Multiplication of rubella and measles viruses in primary rat neural cell cultures: relevance to a postulated triggering mechanism for multiple sclerosis

Atkins, Gregory J.; Mooney, Dorothy A.; Fahy, D. A.; Ng, Shvets; Sheahan, B. J.

doi:10.1111/j.1365-2990.1991.tb00727.x

Cited by 11 publications

(22 citation statements)

References 21 publications

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“…In in vitro cultures infected with the Edmonston vaccine strain, virus antigen was detected in oligodendrocytes but not in neurones until 6 dpi, reflecting the ex vivo findings. This contrasts with an earlier report of infection of purified rat neuronal and glial cultures with the Edmonston MV strain where the virus was detected earlier in neurones than glial cells [36]. In another study a comparison of infection in primary hippocampal neuronal cultures from CD46 transgenic and nontransgenic embryonic mice with the Edmonston vaccine strain found that no infection was detected in the latter when examined up to 6 days [12].…”

Section: Discussioncontrasting

confidence: 58%

Persistent measles virus infection of mouse neural cells lacking known human entry receptors

Abdullah

Earle

Gardiner³

et al. 2009

Neuropathology Appl Neurobio

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Section: Discussioncontrasting

confidence: 58%

Persistent measles virus infection of mouse neural cells lacking known human entry receptors

Abdullah

Earle

Gardiner³

et al. 2009

Neuropathology Appl Neurobio

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“…HB has been previously described to have homologous amino acid stretches with human MBP (Wucherpfenning and Strominger, 1995). Atkins et al (1991) have shown a sequence similarity between the amino‐terminus of human PLP and RV envelope E 1 protein. In this work, we analyzed structural glycoprotein E 2 of RV that was found to induce high specific antibody titers in MS patients (Nath and Wolinsky, 1990).…”

Section: Resultsmentioning

confidence: 99%

“…We searched for a potential viral candidate that would exhibit sufficient molecular mimicry with MOG to induce demyelinating antibodies. We focused on HB and RV, which have long been implicated in MS (Atkins et al, 1991). RV is a togavirus with a molecular biology similar to that of SFV.…”

Section: Discussionmentioning

confidence: 99%

Antibodies directed against rubella virus induce demyelination in aggregating rat brain cell cultures

Duvanel

Honegger

Matthieu

2001

J of Neuroscience Research

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To link the presence of intrathecal virus-specific oligoclonal immunoglobulin G (IgG) in multiple sclerosis patients to a demyelinating activity, aggregating rat brain cell cultures were treated with antibodies directed against two viruses, namely, rubella (RV) and hepatitis B (HB). Anti-RV antibodies in the presence of complement decreased myelin basic protein concentrations in a dose-dependent manner, whereas anti-HB antibodies had no effect. A similar but less pronounced effect was observed on the enzymatic activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase, which is enriched in noncompact membranes of oligodendrocytes. These effects were comparable to those in cultures treated with antibodies directed against myelin oligodendrocyte glycoprotein (MOG), previously found to be myelinotoxic both in vitro and in vivo. Sequence homologies were found between structural glycoprotein E(2) of RV and MOG, suggesting that demyelination was due to molecular mimicry. To support the hypothesis that demyelination was caused by anti-RV IgG that recognized an MOG epitope, we found that anti-RV antibodies depleted MOG in a dose-dependent manner. Further evidence came from the demonstration that anti-RV and anti-MOG IgG colocalized on oligodendrocyte processes and that both revealed by Western blot a 28 kDa protein in CNS myelin, a molecular weight corresponding to MOG. These findings suggest that a virus such as RV exhibiting molecular mimicry with MOG can trigger an autoimmune demyelination.

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“…Despite these investigations there are very few studies that have utilized either primary cells or oligodendrocyte cell lines to study MV infection in this important cell type. In one previous report, Atkins et al (1991) reported that a nonrodent-adapted strain of Edmonston strain of MV multiplied and produced a cytopathic effect in primary cultures of rat oligodendrocytes (Atkins et al, 1991). Viral infection in that study was only monitored by cytopathic effects and no viral immunocytochemistry or ultrastructural investigations were undertaken.…”

Section: Introductionmentioning

confidence: 98%

Infection of human oligodendroglioma cells by a recombinant measles virus expressing enhanced green fluorescent protein

et al. 2002

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One of the hallmarks of the human CNS disease subacute sclerosing panencephalitis (SSPE) is a high level of measles virus (MV) infection of oligodendrocytes. It is therefore surprising that there is only one previous report of MV infection of rat oligodendrocytes in culture and no reports of human oligodendrocyte infection in culture. In an attempt to develop a model system to study MV infection of oligodendrocytes, time-lapse confocal microscopy, immunocytochemistry, and electron microscopy (EM) were used to study infection of the human oligodendroglioma cell line, MO3.13. A rat oligodendrocyte cell line, OLN-93, was also studied as a control. MO3.13 cells were shown to be highly susceptible to MV infection and virus budding was observed from the surface of infected MO3.13 cells by EM. Analysis of the infection in real time and by immunocytochemistry revealed that virus spread occurred by cell-to-cell fusion and was also facilitated by virus transport in cell processes. MO3.13 cells were shown to express CD46, a MV receptor, but were negative for the recently discovered MV receptor, signaling leucocyte activation molecule (SLAM). Immunohistochemical studies on SSPE tissue sections demonstrated that CD46 was also expressed on populations of human oligodendrocytes. SLAM expression was not detected on oligodendrocytes. These studies, which are the first to show MV infection of human oligodendrocytes in culture, show that the cells are highly susceptible to MV infection and this model cell line has been used to further our understanding of MV spread in the CNS.

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Multiplication of rubella and measles viruses in primary rat neural cell cultures: relevance to a postulated triggering mechanism for multiple sclerosis

Cited by 11 publications

References 21 publications

Persistent measles virus infection of mouse neural cells lacking known human entry receptors

Persistent measles virus infection of mouse neural cells lacking known human entry receptors

Antibodies directed against rubella virus induce demyelination in aggregating rat brain cell cultures

Infection of human oligodendroglioma cells by a recombinant measles virus expressing enhanced green fluorescent protein

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