Peripheral nerve protein, P0, as a potential receptor for Theiler's murine encephalomyelitis virus

Libbey, Jane E.; McCright, Ingeborg J.; Tsunoda, Ikuo; Wada, Yoshiaki; Fujinami, Robert S.

doi:10.1080/13550280152058753

Cited by 14 publications

References 43 publications

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Altered Cell Growth and Morphology in a BHK-21 Cell Mutant That Lacks a Receptor for Theiler's Murine Encephalomyelitis Virus

2002

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The receptor for Theiler's murine encephalomyelitis virus (TMEV) remains unknown. In vitro, BHK-21 cells are permissive to infection by TMEV. Selecting mutants of BHK-21 cells produced a cell line (BHKR-) resistant to infection by TMEV. Viral persistence was ruled out by immunofluorescent staining for viral antigens. BHKR- cells were nonpermissive to infection even at high multiplicities of infection. In contrast, cells were able to support one round of virus replication when transfected with infectious TMEV RNA. Binding studies indicated that TMEV was unable to attach to these cells. These data are consistent with the BHKR- cells lacking a receptor for TMEV. Interestingly, BHKR- cells were larger in size and had a significant lag in growth after subculture versus BHK-21 cells. This suggests that the TMEV receptor on BHK-21 cells could play an important role in cell growth and morphology under physiologic conditions. BHKR- cells should facilitate the search for TMEV receptors.

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Altered Cell Growth and Morphology in a BHK-21 Cell Mutant That Lacks a Receptor for Theiler's Murine Encephalomyelitis Virus

2002

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Low-Neurovirulence Theiler's Viruses Use Sialic Acid Moieties on N-linked Oligosaccharide Structures for Attachment

Shah

Lipton

2002

Virology

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Low-neurovirulence BeAn and DA Theiler's murine encephalomyelitis viruses (TMEV) cause persistent infection in the central nervous system (CNS) of susceptible mouse strains, leading to an inflammatory demyelinating process. A role for a specific virus-cell receptor interaction has been posited to explain why only low- and not high-neurovirulence TMEV cause persistent CNS infections. Low- but not high-neurovirulence TMEV use sialic acid for attachment to mammalian cells, which may contribute to neurovirulence attenuation and viral persistence. Analysis of BeAn virus binding and infection in cells with altered (mutated) cell-surface expression of sialic acid containing glyconjugates indicated that both binding and infection are mediated entirely by N-linked glycoproteins. By contrast, GDVII virus binding and infection appears to be dependent only in part on N-linked glycoproteins and not on O-linked glycoproteins or glycolipids. These results indicate that low-neurovirulence BeAn virus uses a sialic acid moiety expressed on an N-linked carbohydrate of a glycoprotein that serves as the protein entry receptor.

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TMEV and Neuroantigens: Myelin Genes and Proteins, Molecular Mimicry, Epitope Spreading, and Autoantibody-Mediated Remyelination

Tsunoda

Fujinami

2005

Experimental Models of Multiple Sclerosis

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The Theiler's murine encephalomyelitis (TMEV) model has been used to study the interactions of virus, myelin and anti-neuroantigen autoimmunity. TMEV and myelin can interrelate during virus entry and persistence. On virus entry, TMEV might use peripheral myelin Po protein as a virus receptor. For persistence, TMEV seems to require myelin functional proteins or structural myelin itself. Here, myelin and oligodendrocyte loss and downregulation of myelin genes would lead to demyelination, but might limit virus spread in the central nervous system. Unlike experimental allergic encephalomyelitis (EAE), a pathogenic role of anti-myelin autoimmunity is unclear in TMEV infection. Anti-myelin autoantibodies have been detected in TMEV infection. Among them, only anti-galactocerebroside (GC) antibody is shown to be myelinotoxic, and has molecular mimicry with TMEV. Myelin-specific T cells play no role in initiation or progression of demyelination in the first two to three months after TMEV infection. However, cellular autoimmunity against several myelin antigens (epitope spreading) can be detected during the late chronic stage.Using the TMEV model, epitope spreading and autoantibody-mediated remyelination have been investigated by recombinant TMEV and anti-neuroantigen (natural) antibodies, respectively Animal models, Autoimmune diseases of the nervous system, Demyelinating diseases, Galactosylceramides, Myelin basic proteins, myelin proteolipid protein, Multiple sclerosis, Picornaviridae infections Chapter B2.

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Peripheral nerve protein, P0, as a potential receptor for Theiler's murine encephalomyelitis virus

Cited by 14 publications

References 43 publications

Altered Cell Growth and Morphology in a BHK-21 Cell Mutant That Lacks a Receptor for Theiler's Murine Encephalomyelitis Virus

Altered Cell Growth and Morphology in a BHK-21 Cell Mutant That Lacks a Receptor for Theiler's Murine Encephalomyelitis Virus

Low-Neurovirulence Theiler's Viruses Use Sialic Acid Moieties on N-linked Oligosaccharide Structures for Attachment

TMEV and Neuroantigens: Myelin Genes and Proteins, Molecular Mimicry, Epitope Spreading, and Autoantibody-Mediated Remyelination

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