Theiler's murine encephalomyelitis virus preferentially infects immature stages of the murine oligodendrocyte precursor cell line BO-1 and blocks oligodendrocytic differentiation in vitro

Pringproa, Kidsadagon; Rohn, Karl; Kummerfeld, Maren; Wewetzer, Konstantin; Baumgärtner, Wolfgang

doi:10.1016/j.brainres.2010.02.068

Cited by 18 publications

(24 citation statements)

References 53 publications

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“…Scale bar = 20 μm. c Quantification of corrected total cell fluorescence of Olig2 expression in uninfected and infected OPCs (***p<0.0001) study, differentiation was also found to be inhibited by TMEV infection, which is consistent with our findings (Pringproa et al 2010).…”

Section: Discussionsupporting

confidence: 93%

Depletion of Olig2 in oligodendrocyte progenitor cells infected by Theiler’s murine encephalomyelitis virus

et al. 2015

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Theiler's murine encephalomyelitis virus (TMEV) infects the central nervous system of mice and causes a demyelinating disease that is a model for multiple sclerosis. During the chronic phase of the disease, TMEV persists in oligodendrocytes and macrophages. Lack of remyelination has been attributed to insufficient proliferation and differentiation of oligodendrocyte progenitor cells (OPCs), but the molecular mechanisms remain unknown. Here, we employed pluripotent stem cell technologies to generate pure populations of mouse OPCs to study the temporal and molecular effects of TMEV infection. Global transcriptome analysis of RNA sequencing data revealed that TMEV infection of OPCs caused significant up-regulation of 1926 genes, whereas 1853 genes were significantly down-regulated compared to uninfected cells. Pathway analysis revealed that TMEV disrupted many genes required for OPC growth and maturation. Down-regulation of Olig2, a transcription factor necessary for OPC proliferation, was confirmed by real-time PCR, immunofluorescence microscopy, and western blot analysis. Depletion of Olig2 was not found to be specific to viral strain and did not require expression of the leader (L) protein, which is a multifunctional protein important for persistence, modulation of gene expression, and cell death. These data suggest that direct infection of OPCs by TMEV may inhibit remyelination during the chronic phase of TMEV-induced demyelinating disease.

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Section: Discussionsupporting

confidence: 93%

Depletion of Olig2 in oligodendrocyte progenitor cells infected by Theiler’s murine encephalomyelitis virus

et al. 2015

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“…The capacity of the initially mostly A2B5‐positive, bipolar BO‐1 cells (http://onlinelibrary.wiley.com/doi/10.1111/nan.12133/suppinfo) to differentiate to either CNPase‐positive, multiprocessed cells with an immature oligodendrocyte morphology (http://onlinelibrary.wiley.com/doi/10.1111/nan.12133/suppinfo) or GFAP‐positive, plump spindloid cells with astrocytic morphology (http://onlinelibrary.wiley.com/doi/10.1111/nan.12133/suppinfo) is known to be dependent on the applied medium [32,48]. Accordingly, 92% of the cells expressed A2B5 in proliferation medium and in oligodendrocytic differentiation medium, whereas only 87% of the cells expressed this marker when cultured in astrocytic differentiation medium (http://onlinelibrary.wiley.com/doi/10.1111/nan.12133/suppinfo).…”

Section: Resultsmentioning

confidence: 99%

STAT3 represents a molecular switch possibly inducing astroglial instead of oligodendroglial differentiation of oligodendroglial progenitor cells in Theiler's murine encephalomyelitis

Sun¹,

Lehmbecker²,

Kalkuhl

et al. 2015

Neuropathology Appl Neurobio

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“…Scanning electron microscopy was performed as described previously32. Briefly, cultured cells were prefixed in glutaraldehyde (2.5%) for 24 hours and subsequently treated with osmium tetroxide (1%) for 2 hours.…”

Section: Methodsmentioning

confidence: 99%

The differentiated airway epithelium infected by influenza viruses maintains the barrier function despite a dramatic loss of ciliated cells

Yang

Beineke³

et al. 2016

Sci Rep

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108

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Virus-host interactions in the respiratory epithelium during long term influenza virus infection are not well characterized. Therefore, we developed an air-liquid interface culture system for differentiated porcine respiratory epithelial cells to study the effect of virus-induced cellular damage. In our well-differentiated cells, α2,6-linked sialic acid is predominantly expressed on the apical surface and the basal cells mainly express α2,3-linked sialic acid. During the whole infection period, release of infectious virus was maintained at a high titre for more than seven days. The infected epithelial cells were subject to apoptosis resulting in the loss of ciliated cells together with a thinner thickness. Nevertheless, the airway epithelium maintained trans-epithelial electrical resistance and retained its barrier function. The loss of ciliated cells was compensated by the cells which contained the KRT5 basal cell marker but were not yet differentiated into ciliated cells. These specialized cells showed an increase of α2,3-linked sialic acid on the apical surface. In sum, our results help to explain the localized infection of the airway epithelium by influenza viruses. The impairment of mucociliary clearance in the epithelial cells provides an explanation why prior viral infection renders the host more susceptible to secondary co-infection by another pathogen.

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Theiler's murine encephalomyelitis virus preferentially infects immature stages of the murine oligodendrocyte precursor cell line BO-1 and blocks oligodendrocytic differentiation in vitro

Cited by 18 publications

References 53 publications

Depletion of Olig2 in oligodendrocyte progenitor cells infected by Theiler’s murine encephalomyelitis virus

Depletion of Olig2 in oligodendrocyte progenitor cells infected by Theiler’s murine encephalomyelitis virus

STAT3 represents a molecular switch possibly inducing astroglial instead of oligodendroglial differentiation of oligodendroglial progenitor cells in Theiler's murine encephalomyelitis

The differentiated airway epithelium infected by influenza viruses maintains the barrier function despite a dramatic loss of ciliated cells

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