ReviewJournal of neurovirology2003
Virus demyelination.
Review in Journal of neurovirology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- Novel Animal Models for Multiple Sclerosis: R-Ras GTPases in Myelin Pathophysiology.Biomolecules · 2025Review
- Temporally resolved single-cell RNA sequencing reveals protective and pathological responses during herpes simplex virus CNS infection.Journal of neuroinflammation · 2025Article
- Genotype-driven sensitivity of mice to tick-borne encephalitis virus correlates with differential host responses in peripheral macrophages and brain.Journal of neuroinflammation · 2025Article
- Inflammation's impact on the interaction between oligodendrocytes and axons.Discovery immunology · 2025Review
- Mechanosensitive Piezo1 channel: an emerging target in demyelination disease.Frontiers in cellular neuroscience · 2025Review
- Bladder and bowel incontinence in COVID-19.Journal of medical virology · 2021Article
- Viral mouse models used to study multiple sclerosis: past and present.Archives of virology · 2021Review
- Unpuzzling COVID-19: tissue-related signaling pathways associated with SARS-CoV-2 infection and transmission.Clinical science (London, England : 1979) · 2020Article
- Neuropathology of COVID-19: a spectrum of vascular and acute disseminated encephalomyelitis (ADEM)-like pathology.Acta neuropathologica · 2020Article
- Anosmia in COVID-19: Mechanisms and Significance.Chemical senses · 2020Article
- Evidence of Human Parvovirus B19 Infection in the Post-Mortem Brain Tissue of the Elderly.Viruses · 2018Article
- Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia.Journal of virology · 2016Article
- Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.Neuropharmacology · 2016Review
- Toxins Targeting the Kv1.3 Channel: Potential Immunomodulators for Autoimmune Diseases.Toxins · 2015Review
- CD8 transverse myelitis in a patient with HIV-1 infection.BMJ case reports · 2014Article
- Damage to the optic chiasm in myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis mice.Magnetic resonance insights · 2014Article
- Expression of HERV-Fc1, a human endogenous retrovirus, is increased in patients with active multiple sclerosis.Journal of virology · 2012Article
- Poly(I:C) promotes TNFα/TNFR1-dependent oligodendrocyte death in mixed glial cultures.Journal of neuroinflammation · 2011Article
- Autoimmunity-related demyelination in infection by Japanese encephalitis virus.Journal of biomedical science · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A number of viruses can initiate central nervous system (CNS) diseases that include demyelination as a major feature of neuropathology. In humans, the most prominent demyelinating diseases are progressive multifocal leukoencephalopathy, caused by JC papovirus destruction of oligodendrocytes, and subacute sclerosing panencephalitis, an invariably fatal childhood disease caused by persistent measles virus. The most common neurological disease of young adults in the developed world, multiple sclerosis, is also characterized by lesions of inflammatory demyelination; however, the etiology of this disease remains an enigma. A viral etiology is possible, because most demyelinating diseases of known etiology in both man and animals are viral. Understanding of the pathogenesis of virus-induced demyelination derives for the most part from the study of animal models. Studies with neurotropic strains of mouse hepatitis virus, Theiler's virus, and Semliki Forest virus have been at the forefront of this research. These models demonstrate how viruses enter the brain, spread, persist, and interact with immune responses. Common features are an ability to infect and persist in glial cells, generation of predominantly CD8(+) responses, which control and clear the early phase of virus replication but which fail to eradicate the infection, and lesions of inflammatory demyelination. In most cases demyelination is to a limited extent the result of direct virus destruction of oligodendrocytes, but for the most part is the consequence of immune and inflammatory responses. These models illustrate the roles of age and genetic susceptibility and establish the concept that persistent CNS infection can lead to the generation of CNS autoimmune responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.