ReviewBrain, behavior, & immunity - health2020
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and glial cells: Insights and perspectives.
Review in Brain, behavior, & immunity - health, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Genetics of COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review.Annals of clinical and translational neurology · 2022Pooled it
- Central nervous system and systemic inflammatory networks associated with acute neurological outcomes in COVID-19.Scientific reports · 2025Article
- Neurobiology of COVID-19-Associated Psychosis/Schizophrenia: Implication of Epidermal Growth Factor Receptor Signaling.Neuropsychopharmacology reports · 2025Review
- Neurological, psychological, psychosocial complications of long-COVID and their management.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Mapping ACE2 and TMPRSS2 co-expression in human brain tissue: implications for SARS-CoV-2 neurological manifestations.Journal of neurovirology · 2024Article
- Long COVID: From olfactory dysfunctions to viral Parkinsonism.World journal of otorhinolaryngology - head and neck surgery · 2024Article
- MST1/2 exerts a pivotal role in inducing neuroinflammation and Coxsackievirus-A10 replication by interacting with innate immunity.Virology journal · 2024Article
- A Comprehensive Review of COVID-19-Related Olfactory Deficiency: Unraveling Associations with Neurocognitive Disorders and Magnetic Resonance Imaging Findings.Diagnostics (Basel, Switzerland) · 2024Review
- Recombinant SARS-CoV-2 Spike Protein and Its Receptor Binding Domain Stimulate Release of Different Pro-Inflammatory Mediators via Activation of Distinct Receptors on Human Microglia Cells.Molecular neurobiology · 2023Article
- Differential Transcriptomic Landscapes of SARS-CoV-2 Variants in Multiple Organs from Infected Rhesus Macaques.Genomics, proteomics & bioinformatics · 2023Article
- Review
- Human microglial models to study host-virus interactions.Experimental neurology · 2023Review
- Long-Term Effects of SARS-CoV-2 in the Brain: Clinical Consequences and Molecular Mechanisms.Journal of clinical medicine · 2023Review
- Coincident Acute Macular Neuroretinopathy and Paracentral Acute Middle Maculopathy in COVID-19.Turkish journal of ophthalmology · 2023Article
- Review
- Review
- Targeting of neuroinflammation by glibenclamide in Covid-19: old weapon from arsenal.Inflammopharmacology · 2023Review
- The viral hypothesis in Alzheimer's disease: SARS-CoV-2 on the cusp.Frontiers in aging neuroscience · 2023Review
- Association between olfactory dysfunction and mood disturbances with objective and subjective cognitive deficits in long-COVID.Frontiers in psychology · 2023Article
- Pathophysiology and mechanisms of hearing impairment related to neonatal infection diseases.Frontiers in microbiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In December 2019, a pneumonia outbreak was reported in Wuhan, Hubei province, China. Since then, the World Health Organization declared a public health emergency of international concern due to a growing number of deaths around the globe, as well as unparalleled economic and sociodemographic consequences. The disease called coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel form of human coronavirus. Although coronavirus infections have been associated with neurological manifestations such as febrile seizures, convulsions, change in mental status, and encephalitis, less is known about the impact of SARS-CoV-2 in the brain. Recently, emerging evidence suggests that SARS-CoV-2 is associated with neurological alterations in COVID-19 patients with severe clinical manifestations. The molecular and cellular mechanisms involved in this process, as well as the neurotropic and neuroinvasive properties of SARS-CoV-2, are still poorly understood. Glial cells, such as astrocytes and microglia, play pivotal roles in the brain response to neuroinflammatory insults and neurodegenerative diseases. Further, accumulating evidence has shown that those cells are targets of several neurotropic viruses that severely impact their function. Glial cell dysfunctions have been associated with several neuroinflammatory diseases, suggesting that SARS-CoV-2 likely has a primary effect on these cells in addition to a secondary effect from neuronal damage. Here, we provide an overview of these data and discuss the possible implications of glial cells as targets of SARS-CoV-2. Considering the roles of microglia and astrocytes in brain inflammatory responses, we shed light on glial cells as possible drivers and potential targets of therapeutic strategies against neurological manifestations in patients with COVID-19. The main goal of this review is to highlight the need to consider glial involvement in the progression of COVID-19 and potentially include astrocytes and microglia as mediators of SARS-CoV-2-induced neurological damage.
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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.