ArticleClinical & developmental immunology2013
Microglia play a major role in direct viral-induced demyelination.
Article in Clinical & developmental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 40 citations in OpenAlex.
- Immunomodulatory Mechanisms Underlying Neurological Manifestations in Long COVID: Implications for Immune-Mediated Neurodegeneration.International journal of molecular sciences · 2025Review
- From Viral Infections to Alzheimer's Disease: Unveiling the Mechanistic Links Through Systems Bioinformatics.The Journal of infectious diseases · 2024Article
- Article
- Review
- Neurogenesis and Viral Infection.Frontiers in immunology · 2022Review
- The Potential Role of COVID-19 in the Pathogenesis of Multiple Sclerosis-A Preliminary Report.Viruses · 2021Review
- Cellular and Molecular Effects of SARS-CoV-2 Linking Lung Infection to the Brain.Frontiers in immunology · 2021Review
- Neural Infection by Oropouche Virus in Adult Human Brain Slices Induces an Inflammatory and Toxic Response.Frontiers in neuroscience · 2021Article
- Ifit2 deficiency restricts microglial activation and leukocyte migration following murine coronavirus (m-CoV) CNS infection.PLoS pathogens · 2020Article
- How to detect and track chronic neurologic sequelae of COVID-19? Use of auditory brainstem responses and neuroimaging for long-term patient follow-up.Brain, behavior, & immunity - health · 2020Review
- Article
- Innate Immune Responses and Viral-Induced Neurologic Disease.Journal of clinical medicine · 2018Review
- Loss of Cx43-Mediated Functional Gap Junction Communication in Meningeal Fibroblasts Following Mouse Hepatitis Virus Infection.Molecular neurobiology · 2018Article
- BALB/c mice infected with DENV-2 strain 66985 by the intravenous route display injury in the central nervous system.Scientific reports · 2018Article
- Role of the Golgi Apparatus in the Blood-Brain Barrier: Golgi Protection May Be a Targeted Therapy for Neurological Diseases.Molecular neurobiology · 2018Review
- Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Demyelinating strain of mouse hepatitis virus infection bridging innate and adaptive immune response in the induction of demyelination.Clinical immunology (Orlando, Fla.) · 2016Article
- Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders.Brain sciences · 2016Review
- Mouse Hepatitis Virus Infection Remodels Connexin43-Mediated Gap Junction Intercellular Communication In Vitro and In Vivo.Journal of virology · 2015Article
- Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia are the resident macrophage-like populations in the central nervous system (CNS). Microglia remain quiescent, unable to perform effector and antigen presentation (APC) functions until activated by injury or infection, and have been suggested to represent the first line of defence for the CNS. Previous studies demonstrated that microglia can be persistently infected by neurotropic mouse hepatitis virus (MHV) which causes meningoencephalitis, myelitis with subsequent axonal loss, and demyelination and serve as a virus-induced model of human neurological disease multiple sclerosis (MS). Current studies revealed that MHV infection is associated with the pronounced activation of microglia during acute inflammation, as evidenced by characteristic changes in cellular morphology and increased expression of microglia-specific proteins, Iba1 (ionized calcium-binding adaptor molecule 1), which is a macrophage/microglia-specific novel calcium-binding protein and involved in membrane ruffling and phagocytosis. During chronic inflammation (day 30 postinfection), microglia were still present within areas of demyelination. Experiments performed in ex vivo spinal cord slice culture and in vitro neonatal microglial culture confirmed direct microglial infection. Our results suggest that MHV can directly infect and activate microglia during acute inflammation, which in turn during chronic inflammation stage causes phagocytosis of myelin sheath leading to chronic inflammatory demyelination.
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What OpenQuestion holds
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.