Evidence map›Paper›PMID 33458558›Full record

ReviewPain reports

Neurobiology of SARS-CoV-2 interactions with the peripheral nervous system: implications for COVID-19 and pain.

Amelia J McFarland, Muhammad S Yousuf, Stephanie Shiers, Theodore J Price

Open access · goldAbstract readReview
In one paragraph

Review in Pain reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 4 pooled it
12.4field-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

70 citing papers in PubMed, 4 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Article
  7. Article
  8. Taste dysfunction in Long COVID.bioRxiv : the preprint server for biology · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

10 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

4 authors at 1 institution in 1 country.

Amelia J McFarlandDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, USA.
Muhammad S YousufDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, USA.
Stephanie ShiersDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, USA.
Theodore J PriceDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, USA.
The University of Texas at Dallas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2 is a novel coronavirus that infects cells through the angiotensin-converting enzyme 2 receptor, aided by proteases that prime the spike protein of the virus to enhance cellular entry. Neuropilin 1 and 2 (NRP1 and NRP2) act as additional viral entry factors. SARS-CoV-2 infection causes COVID-19 disease. There is now strong evidence for neurological impacts of COVID-19, with pain as an important symptom, both in the acute phase of the disease and at later stages that are colloquially referred to as "long COVID." In this narrative review, we discuss how COVID-19 may interact with the peripheral nervous system to cause pain in the early and late stages of the disease. We begin with a review of the state of the science on how viruses cause pain through direct and indirect interactions with nociceptors. We then cover what we currently know about how the unique cytokine profiles of moderate and severe COVID-19 may drive plasticity in nociceptors to promote pain and worsen existing pain states. Finally, we review evidence for direct infection of nociceptors by SARS-CoV-2 and the implications of this potential neurotropism. The state of the science points to multiple potential mechanisms through which COVID-19 could induce changes in nociceptor excitability that would be expected to promote pain, induce neuropathies, and worsen existing pain states.

Indexed as

COVID-19NeuropathyNociceptorSARS-CoV-2

Identifiers

PMID33458558
PMCPMC7803673
OpenAlexW3122855943

What OpenQuestion 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 OpenQuestion graph.