ArticleThe American journal of pathology2006
Oligodendrocytes are a major target of the toxicity of spongiogenic murine retroviruses.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Oligodendrocytes that survive acute coronavirus infection induce prolonged inflammatory responses in the CNS.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Astrocyte Infection Is Required for Retrovirus-Induced Spongiform Neurodegeneration Despite Suppressed Viral Protein Expression.Frontiers in neuroscience · 2019Article
- Evidence of Human Parvovirus B19 Infection in the Post-Mortem Brain Tissue of the Elderly.Viruses · 2018Article
- Rebound from Inhibition: Self-Correction against Neurodegeneration?Journal of clinical & cellular immunology · 2017Article
- Identification of 1,2,3-triazole derivatives that protect pancreatic β cells against endoplasmic reticulum stress-mediated dysfunction and death through the inhibition of C/EBP-homologous protein expression.Bioorganic & medicinal chemistry · 2016Article
- Ecotropic Murine Leukemia Virus Infection of Glial Progenitors Interferes with Oligodendrocyte Differentiation: Implications for Neurovirulence.Journal of virology · 2016Article
- Postinhibitory rebound neurons and networks are disrupted in retrovirus-induced spongiform neurodegeneration.Journal of neurophysiology · 2014Article
- Unique N-linked glycosylation of CasBrE Env influences its stability, processing, and viral infectivity but not its neurotoxicity.Journal of virology · 2013Article
- Senescence-accelerated Mice (SAMs) as a Model for Brain Aging and Immunosenescence.Aging and disease · 2011Article
- Bovine spongiform encephalopathy infection alters endogenous retrovirus expression in distinct brain regions of cynomolgus macaques (Macaca fascicularis).Molecular neurodegeneration · 2011Article
- Retrovirus-induced spongiform neurodegeneration is mediated by unique central nervous system viral targeting and expression of env alone.Journal of virology · 2011Article
- Neuropeptide Y has a protective role during murine retrovirus-induced neurological disease.Journal of virology · 2010Article
- The degree of folding instability of the envelope protein of a neurovirulent murine retrovirus correlates with the severity of the neurological disease.Journal of virology · 2009Article
- The ubiquitin-proteasome system in spongiform degenerative disorders.Biochimica et biophysica acta · 2008Review
- Up-regulation of a cellular protein at the translational level by a retrovirus.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The neurovirulent retroviruses FrCasE and Moloney MLV-ts1 cause noninflammatory spongiform neurodegeneration in mice, manifested clinically by progressive spasticity and paralysis. Neurons have been thought to be the primary target of toxicity of these viruses. However the neurons themselves appear not to be infected, and the possible indirect mechanisms driving the neuronal toxicity have remained enigmatic. Here we have re-examined the cells that are damaged by these viruses, using lineage-specific markers. Surprisingly, these cells expressed the basic helix-loop-helix transcription factor Olig2, placing them in the oligodendrocyte lineage. Olig2+ cells were found to be infected, and many of these cells exhibited focal cytoplasmic vacuolation, suggesting that infection by spongiogenic retroviruses is directly toxic to these cells. As cytoplasmic vacuolation progressed, however, signs of viral protein expression appeared to wane, although residual viral RNA was detectable by in situ hybridization. Cells with the most advanced cytoplasmic effacement expressed the C/EBP-homologous protein (CHOP). This protein is up-regulated as a late event in a cellular response termed the integrated stress response. This observation may link the cellular pathology observed in the brain with cellular stress responses known to be induced by these viruses. The relevance of these observations to oligodendropathy in humans is discussed.
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