Evidence mapPaperPMID 32878468Full record

ReviewASN neuro

Severe Acute Respiratory Syndrome Coronavirus 2 Impact on the Central Nervous System: Are Astrocytes and Microglia Main Players or Merely Bystanders?

Veronica Murta, Alejandro Villarreal, Alberto J Ramos

Abstract readReview
In one paragraph

Review in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Extracellular Vesicles: The Invisible Heroes and Villains of COVID-19 Central Neuropathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Veronica MurtaLaboratorio de Neuropatología Molecular, Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis," Facultad de Medicina, UBA-CONICET, Universidad de Buenos Aires, Ciudad de Buenos Aires, Argentina.ORCID 0000-0001-7830-351X
Alejandro VillarrealLaboratorio de Neuropatología Molecular, Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis," Facultad de Medicina, UBA-CONICET, Universidad de Buenos Aires, Ciudad de Buenos Aires, Argentina.
Alberto J RamosLaboratorio de Neuropatología Molecular, Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis," Facultad de Medicina, UBA-CONICET, Universidad de Buenos Aires, Ciudad de Buenos Aires, Argentina.ORCID 0000-0003-4009-6337

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With confirmed coronavirus disease 2019 (COVID-19) cases surpassing the 18 million mark around the globe, there is an imperative need to gain comprehensive understanding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the main clinical manifestations of COVID-19 are associated with respiratory or intestinal symptoms, reports of neurological signs and symptoms are increasing. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the central nervous system (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood-brain barrier. Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS rennin-angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for Middle East respiratory syndrome coronavirus (MERS-CoV). Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes, and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to disbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this comprehensive review, we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV; explore the potential role for astrocytes and microglia in the infection and neuroinflammation; and compare them with the previously described human and animal CoV that showed neurotropism to propose possible underlying mechanisms.

Indexed as

BetacoronavirusCoronavirus InfectionsPandemicsPneumonia, ViralAnimalsAstrocytesCentral Nervous SystemCOVID-19HumansInflammationMicrogliaMiddle East Respiratory Syndrome CoronavirusSARS-CoV-2Severe acute respiratory syndrome-related coronaviruscentral nervous systemcoronavirusCOVID-19gliaMERSSARS

Identifiers

PMID32878468
PMCPMC7476346

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 Socratic graph.