Evidence map›Paper›PMID 33000221›Full record

ArticleMolecular medicine reports2020

Neuropilin‑1 as a new potential SARS‑CoV‑2 infection mediator implicated in the neurologic features and central nervous system involvement of COVID‑19.

Julie Davies, Harpal S Randeva, Kamaljit Chatha, Marcia Hall, Demetrios A Spandidos, Emmanouil Karteris, Ioannis Kyrou

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 6 pooled it
12.8field-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

122 citing papers in PubMed, 6 syntheses or guidelines pooled it, 175 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. SARS-CoV-2 cell entry beyond the ACE2 receptor.Molecular biology reports · 2022
    Pooled it
  6. Pooled it
  7. Trial
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

62 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Julie DaviesCentre for Genome Engineering and Maintenance, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Harpal S RandevaWarwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK.
Kamaljit ChathaWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.
Marcia HallCentre for Genome Engineering and Maintenance, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Demetrios A SpandidosLaboratory of Clinical Virology, Medical School, University of Crete, 71409 Heraklion, Greece.
Emmanouil KarterisCentre for Genome Engineering and Maintenance, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Ioannis KyrouWarwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK.
Brunel University of London · GBUniversity Hospitals Coventry and Warwickshire NHS Trust · GBUniversity of Crete · GRUniversity of Warwick · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection by the severe acute respiratory syndrome (SARS) coronavirus‑2 (SARS‑CoV‑2) is the cause of the new viral infectious disease (coronavirus disease 2019; COVID‑19). Emerging evidence indicates that COVID‑19 may be associated with a wide spectrum of neurological symptoms and complications with central nervous system (CNS) involvement. It is now well‑established that entry of SARS‑CoV‑2 into host cells is facilitated by its spike proteins mainly through binding to the angiotensin‑converting enzyme 2 (ACE‑2). Preclinical studies have suggested that neuropilin‑1 (NRP1), which is a transmembrane receptor that lacks a cytosolic protein kinase domain and exhibits high expression in the respiratory and olfactory epithelium, may also be implicated in COVID‑19 by enhancing the entry of SARS‑CoV‑2 into the brain through the olfactory epithelium. In the present study, we expand on these findings and demonstrate that the NRP1 is also expressed in the CNS, including olfactory‑related regions such as the olfactory tubercles and paraolfactory gyri. This furthers supports the potential role of NRP1 as an additional SARS‑CoV‑2 infection mediator implicated in the neurologic manifestations of COVID‑19. Accordingly, the neurotropism of SARS‑CoV‑2 via NRP1‑expressing cells in the CNS merits further investigation.

Indexed as

BetacoronavirusBrainCentral Nervous SystemCoronavirus InfectionsCOVID-19Databases, GeneticHumansNeuropilin-1PandemicsPneumonia, ViralReceptors, CoronavirusReceptors, VirusSARS-CoV-2Neuropilin-1Receptors, CoronavirusReceptors, Virus

Identifiers

PMID33000221
PMCPMC7533503
OpenAlexW3084572366

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.