virology, Virus, Virus infection, Webb, West nile virus.
Abstract
Many viruses, with lipid envelopes derived from the host cell membranes, have been implicated in the aetiology of multiple sclerosis (MS), and epidemiological studies support an infectious agent. Alternatively the disease is thought by other workers to be auto‐immune in nature, and recently much attention has been focused on immunological sensitivity to glycolipids in MS patients. In this paper it is proposed that CNS demyelination could arise in susceptible individuals (HLA type) from an immune response to glycolipids, triggered by the carrier effect of one or more enveloped neurotropic viruses.
Url:
DOI: 10.1111/j.1365-2990.1984.tb00335.x
Affiliations:
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Le document en format XML
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<term>Blocks receptors</term>
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<term>Canine distemper</term>
<term>Canine distemper virus</term>
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<term>Ilyas davison</term>
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<term>Immune system</term>
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<term>Langat virus</term>
<term>Leibowitz gregson</term>
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<term>Many viruses</term>
<term>Marcus schwarting</term>
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<term>Semliki forest virus</term>
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<term>Viral protein spikes</term>
<term>Viral proteins</term>
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<front><div type="abstract" xml:lang="en">Many viruses, with lipid envelopes derived from the host cell membranes, have been implicated in the aetiology of multiple sclerosis (MS), and epidemiological studies support an infectious agent. Alternatively the disease is thought by other workers to be auto‐immune in nature, and recently much attention has been focused on immunological sensitivity to glycolipids in MS patients. In this paper it is proposed that CNS demyelination could arise in susceptible individuals (HLA type) from an immune response to glycolipids, triggered by the carrier effect of one or more enveloped neurotropic viruses.</div>
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