Evidence map›Paper›PMID 35746718›Full record

ReviewViruses2022

Characterization of SARS-CoV-2 Evasion: Interferon Pathway and Therapeutic Options.

Mariem Znaidia, Caroline Demeret, Sylvie van der Werf, Anastassia V Komarova

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Review
  3. COVID-19, the disease that changed the world.Medicine and pharmacy reports · 2026
    Review
  4. Article
  5. Article
  6. Acute SARS-CoV-2 infection.Nature reviews. Disease primers · 2025
    Review
  7. Review
  8. Review
  9. Classification and regulatory interactions of key transcription factors in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  10. Review
  11. Unraveled role of TLR7-mediated interferon signaling activation in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

4 authors at 1 institution in 1 country.

Mariem ZnaidiaGénétique Moléculaire des Virus à ARN Unit, Department of Virology, Institut Pasteur, Université Paris Cité, CNRS UMR3569, 75015 Paris, France.
Caroline DemeretGénétique Moléculaire des Virus à ARN Unit, Department of Virology, Institut Pasteur, Université Paris Cité, CNRS UMR3569, 75015 Paris, France.ORCID 0000-0002-1103-6805
Sylvie van der WerfGénétique Moléculaire des Virus à ARN Unit, Department of Virology, Institut Pasteur, Université Paris Cité, CNRS UMR3569, 75015 Paris, France.
Anastassia V KomarovaGénétique Moléculaire des Virus à ARN Unit, Department of Virology, Institut Pasteur, Université Paris Cité, CNRS UMR3569, 75015 Paris, France.ORCID 0000-0002-9998-8447
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. SARS-CoV-2 is characterized by an important capacity to circumvent the innate immune response. The early interferon (IFN) response is necessary to establish a robust antiviral state. However, this response is weak and delayed in COVID-19 patients, along with massive pro-inflammatory cytokine production. This dysregulated innate immune response contributes to pathogenicity and in some individuals leads to a critical state. Characterizing the interplay between viral factors and host innate immunity is crucial to better understand how to manage the disease. Moreover, the constant emergence of new SARS-CoV-2 variants challenges the efficacy of existing vaccines. Thus, to control this virus and readjust the antiviral therapy currently used to treat COVID-19, studies should constantly be re-evaluated to further decipher the mechanisms leading to SARS-CoV-2 pathogenesis. Regarding the role of the IFN response in SARS-CoV-2 infection, in this review we summarize the mechanisms by which SARS-CoV-2 evades innate immune recognition. More specifically, we explain how this virus inhibits IFN signaling pathways (IFN-I/IFN-III) and controls interferon-stimulated gene (ISG) expression. We also discuss the development and use of IFNs and potential drugs controlling the innate immune response to SARS-CoV-2, helping to clear the infection.

Indexed as

COVID-19 Drug TreatmentInterferon Type IAntiviral AgentsHumansImmune EvasionImmunity, InnateInterferonsPandemicsSARS-CoV-2Antiviral AgentsInterferonsInterferon Type Iantagonisminnate immunityinterferonSARS-CoV-2therapyvirus–host interactions

Identifiers

PMID35746718
PMCPMC9231409
OpenAlexW4282831080

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.