ArticleVirology2006
Human coronavirus OC43 infection induces chronic encephalitis leading to disabilities in BALB/C mice.
Article in Virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 2 of them syntheses that pooled it.
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
134 citing papers in PubMed, 2 syntheses or guidelines pooled it, 196 citations in OpenAlex.
- Neurological manifestations of COVID-19 and other coronavirus infections: A systematic review.Clinical neurology and neurosurgery · 2020Pooled it
- Respiratory Syndrome Coronavirus Infections: Possible Mechanisms of Neurological Implications-A Systematic Review.Frontiers in neurology · 2020Pooled it
- Porcine hemagglutinating encephalomyelitis virus nucleocapsid protein targets RIG-I and IRF3 to evade IFN immunity.Journal of virology · 2026Article
- Farm animal coronaviruses: the solution is in vaccines.The veterinary quarterly · 2025Review
- Current Status and Challenges of Vaccine Development for Seasonal Human Coronaviruses.Vaccines · 2025Review
- From zoonotic spillover to endemicity: the broad determinants of human coronavirus tropism.mBio · 2025Review
- Human coronavirus OC43 infection in human cerebral organoids: novel insights on pathogenesis and potential therapeutic interventions.Journal of biomedical science · 2025Article
- Monkeypox virus spreads from cell-to-cell and leads to neuronal death in human neural organoids.Nature communications · 2025Article
- The age-dependent neuroglial interaction with peripheral immune cells in coronavirus-induced neuroinflammation with a special emphasis on COVID-19.Biogerontology · 2025Review
- SARS-CoV-2: A synergy to the Alzheimer's disease.Journal of neurovirology · 2025Review
- Review
- Utilizing HCoV-OC43 to better understand the neurological impact of COVID-19.Brain, behavior, & immunity - health · 2024Article
- COVID-19 and the impact on Alzheimer's disease pathology.Journal of neurochemistry · 2024Review
- Indomethacin inhibits human seasonal coronaviruses at late stages of viral replication in lung cells: Impact on virus-induced COX-2 expression.Journal of virus eradication · 2024Article
- Phase Separation of SARS-CoV-2 Nucleocapsid Protein with TDP-43 Is Dependent on C-Terminus Domains.International journal of molecular sciences · 2024Article
- Neurological Complications of COVID-19: Unraveling the Pathophysiological Underpinnings and Therapeutic Implications.Viruses · 2024Review
- A glimpse into viral warfare: decoding the intriguing role of highly pathogenic coronavirus proteins in apoptosis regulation.Journal of biomedical science · 2024Review
- Human coronavirus OC43 nanobody neutralizes virus and protects mice from infection.Journal of virology · 2024Article
- Review
- Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The notion that an infectious respiratory pathogen can damage the central nervous system (CNS) and lead to neurological disease was tested using a human respiratory coronavirus, the OC43 strain of human coronavirus (HCoV-OC43). First, primary cell cultures were used to determine the susceptibility of each type of neural cells to virus infection. Neurons were the target cells, undergoing degeneration during infection, in part due to apoptosis. Second, neuropathogenicity was investigated in susceptible mice. Intracerebral inoculation of HCoV-OC43 into BALB/c mice led to an acute encephalitis with neuronal cell death by necrosis and apoptosis. Infectious virus was apparently cleared from surviving animals, whereas viral RNA persisted for several months. Some of the animals surviving to acute encephalitis presented an abnormal limb clasping reflex and a decrease in motor activity starting several months post-infection. These results suggest that viral persistence could be associated with an increased neuronal degeneration leading to neuropathology and motor deficits in susceptible individuals.
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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.