Evidence map›Paper›PMID 36007063›Full record

ArticlePLoS pathogens2022

SARS-CoV-2 ORF6 disrupts innate immune signalling by inhibiting cellular mRNA export.

Ross Hall, Anabel Guedán, Melvyn W Yap, George R Young, Ruth Harvey, Jonathan P Stoye, Kate N Bishop

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-weighted citation impact, top 5% 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, 48 citations in OpenAlex.

  1. A multimodaliScience · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. ThebioRxiv : the preprint server for biology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 1 institution in 1 country.

Ross HallRetroviral Replication Laboratory, The Francis Crick Institute, London, United Kingdom.
Anabel GuedánRetroviral Replication Laboratory, The Francis Crick Institute, London, United Kingdom.
Melvyn W YapRetroviral Replication Laboratory, The Francis Crick Institute, London, United Kingdom.
George R YoungBioinformatics and Biostatistics STP, The Francis Crick Institute, London, United Kingdom.
Ruth HarveyWorld Influenza Centre, The Francis Crick Institute, London, United Kingdom.
Jonathan P StoyeRetrovirus-Host Interactions Laboratory, The Francis Crick Institute, London, United Kingdom.
Kate N BishopRetroviral Replication Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0003-3991-614X
The Francis Crick Institute · GB

Funding

Cancer Research UK FC001042Cancer Research UK FC001162Medical Research Council FC001162Medical Research Council MR/W005611/1Wellcome Trust 108012/Z/15/ZWellcome Trust FC001042Wellcome Trust FC001162
6 · The paper itself

Abstract

SARS-CoV-2 is a betacoronavirus and the etiological agent of COVID-19, a devastating infectious disease. Due to its far-reaching effect on human health, there is an urgent and growing need to understand the viral molecular biology of SARS-CoV-2 and its interaction with the host cell. SARS-CoV-2 encodes 9 predicted accessory proteins, which are presumed to be dispensable for in vitro replication, most likely having a role in modulating the host cell environment to aid viral replication. Here we show that the ORF6 accessory protein interacts with cellular Rae1 to inhibit cellular protein production by blocking mRNA export. We utilised cell fractionation coupled with mRNAseq to explore which cellular mRNA species are affected by ORF6 expression and show that ORF6 can inhibit the export of many mRNA including those encoding antiviral factors such as IRF1 and RIG-I. We also show that export of these mRNA is blocked in the context of SARS-CoV-2 infection. Together, our studies identify a novel mechanism by which SARS-CoV-2 can manipulate the host cell environment to supress antiviral responses, providing further understanding to the replication strategies of a virus that has caused an unprecedented global health crisis.

Indexed as

COVID-19SARS-CoV-2Antiviral AgentsHumansImmunity, InnateNuclear Matrix-Associated ProteinsNucleocytoplasmic Transport ProteinsRNA, MessengerViral ProteinsAntiviral AgentsNuclear Matrix-Associated ProteinsNucleocytoplasmic Transport ProteinsORF6 protein, SARS-CoV-2RAE1 protein, humanRNA, MessengerViral Proteins

Identifiers

PMID36007063
PMCPMC9451085
OpenAlexW4293093272

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.