Evidence map›Paper›PMID 37537664›Full record

ArticleJournal of neuroinflammation2023

Differential effects of SARS-CoV-2 variants on central nervous system cells and blood-brain barrier functions.

Alizé Proust, Christophe J Queval, Ruth Harvey, Lorin Adams, Michael Bennett, Robert J Wilkinson

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% of its field
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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  15. Infections withFrontiers in aging neuroscience · 2025
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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

6 authors at 1 institution in 2 countries.

Alizé ProustTuberculosis Laboratory, The Francis Crick Institute, London, NW1 1AT, UK. alize.proust@crick.ac.uk.
Christophe J QuevalHigh Throughput Screening Laboratory, The Francis Crick Institute, London, NW1 1AT, UK.
Ruth HarveyWorldwide Influenza Centre, The Francis Crick Institute, London, NW1 1AT, UK.
Lorin AdamsWorldwide Influenza Centre, The Francis Crick Institute, London, NW1 1AT, UK.
Michael BennettWorldwide Influenza Centre, The Francis Crick Institute, London, NW1 1AT, UK.
Robert J WilkinsonTuberculosis Laboratory, The Francis Crick Institute, London, NW1 1AT, UK.
The Francis Crick Institute · GB

Funding

Cancer Research UK CC2112Medical Research Council MR/R006237/1Wellcome Trust CC2112
6 · The paper itself

Abstract

backgroundAlthough mainly causing a respiratory syndrome, numerous neurological symptoms have been identified following of SARS-CoV-2 infection. However, how the virus affects the brain and how the mutations carried by the different variants modulate those neurological symptoms remain unclear.

methodsWe used primary human pericytes, foetal astrocytes, endothelial cells and a microglial cell line to investigate the effect of several SARS-CoV-2 variants of concern or interest on their functional activities. Cells and a 3D blood-brain barrier model were infected with the wild-type form of SARS-CoV-2, Alpha, Beta, Delta, Eta, or Omicron (BA.1) variants at various MOI. Cells and supernatant were used to evaluate cell susceptibility to the virus using a microscopic assay as well as effects of infection on (i) cell metabolic activity using a colorimetric MTS assay; (ii) viral cytopathogenicity using the xCELLigence system; (iii) extracellular glutamate concentration by fluorometric assay; and (iv) modulation of blood-brain barrier permeability.

resultsWe demonstrate that productive infection of brain cells is SARS-CoV-2 variant dependent and that all the variants induce stress to CNS cells. The wild-type virus was cytopathic to all cell types except astrocytes, whilst Alpha and Beta variants were only cytopathic for pericytes, and the Omicron variant cytopathic for endothelial cells and pericytes. Lastly wild-type virus increases blood-brain barrier permeability and all variants, except Beta, modulate extracellular glutamate concentration, which can lead to excitotoxicity or altered neurotransmission.

conclusionsThese results suggest that SARS-CoV-2 is neurotropic, with deleterious consequences for the blood-brain barrier integrity and central nervous system cells, which could underlie neurological disorders following SARS-CoV-2 infection.

Indexed as

COVID-19SARS-CoV-2Blood-Brain BarrierEndothelial CellsGlutamic AcidHumansGlutamic AcidAstrocytesBlood–brain barrierBrainBrain microvascular endothelial cellsCentral nervous systemExcitotoxicityMicrogliaPericytesSARS-CoV-2

Identifiers

PMID37537664
PMCPMC10398935
OpenAlexW4385549237

What Socratic holds

Textmetadata
LicenceCC BY
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.