Evidence map›Paper›PMID 35436306›Full record

ArticlePloS one2022

An endogenously activated antiviral state restricts SARS-CoV-2 infection in differentiated primary airway epithelial cells.

Lindsay Broadbent, Connor G G Bamford, Guillermo Lopez Campos, Sheerien Manzoor, David Courtney, Ahlam Ali, Olivier Touzelet, Conall McCaughey, Ken Mills, Ultan F Power

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Mechanisms by which the cystic fibrosis transmembrane conductance regulator may influence SARS-CoV-2 infection and COVID-19 disease severity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  12. iScience · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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

10 authors at 2 institutions in 1 country.

Lindsay BroadbentWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.ORCID 0000-0002-8755-6946
Connor G G BamfordWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
Guillermo Lopez CamposWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
Sheerien ManzoorWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
David CourtneyWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
Ahlam AliWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
Olivier TouzeletWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
Conall McCaugheyRegional Virus Laboratory, Belfast Health and Social Care Trust, Belfast, Northern Ireland, United Kingdom.
Ken MillsPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast, United Kingdom.
Ultan F PowerWellcome-Wolfson Institute for Experimental Medicine, Queens University Belfast, Belfast, Northern Ireland, United Kingdom.
Queen's University Belfast · GBBelfast Health and Social Care Trust · GB

Funding

Department of Health MC_PC_19057Medical Research Council MC_PC_19057
6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of the coronavirus disease-19 (COVID-19) pandemic, was identified in late 2019 and caused >5 million deaths by February 2022. To date, targeted antiviral interventions against COVID-19 are limited. The spectrum of SARS-CoV-2 infection ranges from asymptomatic to fatal disease. However, the reasons for varying outcomes to SARS-CoV-2 infection are yet to be elucidated. Here we show that an endogenously activated interferon lambda (IFNλ1) pathway leads to resistance against SARS-CoV-2 infection. Using a well-differentiated primary nasal epithelial cell (WD-PNEC) culture model derived from multiple adult donors, we discovered that susceptibility to SARS-CoV-2 infection, but not respiratory syncytial virus (RSV) infection, varied. One of four donors was resistant to SARS-CoV-2 infection. High baseline IFNλ1 expression levels and associated interferon stimulated genes correlated with resistance to SARS-CoV-2 infection. Inhibition of the JAK/STAT pathway in WD-PNECs with high endogenous IFNλ1 secretion resulted in higher SARS-CoV-2 titres. Conversely, prophylactic IFNλ treatment of WD-PNECs susceptible to infection resulted in reduced viral titres. An endogenously activated IFNλ response, possibly due to genetic differences, may be one explanation for the differences in susceptibility to SARS-CoV-2 infection in humans. Importantly, our work supports the continued exploration of IFNλ as a potential pharmaceutical against SARS-CoV-2 infection.

Indexed as

COVID-19Respiratory Syncytial Virus InfectionsAntiviral AgentsEpithelial CellsHumansInterferonsJanus KinasesSARS-CoV-2Signal TransductionSTAT Transcription FactorsAntiviral AgentsInterferonsJanus KinasesSTAT Transcription Factors

Identifiers

PMID35436306
PMCPMC9015133
OpenAlexW4225985335

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.